Biomedical subjects

F G Spinale

Publications and source records attributed to F G Spinale.

At least 145 records · Page 8Linked to original sources

PubMed1994

Myocardial effects of repetitive episodes of rapid ventricular pacing in conscious dogs: surgical creation, echocardiographic evaluation, and morphometric analysis.

The interactions of the systemic and myocardial adaptations during and after rapid ventricular pacing, a model of heart failure, were assessed in conscious, unstressed dogs. Ultrasonic probes and vascular catheters were surgically implanted into dogs for measurements of blood flows and pressures during 3 weeks of pacing and after 2 months of recovery. Three weeks of tachycardia (260 beats/min) resulted in a marked reduction in hemodynamic parameters and left ventricular dilatation, with caudal wall thinning throughout the pacing period and 1 week of recovery. Sinus rhythm resumed after the pacer was turned off, with return toward normal in hemodynamic parameters; however, left ventricular dilatation and ventricular remodeling, with significant fibrosis, loss of myocytes, and hypertrophy of the surviving cells were still present after 2 months of recovery. In conclusion, even though hemodynamic parameters normalized during recovery, adaptive myocardial remodeling caused permanent ventricular fibrosis, hypertrophy, and increased cardiac filling pressures.

Animals↗

PubMed1994

The novel effects of 3,5,3'-triiodo-L-thyronine on myocyte contractile function and beta-adrenergic responsiveness in dilated cardiomyopathy.

Medical management of patients with chronic left ventricular dysfunction continues to be a difficult problem. Recent clinical and experimental studies have suggested that 3,5,3'-triiodo-L-thyronine improves left ventricular pump function. However, whether 3,5,3'-triiodo-L-thyronine directly improves myocyte contractile function in cardiomyopathic states is unknown. Accordingly, this study examined the direct effects of 3,5,3'-triiodo-L-thyronine on isolated myocyte contractile function in cardiocytes obtained from control (n = 6) pigs and pigs with tachycardia-induced dilated cardiomyopathy (atrial pacing at 240 beats/min for 3 weeks; n = 6). Myocyte percent shortening and velocity of shortening were obtained at baseline and in the presence of 3,5,3'-triiodo-L-thyronine doses of 80 and 100 pmol/L. For both control and dilated cardiomyopathy groups, 3,5,3'-triiodo-L-thyronine caused a significant increase in myocyte contractile function. For example, a 100 pmol/L dose of 3,5,3'-triiodo-L-thyronine increased myocyte velocity of shortening by 51% in control myocytes and by 54% in dilated cardiomyopathy myocytes compared with baseline. A second series of experiments was performed to determine whether 3,5,3'-triiodo-L-thyronine altered the responsiveness of the beta-adrenergic receptor system in control and dilated cardiomyopathy myocytes. Myocyte contractile function was examined during beta-adrenergic stimulation with isoproterenol alone and in myocytes preincubated with 3,5,3'-triiodo-L-thyronine doses of 80 and 100 pmol/L to which isoproterenol was added. Isoproterenol alone increased velocity of shortening by 139% in control and by 233% in dilated cardiomyopathy myocytes compared with baseline. This was significantly greater than the increase with 3,5,3'-triiodo-L-thyronine alone. 3,5,3'-triiodo-L-thyronine followed by isoproterenol increased velocity of shortening by 245% in control and 313% in dilated cardiomyopathy myocytes compared with baseline. This was significantly greater than the response with 3,5,3'-triiodo-L-thyronine or isoproterenol alone and appeared to be greater than an additive response. The results from this study clearly demonstrated that 3,5,3'-triiodo-L-thyronine directly augmented myocyte contractile function in both control and dilated cardiomyopathy myocytes. In addition, 3,5,3'-triiodo-L-thyronine enhanced the contractile response to beta-adrenergic stimulation in dilated cardiomyopathy. This study provides unique evidence to suggest that 3,5,3'-triiodo-L-thyronine may be a useful adjunct to conventional inotropic support in the setting of advanced left ventricular dysfunction.

Animals↗

PubMed1994

The direct effects of protamine sulfate on myocyte contractile processes.

The use of protamine sulfate in patients has been associated with circulatory collapse and is suspected to directly depress left ventricular function. However, the cellular basis for these changes that occur after protamine administration are unknown. Accordingly, the first objective of this study was to determine the direct effects of protamine on isolated myocyte contractile function. Myocytes were isolated from porcine hearts and contractile function was examined at baseline and then after the administration of protamine in concentrations of 20, 40, or 80 micrograms/ml. These concentrations were chosen because they reflect the serum concentrations of protamine commonly obtained in patients. The presence of protamine resulted in a dose-dependent decline in myocyte contractile function. For example, in the presence of a 20 microgram/ml concentration of protamine myocyte contractile function did not change significantly from baseline values, whereas an 80 microgram/ml protamine concentration caused myocyte percent and velocity of shortening to fall by more than 35% from baseline values. In light of the fact that protamine directly depressed myocyte contractile function, a second objective of this study was to examine potential cellular mechanisms responsible for this effect. Accordingly, in the next series of experiments, the effects of protamine on the myocyte sarcolemmal beta-adrenergic receptor system were examined by measuring myocyte contractile function with the beta-adrenergic agonist isoproterenol (25 nmol/L), as well as with the concomitant addition of protamine and isoproterenol. In the presence of protamine, myocyte beta-adrenergic responsiveness was significantly reduced. For example, in the presence of an 80 microgram/ml dose of protamine, both myocyte percent and velocity of shortening fell by greater than 50% when compared with isoproterenol alone values (p < 0.05). To determine the reversibility of these protamine effects, we performed additional experiments in the presence of heparin. Incubation with heparin before protamine addition prevented the negative effects of protamine on myocyte function. However, the addition of heparin after protamine incubation failed to reverse the negative effects of protamine on myocyte function. In a final set of experiments, the effects of protamine on isolated myocyte electrophysiologic properties were examined using microelectrode techniques at baseline and with either 40 or 80 micrograms/ml doses of protamine. Myocyte resting membrane potential changed from baseline with the addition of a 40 micrograms/ml dose of protamine (-79.2 +/- 0.5 versus -75.2 +/- 0.8 mV (p < 0.05), with no further change at an 80 micrograms/ml dose of protamine (-73.0 +/- 1.3 mV).(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗

PubMed1994

The relation between latissimus dorsi skeletal muscle structure and contractile function after cardiomyoplasty.

Past reports suggest that structural changes within the latissimus dorsi muscle occur with chronic electrical stimulation during cardiomyoplasty. However, the specific changes in the structure of the latissimus dorsi muscle and the relation to muscle contractile function with cardiomyoplasty are unknown. Accordingly, this study examined regional changes in latissimus dorsi muscle structure and function after cardiomyoplasty. The left latissimus dorsi muscle was mobilized and wrapped around the heart in pigs with the use of standardized techniques and the latissimus dorsi muscle chronically paced at ambient heart rates (90 beats/min; 20 Hz, 5 V amplitude, n = 6). After 6 weeks, the paced latissimus dorsi muscle and the contralateral control muscle were removed and divided into proximal (0 to 3 cm), middle (3 to 6 cm), and distal (6 to 12 cm) regions. By computer-assisted morphometry, muscle cell myofibril volume, cross-sectional area, and collagen percent area were determined. In the paced latissimus dorsi muscle, myofibril volumes increased by more than 50% in the proximal and middle regions compared with those in the contralateral control muscle. However, myofibril volumes were significantly lower in the distal region of the paced latissimus dorsi muscle compared with those in control muscles (33% +/- 5% versus 20% +/- 3%, p < 0.05). In the paced latissimus dorsi muscle, cross-sectional area was significantly reduced from that of control muscles in all regions. A further reduction in cross-sectional area was noted in the distal region of the paced latissimus dorsi muscle compared with that in both the contralateral control muscle and the proximal and middle regions of the paced latissimus dorsi muscle. Collagen content significantly increased in the paced latissimus dorsi muscle compared with that in control muscle with a more fibrotic pattern observed in the distal region. Latissimus dorsi muscle strips (less than 2 mm2 cross-sectional area) were harvested, and peak and velocity of tension development were examined after field electrical stimulation at 0.2 to 1.2 Hz. At 0.2 Hz, the velocity of tension development was unchanged in the paced latissimus dorsi muscle compared with that in control muscle. However, peak tension development degraded by only 28% in the paced latissimus dorsi muscles but fell by 51% in control muscles with increased stimulation frequencies. In summary, the contractile function of the chronically stimulated latissimus dorsi muscle was associated with fatigue resistance and increased contractile protein content. However, more distal regions of the paced latissimus dorsi muscle demonstrated atrophy and fibrosis.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1994

Hypothermic potassium cardioplegia impairs myocyte recovery of contractility and inotropy.

Acute postoperative left ventricular dysfunction after hypothermic, crystalloid potassium cardioplegia occasionally occurs. This project examined myocyte contractility and inotropic responsiveness after hypothermic arrest with and without potassium cardioplegia. Isolated swine left ventricular myocytes were placed in a thermostatically controlled chamber (37 degrees C) that contained a standard cell medium, pulse stimulated at 1 Hz, and steady-state contractions were measured by computer-assisted video microscopy with and without isoproterenol (25 nmol/L). After baseline measurements were taken the myocytes were randomly assigned to the following treatments: (1) control group with infusion of 37 degrees C crystalloid solution and maintained at 37 degrees C for 3 hours (n = 23), (2) hypothermia group with infusion of 4 degrees C crystalloid without potassium and stored at 4 degrees C for 3 hours (n = 22), (3) hypothermic cardioplegia group with infusion of a crystalloid cardioplegia (oxygenated, buffered 4 degrees C Ringer's solution with 24 mEq/L K+) and then stored at 4 degrees C for 3 hours (n = 35). After treatment the myocytes were then rewarmed to 37 degrees C by infusion of medium, and contractile measurements were repeated. In the control group, the percent and velocity of shortening were identical to those in baseline measurements: 6.4% +/- 0.4% and 53 +/- 5 microns/sec, respectively, and these values remained unchanged in the hypothermia group: 6.5% +/- 0.4% and 51 +/- 3 microns/sec, respectively. However, in the hypothermic cardioplegia group, the percent and velocity of shortening were significantly lower with rewarming: 4.8% +/- 0.4% and 35 +/- 3 microns/sec, respectively, p < 0.05). Isoproterenol caused increased percent and velocity of shortening in both the control and hypothermia groups: 10.0% +/- 0.6% and 9.5% +/- 0.9% and 81.6 +/- 8 microns/sec and 71.4 +/- 8 microns/sec, respectively. This response was significantly blunted in the cardioplegia group (8.9% +/- 0.8% and 56.9 +/- 7 microns/sec, p < 0.05). With an isolated myocyte system that is independent of extracellular and perfusion effects, hyperkalemic cardioplegic solution resulted in depressed myocyte contractile performance after rewarming. Potassium cardioplegia also caused a blunted inotropic responsiveness on rewarming. A potential contributory factor for the depressed left ventricular function after the use of potassium cardioplegia is a direct depression in myocyte contractility.

Analysis of Variance↗

PubMed1993

The cellular basis for the blunted response to beta-adrenergic stimulation in supraventricular tachycardia-induced cardiomyopathy.

Chronic tachycardia-induced dilated cardiomyopathy causes increased plasma catecholamines and alterations in beta-adrenergic responsiveness in vivo. However, whether isolated myocyte contractile response to beta-stimulation is directly affected by the development of cardiomyopathy and how these changes are related to alterations in the beta-adrenergic receptor system remain unclear. Accordingly, isolated myocyte function and beta-adrenergic responsiveness were examined in two groups of 12 pigs each: sham controls, and with supraventricular tachycardia induced cardiomyopathy (SVT; pace: 240 beats/min, 3 weeks). Isolated LV myocyte percent and velocity of shortening were examined at baseline, with isoproterenol (2-100 nM), and forskolin (0.1-4 microM). Baseline percent and velocity of shortening were significantly reduced with SVT compared to controls (1.6 +/- 0.1 vs 5.4 +/- 0.2%, 56 +/- 3 vs 25 +/- 1 micron/s, respectively, P < 0.05). The maximal increase in the percent and velocity of shortening with isoproterenol was significantly blunted in the SVT myocytes compared with controls (3.2 +/- 0.4 vs 9.7 +/- 1.0%, 48.0 +/- 5.3 vs 122.6 +/- 15.5 micron/s, respectively, P < 0.05). Similarly, maximal increase in the percent and velocity of shortening with forskolin were reduced with SVT compared to controls (3.3 +/- 0.4 vs 10.5 +/- 0.6%, 50.7 +/- 6.4 vs 120.1 +/- 9.7 micron/s, respectively, P < 0.05). In order to determine the cellular basis for these changes in beta-adrenergic response, myocyte structure, sarcolemmal beta-receptor density and affinity, and adenylate cyclase activity were examined. There was a 25% reduction in beta-receptor number with SVT (P < 0.05) but no change in affinity. Basal adenylate cyclase activity was lower with SVT compared to control (46 +/- 3 vs 77 +/- 10 pmol cyclic AMP/mg/min, P < 0.05), and exhibited a blunted response with both isoproterenol (1 mM; 106 +/- 19 vs 203 +/- 26 pmol cyclic AMP/mg/min, P < 0.05) and forskolin (100 microns: 209 +/- 35 vs 378 +/- 58 pmol cyclic AMP/mg/min, P < 0.05). Finally, myofibrillar content within SVT myocytes was significantly reduced from controls (43 +/- 7 vs 63 +/- 4%, P < 0.05). In summary, the cellular basis for the depressed myocyte contractile response to beta-stimulation with tachycardia induced SVT are probably due to several factors which include: decreased expression of beta-receptors, alterations in beta-receptor transduction, reduced adenylate cyclase activity, and decreased myocyte contractile protein content.

Adenylyl Cyclases↗

PubMed1993

Effects of cardiomyoplasty on biventricular function in canine chronic heart failure.

Dynamic cardiomyoplasty, the use of skeletal muscle to assist the heart, is a new therapy for the treatment of heart failure. However, the effects of cardiomyoplasty on biventricular function and the synchrony of ventricular contraction are not fully known. We assessed the efficacy of latissimus dorsi muscle (LDM) dynamic cardiomyoplasty in a chronic model of biventricular failure. Five dogs received doxorubicin (1 mg.kg-1.wk-1) for up to 12 weeks to induce heart failure and then underwent a biventricular cardiomyoplasty. After operation, the muscle was progressively stimulated according to an established protocol. When training was complete (10 weeks), radionuclide ventriculographic and catheterization data were obtained. Peak left ventricular (LV) systolic pressure and its first derivative were unchanged, whereas LV end-diastolic pressure decreased slightly with LDM assistance (11.0 +/- 1.6 to 9.6 +/- 1.5 mm Hg; p < 0.05). Right ventricular (RV) systolic pressure increased significantly with LDM assistance from 21 +/- 2 to 26 +/- 3 mm Hg (p < 0.05), whereas its first derivative and RV end-diastolic pressure were unchanged. Dynamic cardiomyoplasty significantly improved LV ejection fraction from 0.18 +/- 0.07 without LDM assistance to 0.31 +/- 0.05 with LDM assistance (p < 0.05); similarly RV ejection fraction increased from 0.32 +/- 0.07 to 0.45 +/- 0.06 with LDM assistance (p < 0.05). The temporal sequence of LV wall motion was assessed by phase analysis of the radionuclide ventriculograms. With skeletal muscle assistance, standard deviation ("spread") decreased from 31.6 +/- 17.4 to 20.0 +/- 15.4 degrees (p < 0.06), whereas skewness ("symmetry") was unchanged. Dynamic cardiomyoplasty improved both LV and RV ejection fractions without increasing diastolic pressure.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1993

Comparison of three blood-processing techniques during and after cardiopulmonary bypass.

The return of extracorporeal circuit blood at the termination of cardiopulmonary bypass is an important feature of blood conservation during open heart procedures. However, the relative benefits and disadvantages of different circuit blood salvage methods remain unclear. Accordingly, the purpose of this study was to examine whether quantifiable differences exist between three different circuit blood-salvaging techniques: direct infusion, centrifugation, and ultrafiltration. Sixty patients with very similar preoperative characteristics were randomly assigned to each of the three groups, and blood coagulation screens, plasma profiles, and respiratory function were determined at 20 minutes and at 6 and 18 hours after cardiopulmonary bypass. Early after cardiopulmonary bypass (20 minutes), the plasma colloid osmotic pressure and fibrinogen and platelet concentrations were significantly higher with ultrafiltration (p < 0.05) versus those observed for the other two methods. The plasma thromboplastin times were significantly (p < 0.05) longer after cardiopulmonary bypass with centrifugation as compared to direct infusion and ultrafiltration. However, the coagulation profiles and plasma composition normalized by 18 hours after cardiopulmonary bypass with all three blood-salvaging methods. There were no significant differences in terms of blood utilization or chest tube drainage over the entire postoperative period among any of the circuit blood-salvaging methods. These results suggest that ultrafiltration of postcardiopulmonary circuit blood may preserve plasma colloid pressure and platelet concentration in the early postoperative period, but these differences do not persist. Thus, for routine cardiopulmonary bypass procedures, direct infusion, centrifugation, and ultrafiltration may all be satisfactory methods of circuit blood salvage.

Blood Coagulation Tests↗

PubMed1993

Assessment of right ventricular contractile performance after pulmonary resection.

Right ventricular (RV) performance deteriorates after pulmonary resection. The mechanism remains unclear and could be related to changes in loading conditions or contractility. To assess the role of alteration in RV contractility, we developed a simple and reliable means to measure RV contractile performance in adult patients. Using thermodilution methods and rapid volume infusion in the preoperative setting, the relationship between RV stroke work (RVSWI) and end-diastolic volume (RVEDVI), termed the preload recruitable stroke work relation, was plotted using linear regression. Experimental studies have demonstrated that the preload recruitable stroke work relation is a linear and load-insensitive index of RV contractile performance. Our study confirms this finding in adult patients: RVSWI = 0.33 (RVEDVI) - 20.4 (n = 108; r = 0.94; p < 0.01). Examination of RV pump function and hemodynamic parameters in the early postresection period (up to 24 hours postoperatively) revealed significant changes in loading conditions, but isochronal RVEDVI and RVSWI values were within the confidence limits of the preload recruitable stroke work relation. Thus, depressed RV contractility does not appear to play a predominant role in this early postoperative period. Further study in a larger patient population will be required to verify this observation and to assess RV performance beyond 24 hours after resection.

Female↗

PubMed1993

Contractile properties of isolated porcine ventricular myocytes.

OBJECTIVE: The aim was to examine the structure, function, and inotropic responsiveness of isolated porcine myocytes. METHODS: Left ventricular myocytes were harvested from six pigs with normal echocardiographic and pressure indices of left ventricular function: fractional shortening 30 (SEM 2)%, peak+dP/dt 1225(110) mm Hg.s-1, end diastolic pressure 7(2) mm Hg, and cardiac output 2.8(0.5) litres.min-1. Indices of myocyte contractility were examined using a computer assisted video edge detection system which included the percent and velocity of myocyte shortening. Myocyte contractions were recorded by alternating field stimulation at 1 Hz and measurements performed in the presence of 2-10 mM extracellular Ca2+. Contractile properties of isolated porcine myocytes were examined unattached (n = 20) or following attachment to a basement membrane substrate (n = 63). RESULTS: Left ventricular myocytes were successfully obtained from all pigs with a 68% average yield of viable myocytes. Isolated myocyte length was 128(6) microns with an average profile surface area of 2226(51) microns 2 (coefficients of variation of 25% and 35% respectively). Electron microscopic examination showed normal cytoarchitecture with 62(4)% myofibrils by volume. Baseline extent and velocity of shortening for unattached myocytes was 6.2% and 77(10) microns.s-1 respectively. Baseline extent and velocity of shortening for myocytes adherent to a basement substrate were 4.9(0.4)% and 64(7) microns.s-1. These indices of myocyte contractile function increased from baseline values for both the unattached and attached cells with increased extracellular Ca2+. CONCLUSIONS: Isolated porcine left ventricular myocytes retain normal cytoarchitecture and composition, respond to field stimulation, and are responsive to extracellular Ca2+. Myocytes adherent to a basement membrane substrate were capable of contracting against this resistive load.

Animals↗

PubMed1993

Cardiocyte contractile performance in experimental biventricular volume-overload hypertrophy.

Previous studies have shown that the right ventricle (RV) appears to tolerate volume overloading better than does the left ventricle (LV). To determine whether this dichotomous response is due to intrinsic differences in the contractile performance of volume hypertrophied RV vs. LV cardiac muscle cells, or cardiocytes, we characterized the contractile performance of cardiocytes isolated from an experimental feline model of biventricular volume overload (n = 7 cats), wherein a peripheral arteriovenous fistula (AVF) produced an identical duration and degree of volume overload for both ventricles; sham-operated cats served as the appropriate controls (n = 7). Cardiocyte contractile function was defined by laser diffraction measurement of sarcomere motion. For the AVF cats, there was a 2.4-fold increase in cardiac output, a significant increase in the RV and LV weight-to-body weight ratios, and a significant increase in cell surface area for the RV and LV cardiocytes. Despite this, cardiocyte contractile function in the AVF cats was entirely normal. Thus there was no significant difference between RV and LV cardiocytes from control cats in the extent or velocity of sarcomere shortening either in 1 cP superfusate or in higher viscosity superfusates, and comparison of RV and LV cells from the AVF cats to those from sham-operated cats again revealed no significant differences. Furthermore, cardiocyte relengthening properties showed no significant differences between AVF and control groups. In summary, this study shows that contractile dysfunction is not an inherent property of either RV or LV cardiac muscle cells hypertrophying in response to substantial volume overloading when preload is increased but afterload is normal.

Animals↗

PubMed1993

Cell and sarcomere contractile performance from the same cardiocyte using video microscopy.

The relationship between whole cell and sarcomere contractile performance from within the same myocyte remains unclear. In the present study, the dynamic properties of whole cell and sarcomere contractile performance were examined from the same myocyte by computer-assisted video microscopy. Isolated canine left ventricular myocytes were field stimulated at 1 Hz, and whole cell and sarcomere contractile performance was measured in the unloaded unattached state (n = 16) and after attachment to a basement membrane substrate (n = 18). Whole cell and sarcomere contractile measurements were obtained immediately on initiation of electrical stimulation as well as at steady state, after which measurements were repeated in the presence of 25 nM isoproterenol. Video-microscopic images of whole cell and sarcomere contractions were obtained at final magnifications of x1,100 and x5,500, respectively. By use of a 240-Hz high-scan-rate charge-coupled device camera and a video-based edge-detection system synchronized with the camera video output, the myocyte and sarcomere motion data were digitized. Steady-state percentage and velocity of shortening for whole cells and sarcomeres were 4.75 +/- 0.30% and 56.50 +/- 2.37 microns/s and 8.63 +/- 0.60% and 2.24 +/- 0.46 microns/s, respectively, for the attached myocytes and 8.63 +/- 0.48% and 71.38 +/- 6.14 microns/s and 11.73 +/- 3.22% and 2.72 +/- 0.62 microns/s, respectively, for the unattached myocytes. With the initiation of electrical stimulation, the extent of the shortening-velocity of relengthening relationship increased in a linear fashion for the attached (whole cell, r = 0.87; sarcomere, r = 0.90; both P < 0.001) and unattached myocytes (whole cell, r = 0.83; sarcomere, r = 0.88; both P < 0.001). In all experiments, isoproterenol significantly increased the slope of these linear relationships (P < 0.01). Furthermore, the relationship between whole cell and sarcomere velocity of shortening was highly linear (r > 0.91, P < 0.001). In summary, this study demonstrated that the video-based edge-detection technique could be adapted to measure cell and sarcomere contractile performance from the same myocyte. Furthermore, a significant linear relationship exists between whole cell and sarcomere contractile dynamics with alterations in both load and inotropic state.

Animals↗

PubMed1993

Identification of patients at risk for excessive blood loss during coronary artery bypass surgery: thromboelastography versus coagulation screen.

In light of the potential morbidity associated with transfusion of blood products, a reliable preoperative screening test to identify cardiothoracic surgical patients who are at potential risk for increased intraoperative blood loss would be useful. Accordingly, we examined the efficacy of a variety of coagulation tests to predict intraoperative blood loss in 60 patients presenting for coronary artery bypass surgery (CABG). A complete coagulation screen, activated clotting time (ACT), and thromboelastograph (TEG) were performed before surgery. Intraoperative blood loss was determined by weighing sponges and measuring the quantity of blood in suction canisters. The duration of cardiopulmonary bypass was 100 +/- 4 min, and total surgery time was 5.0 +/- 0.1 h. Total crystalloid and colloid requirements were 5.5 +/- 0.2 and 1.4 +/- 0.1 L. Forty-eight percent of the patients required blood with an average requirement of 2.5 +/- 0.5 units. Total intraoperative blood loss averaged 1590 +/- 95 mL with a range from 640 to 3928 mL. Using multiple linear regression, all coagulation and TEG variables were used to model perioperative blood loss. Results showed that all components of the TEG failed to predict blood loss (r < 0.25, P > 0.78). However, three components of the routine coagulation assay, including bleeding time, prothrombin time, and platelet count could be modeled to predict perioperative blood loss (r = 0.75, P < 0.05). Although TEG has been shown to have potential in identifying postcardiopulmonary bypass coagulopathies, these results suggest that it does not appear to be useful in determining the coagulation status of CABG patients preoperatively.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

PubMed1993

Structural basis for changes in left ventricular function and geometry because of chronic mitral regurgitation and after correction of volume overload.

Left ventricular function and myocyte structure were examined in three groups of dogs: (1) 3 months of mitral regurgitation caused by chordal rupture (n = 7); (2) chronic mitral regurgitation followed by mitral valve replacement and a 3-month recovery period (n = 7), and (3) sham controls (n = 8). The left ventricular end-systolic stiffness constant (Kess) was measured as an index of left ventricular contractile function with stress-strain relationships obtained by cinecatheterization. Isolated myocyte structure and composition were examined with computer-assisted morphometry and nuclear area computed with deoxyribonucleic acid fluorescence. Left ventricular contractile function was significantly depressed with chronic mitral regurgitation compared with control values (Kess, 2.1 +/- 0.1 versus 3.6 +/- 0.2; p < 0.05) and returned to control values with mitral valve replacement (3.8 +/- 0.2). Left ventricular mass significantly increased in both the mitral regurgitation and mitral valve replacement groups compared with control values (121 +/- 10, 120 +/- 5 versus 95 +/- 9 gm, respectively; p < 0.05). Myocyte length increased with mitral regurgitation beyond control values (194 +/- 4 versus 218 +/- 8 microns; p < 0.05) and increased beyond mitral regurgitation values after mitral valve replacement (231 +/- 7 microns; p < 0.05). Myocyte volume with mitral regurgitation increased slightly beyond control values (33.5 +/- 0.7 versus 37.6 +/- 1.3 microns3; p = 0.15) and significantly increased with mitral valve replacement (40.1 +/- 1.2 microns3; p < 0.05). Myocyte myofibril volume significantly declined with mitral regurgitation compared with control values (14.8 +/- 1.5 versus 22.2 +/- 0.7 microns3; p < 0.05) and significantly increased beyond both mitral regurgitation and control values with mitral valve replacement (27.1 +/- 1.1 microns3; p < 0.05). Myocyte nuclear area with mitral regurgitation remained unchanged from control values (1430 +/- 122 versus 1163 +/- 89 microns2) but increased significantly with mitral valve replacement (2209 +/- 250 microns2; p < 0.05). In summary, the left ventricular contractile dysfunction with chronic mitral regurgitation is accompanied by increased myocyte length and reduced myofibril content. In contrast, the left ventricular hypertrophy and improved left ventricular pump function with mitral valve replacement were due to increased myocyte volume and increased contractile protein content.

Animals↗

PubMed1992

Effect of pulmonary resection on right ventricular function.

The effect of pulmonary resection on right ventricular (RV) performance and its possible contribution to morbidity or mortality remain unclear. Using thermodilution methods and a fast-response thermistor positioned in the pulmonary artery, it is now possible to measure RV end-diastolic volume and RV ejection fraction. Using this technique, RV performance during and after major pulmonary resection was studied in 15 patients. Significant RV dysfunction was demonstrated in the postoperative period. Right ventricular end-diastolic volume increased significantly on postoperative day 1 (177 +/- 9 mL) and postoperative day 2 (172 +/- 4 mL) versus early postoperatively (153 +/- 10 mL) (p less than 0.05). By postoperative day 2, RV ejection fraction was significantly decreased (0.36 +/- 0.03) from preoperative (0.45 +/- 0.02) and early postoperative (0.40 +/- 0.01) values (p less than 0.05). Although pulmonary artery pressures rose modestly in the postoperative period, and pulmonary vascular resistance increased by postoperative day 2, pulmonary vascular resistance remained significantly lower or unchanged from baseline values. We speculate that the etiology of the RV dysfunction after pulmonary resection may be multifactorial. Changes in RV afterload or alteration in RV contractility may be factors.

Adult↗

PubMed1992

Retrograde versus antegrade cardioplegia: impact on right ventricular function.

Retrograde cardioplegia administered through the coronary sinus has several documented advantages over antegrade cardioplegia but has been thought to provide inadequate right ventricular myocardial protection. We prospectively compared the effects of retrograde and antegrade cardioplegia on right ventricular performance in patients undergoing myocardial revascularization. Two groups of similar age, extent of disease, and preoperative left ventricular ejection fraction received retrograde (n = 16) or antegrade (n = 14) crystalloid cardioplegia. A right ventricular rapid-response thermistor catheter, previously developed and validated in our institution, was used to measure right atrial pressure, pulmonary artery pressure, right ventricular ejection fraction, end-diastolic volume index, and stroke volume index before bypass (baseline) and at several intervals after bypass. There were no differences in cross-clamp time, heart rate, cardiac enzymes, inotrope requirements, or arrhythmias between the two groups. Right ventricular parameters were equivalent in both groups at all time intervals except 30 minutes after bypass, at which time right ventricular end-diastolic volume index was lower (80 +/- 6 versus 93 +/- 6 mL/m2; p less than 0.05) and right ventricular stroke volume index was higher (35 +/- 3 versus 29 +/- 2 mL/m2, p less than 0.05) in the retrograde group compared with the antegrade group, indicating better right ventricular function with retrograde cardioplegia early after bypass. In both groups, right ventricular end-diastolic volume index was higher than baseline (p less than 0.05) during the first 4 hours after bypass. No other important differences were found.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

PubMed1992

Myocardial Na+,K(+)-ATPase in tachycardia induced cardiomyopathy.

Na+,K(+)-ATPase is a major determinant of myocyte homeostasis and excitation-contraction. Cardiac glycosides such as digitalis and ouabain increase the inotropic state of the heart through the inhibition of Na+,K(+)-ATPase. While cardiac glycosides are commonly used in the setting of congestive heart failure, optimal therapy would depend upon an intact Na+,K(+)-ATPase system. Changes in Na+,K(+)-ATPase activity and glycoside receptor density with the development of cardiomyopathy have not been well defined. Accordingly, left ventricular (LV) function and Na+,K(+)-ATPase activity and glycoside binding were examined in 7 pigs with dilated cardiomyopathy and in 7 controls. Dilated cardiomyopathy was produced by pacing induced supraventricular tachycardia (SVT) for 3 weeks at 240 bpm. Left ventricular function was examined by simultaneous echocardiography and catheterization. Left ventricular fractional shortening significantly decreased with SVT (34 +/- 2 vs. 10 +/- 2%, P less than 0.05) and LV diastolic dimension and pressure significantly increased (3.8 +/- 0.3 vs. 5.1 +/- 0.4 cm, and 8 +/- 2 vs. 27 +/- 2 mmHg, respectively, P less than 0.05) as compared to controls. Na+,K(+)-ATPase activity was assayed as potassium dependent p-nitrophenol-phosphatase activity. Glycoside receptor density (Bmax) and affinity (KD) was determined using [3H]-ouabain binding assays. Na+,K(+)-ATPase activity, Bmax, and KD all significantly fell from control values with SVT induced cardiomyopathy (0.64 +/- 0.06 vs. 0.45 +/- 0.12 micrograms pNP/mg/h, 5.5 +/- 0.4 vs. 1.9 +/- 0.4 pmol/mg, and 15 +/- 3 vs. 9 +/- 3 nM, respectively, P less than 0.05). The distribution of Na+,K(+)-ATPase in LV sections taken from control and SVT hearts were examined using immunohistochemical techniques. A patchy distribution of Na+,K(+)-ATPase along the sarcolemma in SVT sections was observed as opposed to a more uniform distribution in control myocytes. There was no observable change in the relative content and distribution of the Na+,K(+)-ATPase isoforms alpha 2 and alpha 3 in the SVT sections as compared to controls. In an additional set of experiments, changes in LV as well as isolated myocyte responsiveness to ouabain were examined. Left ventricular fractional shortening and peak dP/dt were measured following administration of 20-60 micrograms/Kg of ouabain in control (n = 3) and SVT (n = 3) pigs. In the control group, 40 micrograms/Kg caused a 25% in LV fractional shortening and a 60% increase in peak dP/dt from baseline. Cumulative doses of 60 micrograms/Kg in the control pigs resulted in over a 75% increase in peak dP/dt from baseline values.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1992

Effect of chronic supraventricular tachycardia on left ventricular function and structure in newborn pigs.

OBJECTIVES: The purpose of this study was to examine the effects of supraventricular pacing tachycardia on left ventricular function and myocardial structure in newborn, immature pigs and to determine whether immature pigs respond to supraventricular tachycardia differently from adults. BACKGROUND: Previous studies have shown that supraventricular tachycardia causes dilated cardiomyopathy in adult animals; however, in humans, supraventricular tachycardia-induced congestive heart failure occurs most frequently in children and newborns. Because some clinical diseases may cause myocardial failure in adults but rarely do so in children, it was hypothesized that the effects of supraventricular tachycardia in newborns may be different from those in adults. METHODS: In two groups of newborn swine (3 weeks of age), left ventricular volume, mass and function were assessed with simultaneous echocardiography and cardiac catheterization and myocardial structure was examined with light and electron microscopy. Six piglets underwent 3 weeks of left atrial pacing tachycardia (240 beats/min) and six littermates served as a control group. Both groups were followed up for 3 weeks. RESULTS: At the end of the protocol, left ventricular dimensions increased in the piglets with supraventricular tachycardia compared with values in the control group, but there were no differences in left ventricular mass. Systolic function, assessed by fractional shortening, peak ejection rate and maximal rate of pressure development, was decreased in the group with supraventricular tachycardia. The fractional shortening-end-systolic stress relation in the piglets with supraventricular tachycardia decreased below normal values. Left ventricular diastolic function assessed by the relaxation time constant was prolonged, the peak filling rate was decreased and left ventricular stiffness was increased in the supraventricular tachycardia group. The morphologic data demonstrated that supraventricular tachycardia did not change total myocyte volume but did decrease total myofibrillar volume. CONCLUSIONS: Supraventricular tachycardia caused dilated cardiomyopathy in immature pigs. These changes in left ventricular function were associated with a decrease in cellular contractile proteins. Thus, the effects of supraventricular tachycardia on left ventricular function and structure in immature animals were comparable to previous findings in mature animals.

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