Biomedical subjects

A J Buda

Publications and source records attributed to A J Buda.

At least 19 recordsLinked to original sources

PubMed1995

Intracoronary nitric oxide improves postischemic coronary blood flow and myocardial contractile function.

In the present study a novel nitric oxide (NO) donor, CAS-1609, was utilized as a means of coronary NO replenishment in a canine model of myocardial ischemia-reperfusion. Administration of CAS-1609 (1.25 mg iv) 10 min before reperfusion, followed by a 1 mg/h intracoronary infusion throughout the 4.5-h reperfusion period, resulted in significant improvement in postischemic transmural myocardial blood flow (0.66 +/- 0.09 vs. 0.37 +/- 0.08 ml.min-1.g-1 for saline vehicle, P < 0.05). Dogs receiving NO supplementation also exhibited a significant recovery of myocardial contractility after 4.5 h of reperfusion (30 +/- 2% area ejection fraction vs. 22 +/- 2% for saline vehicle, P < 0.05). Moreover, myocardial necrosis as a percentage of the area at risk was reduced from 28.9 +/- 4.3% in the saline group to 8.5 +/- 2.6% in the CAS-1609 group (P < 0.01), while ischemic zone myeloperoxidase activity, indicative of neutrophil infiltration, was also attenuated by 70% with NO therapy. Injection of acetylcholine and nitroglycerin into the left circumflex coronary artery revealed a significant impairment of vasodilator responses in the saline vehicle dogs at 2 h of reperfusion. However, dogs treated with the NO donor demonstrated postischemic vasodilator responses which were similar to baseline (P = not significant vs. baseline). These studies demonstrate that intracoronary administration of NO significantly augments postischemic coronary blood flow and contractile function following ischemia and reperfusion. In addition, NO therapy reduces coronary vascular injury, attenuates myocardial necrosis, and reduces neutrophil infiltration. The cardioprotective actions of intracoronary NO administration may be related to the potent antineutrophil actions of NO.

Animals↗

PubMed1994

Regional effects of myocardial ischemia on epicardially recorded canine first heart sounds.

To determine whether focal changes in myocardial material properties are important in determining the response of first heart sound acceleration amplitude and frequency to myocardial ischemia, cardiac vibrations were simultaneously recorded from ischemic and nonischemic regions of canine epicardium by use of ultralight acceleration transducers. Cardiac acceleration and hemodynamics were recorded before and 5 min, 15 min, 1 h, and 2 h after left circumflex coronary artery occlusion. Peak-to-peak amplitude declined transiently in the nonischemic zone during early occlusion (P < 0.05) but was not decreased at any time in the ischemic myocardium. The median frequency of first heart sound vibrations in the ischemic region increased 31% within 5 min after occlusion (P < 0.01) and remained elevated for 2 h (P < 0.05). Nonischemic zone frequency was not statistically different from baseline at any time point. The disparate regional response of first heart sound vibrational frequency to myocardial ischemia suggests that propagating mechanical transients and myocardial contractile acceleration, rather than resonant vibrations, produce the first heart sound.

Animals↗

PubMed1994

A novel sialyl LewisX analog attenuates neutrophil accumulation and myocardial necrosis after ischemia and reperfusion.

BACKGROUND: Polymorphonuclear leukocytes (PMNs) have been shown to mediate coronary vascular and myocardial tissue injury after coronary artery ischemia and reperfusion. Previous studies using specific monoclonal antibodies directed against P-selectin and L-selectin have demonstrated the involvement of the selectin family of glycoproteins in the early phase of PMN-induced myocardial ischemia-reperfusion injury. We examined the effects of a novel oligosaccharide analog of sialyl LewisX (SLeX), which blocks both P-selectin and E-selectin in an acute canine model of myocardial ischemia and reperfusion. METHODS AND RESULTS: Anesthetized, open-chest dogs were subjected to 1.5 hours of left circumflex coronary artery (LCx) occlusion followed by 4.5 hours of reperfusion and randomly received the SLeX analog CY-1503 (5 mg/kg IV), the nonfucosylated analog of CY-1503, SLN (5 mg/kg IV), or saline 5 minutes before reperfusion. The investigators were blinded to the treatment until all the data analysis was completed. All three groups of dogs exhibited similar and severe reductions in transmural myocardial blood flow in the LCx region as well as pronounced myocardial contractile dysfunction during occlusion, suggesting comparable degrees of myocardial ischemia. After reperfusion, dogs receiving saline (n = 6) displayed an enhanced degree of myocardial injury that was evidenced by a dramatic elevation in plasma creatine kinase (CK) activity, PMN accumulation, and myocardial necrosis. Plasma CK activity increased from 1.9 +/- 0.5 IU/microgram protein at baseline to 73.0 +/- 11.0 IU/micrograms protein (P < .001) at 4.5 hours of reperfusion and myocardial PMN accumulation, as measured by cardiac myeloperoxidase (MPO) activity, and was significantly enhanced (P < .01) within the necrotic zone compared with the nonischemic zone (4.3 +/- 0.6 versus 0.7 +/- 0.1 U/100 mg tissue). After 4.5 hours of reperfusion, 36% of the myocardium within the ischemic zone and 17% of the left ventricle became necrotic in the dogs receiving saline. Treatment with CY-1503 (n = 6) significantly (P < .05) blunted plasma CK activity by more than 50% throughout the reperfusion period, reduced necrotic zone PMN accumulation by 63% (P < .05), and reduced myocardial necrosis in the area at risk by 65% (P < .01) and by 72% within the left ventricle (P < .01). In contrast, administration of the nonfucosylated analog of CY-1503, SLN (n = 6), failed to exert any detectable cardioprotective effects after myocardial ischemia and reperfusion. CONCLUSIONS: Our results provide strong evidence that treatment with a unique carbohydrate analog of SLeX, CY-1503, significantly reduces the degree of myocardial injury associated with coronary artery ischemia and reperfusion. The profound cardioprotection appears to be related to a reduction in PMN accumulation within the ischemic-reperfused myocardium. Additional studies investigating more-prolonged periods of reperfusion are required to determine whether CY-1503 treatment merely delays the onset or actually reduces the full extent of myocardial necrosis after ischemia and reperfusion.

Animals↗

PubMed1992

Rapid reduction of left ventricular hypertrophy in acromegaly after suppression of growth hormone hypersecretion.

OBJECTIVE: To examine the possible role of growth hormone as a pathogenetic factor in the development of myocardial hypertrophy in acromegaly. DESIGN: An uncontrolled clinical trial. SETTING: Tertiary-care medical center. PATIENTS: Sixteen patients with acromegaly were stratified into two groups: Group I (n = 10) had left ventricular hypertrophy (LVH), and group II (n = 6) did not have LVH. INTERVENTION: Therapy with octreotide acetate (SMS 201-995), a long-acting somatostatin analog (mean dose, 538 micrograms/d), was administered for 2 months. MEASUREMENTS: Plasma growth hormone and insulin-like growth factor I (IGF-I) concentrations, hand volume, and echocardiographic left ventricular dimensions and mass were measured at baseline and at 1 week and 2 months after the start of therapy. RESULTS: Before octreotide therapy, both groups had similar hand volumes and similar growth hormone and IGF-I hypersecretion. Both groups showed a reduction in growth hormone at 2 months (mean reduction, 13.7 micrograms/L in patients with LVH [P < 0.01] and 14.1 micrograms/L in patients without LVH [P < 0.05]). Plasma IGF-I was also decreased (mean reduction, 305 micrograms/L in patients with LVH [P < 0.01] and 304 micrograms/L in patients without LVH [P < 0.05]). Reduction of growth hormone and IGF-I hypersecretion in patients with LVH was associated with a rapid decrease in left ventricular mass (339 g to 299 g, P < 0.01) within 1 week, which was sustained at 2 months (274 g, P < 0.04). Patients without LVH showed no statistical change in left ventricular mass. In patients with LVH, the decrease in left ventricular mass correlated with the octreotide-induced decrease in growth hormone (r = 0.79, P less than 0.05) but not with blood pressure. Blood pressure, left ventricular dimensions, and percent of fractional shortening were not altered by therapy in either group. Hand volume decreased in both groups. CONCLUSIONS: Normalization of growth hormone secretion is associated with reduction of left ventricular mass in acromegalic patients with LVH within 1 week of initiating therapy with octreotide.

Acromegaly↗

PubMed1992

Metabolic effects of adenosine on regional myocardial ischemia by phosphorus 31 nuclear magnetic resonance spectroscopy.

The metabolic effects of adenosine on regionally ischemic myocardium were investigated in an open-chest rabbit model by means of phosphorus 31 nuclear magnetic resonance (NMR) spectroscopy. Sixteen anesthetized New Zealand white rabbits were subjected to thoracotomy; a reversible snare occluder was placed around a large branch of the left circumflex coronary artery, and an NMR surface coil was positioned adjacent to the myocardium perfused by this vessel. The animals were placed in a 2.0 T CSI spectrometer (GE Medical Systems, Fremont, Calif.), and baseline spectra were acquired. Eight animals were treated with intravenous adenosine (25 mg/kg), and eight rabbits served as control subjects. All animals were subjected to a 10-minute period of ischemia followed by a period of reperfusion. NMR spectra were acquired during both intervals. During the occlusion period, expected increases in inorganic phosphate levels and decreases in phosphocreatine levels were observed in both groups; however, inorganic phosphate increased less in adenosine-treated animals (adenosine: 33 +/- 2.8% total spectral area during occlusion vs control: 41 +/- 3.1%) and phosphocreatine diminished less with adenosine (adenosine: 26 +/- 3% vs control: 13 +/- 1.2%; p < 0.002). No significant differences were seen in beta-adenosine triphosphate levels. In both groups the metabolite levels during reperfusion recovered to near baseline values, although phosphocreatine remained slightly higher in the treated group during early reperfusion. An apparent cardioprotective effect of adenosine on relative phosphocreatine and inorganic phosphate levels can be observed in intact rabbits by means of phosphorus 31 NMR spectroscopy.

Adenosine↗

PubMed1992

Ischemic expansion during acute myocardial infarction and reversal by coronary reperfusion.

Previous studies have shown that infarct expansion occurs at least 1 day after a large transmural infarction. To assess whether regional left ventricular expansion is evident within hours of an acute myocardial infarction, 25 adult mongrel dogs underwent left circumflex coronary artery occlusion for 2 hours and 22 of these were subsequently reperfused. Two-dimensional echocardiography was used to record left ventricular topography and function at baseline, at 2 hours of occlusion, and following reperfusion. Short-axis midpapillary echocardiograms were analyzed using a microcomputer digitizing routine by establishing a 360-degree circumferential map of the left ventricle. The central ischemic zone was defined as that region with the most depressed contractility after 2 hours of occlusion, and the normal zone was set at 180 degree away from the central ischemic zone. Endocardial and epicardial segment lengths and wall thickness were measured for both the normal zone and the central ischemic zone at end diastole. After 2 hours of occlusion, diastolic central ischemic endocardial (1.3 +/- 0.05 to 1.42 +/- 0.04 cm, p less than 0.01) and central ischemic epicardial (1.84 +/- 0.06 to 1.93 +/- 0.06 cm, p less than 0.05) segment lengths were significantly increased. There were no significant changes in segment lengths or wall thickness in the normal zone. After 2 hours of occlusion, there was significant diastolic left ventricular (LV) dilatation (LV area increased from 18.2 +/- 1.3 to 21.0 +/- 1.3 cm2, p less than 0.01). Furthermore, central ischemic endocardial and epicardial segment length changes from baseline to occlusion correlated significantly with LV dilatation (r = 0.56, p less than 0.003; r = 0.55, p less than 0.004 respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1992

Time-frequency transforms: a new approach to first heart sound frequency dynamics.

This study employed a new analytical tool, the Binomial joint time-frequency transform, to test the hypothesis that first heart sound frequency rises during the isovolumic contraction period. Cardiac vibrations were recorded from eight open chest dogs using an ultralight accelerometer cemented directly to the epicardium of the anterior left ventricle. The frequency response of the recording system was flat +/- 3 dB from 0.1 to 400 Hz. Three characteristic time-frequency spectral patterns were evident in the animals investigated: 1) A frequency component that rose from approximately 40-140 Hz in a 30-50 ms interval immediately following the ECG R-wave. 2) A slowly varying or static frequency of 60-100 Hz beginning midway through the isovolumic contraction period. 3) Broad-band peaks occurring at the time of the Ia and Ib high frequency components. The presence of rapid frequency dynamics limits the usefulness of stationary analysis techniques for the first heart sound. The Binomial transform provided much better resolution than the spectrograph or spectrogram, the two most common non-stationary signal analysis techniques. By revealing the onset and dynamics of first heart sound frequencies, time-frequency transforms may allow mechanical assessment of individual cardiac structures.

Animals↗

PubMed1992

Effect of reduction in myocardial edema on myocardial blood flow and ventricular function after coronary reperfusion.

The contribution of myocardial edema to the no-reflow phenomenon, left ventricular functional recovery, and infarct size after coronary occlusion and reperfusion is uncertain. To examine this, we studied 26 open-chest dogs after coronary occlusion and reperfusion. Twelve dogs received hypertonic mannitol 30 min before reperfusion, which increased serum osmolality (P less than 0.01 vs. control). Fourteen control dogs received a similar volume of saline that had no effect on serum osmolality. Tissue biopsies of central ischemic and normal myocardial areas were analyzed by proton nuclear magnetic resonance relaxation spectroscopy to assess edema content. Hypertonic mannitol resulted in a significant decrease in ischemic tissue T1 (767.0 +/- 16.3 vs. 818.6 +/- 19.0 ms, P less than 0.05) compared with the control group. Despite this, no significant differences were found between the mannitol and control groups in 4-h reperfusion subendocardial blood flow or left ventricular wall thickening. In addition, mannitol administered before reperfusion did not modify infarct size compared with the control group (infarct/risk area, 41.0 +/- 1.4 vs. 37.9 +/- 1.9%, P not significant). In conclusion, no benefit is produced in reperfusion blood flow or functional recovery by reducing edema in postischemic myocardial tissue. This suggests that mechanisms other than myocardial edema are responsible for myocardial no reflow and contractile dysfunction after coronary reperfusion. Furthermore, hypertonic mannitol administered before reperfusion does not reduce infarct size.

Animals↗

PubMed1991

Changes in left ventricular diastolic filling during the development of left ventricular hypertrophy: observations using Doppler echocardiography in a unique canine model.

To examine changes in diastolic left ventricular filling during the development of left ventricular hypertrophy, serial pulsed Doppler echocardiographic studies were performed in a canine model of left ventricular hypertrophy induced by neurogenic pressor episodes. This model is unique since left ventricular hypertrophy develops without sustained hypertension. The neurogenic pressor episodes produced progressive increases in left ventricular mass of 17% by 3 weeks (p less than 0.03) and 23% by 9 weeks (p less than 0.001). During the course of hypertrophy development, there were no changes in resting heart rate, blood pressure, left ventricular volumes or ejection fraction, or end-systolic wall stress. However, peak early filling (peak E) velocity decreased from 65 +/- 5 cm/sec to 53 +/- 4 cm/sec by 3 weeks (p less than 0.05) and remained depressed at 9 weeks. In addition, peak E/A (the ratio of early to late peak filling) decreased by 3 weeks (p less than 0.01) and the contribution of atrial filling to total left ventricular diastolic filling increased by 9 weeks (p less than 0.005). There were significant correlations between the changes in left ventricular mass and the change in peak E velocity at 3 weeks (r = -0.92, p less than 0.001) but not at 9 weeks. These data indicate that left ventricular filling abnormalities occur early in the course of the development of left ventricular hypertrophy, are not a result of loading alterations related to sustained hypertension, and do not change significantly following increasing stages of hypertrophy.

Animals↗

PubMed1991

Transmural distribution of myocardial edema by NMR relaxometry following myocardial ischemia and reperfusion.

To determine the distribution and extent of myocardial edema resulting from ischemia and reperfusion, seven open-chest dogs underwent occlusion of the left circumflex coronary artery for 2 hours (group I), and 10 underwent occlusion for 2 hours and reperfusion for 2 hours (group II). Proton nuclear magnetic resonance spectroscopy (T1 and T2 relaxation times) and percent water content were determined to quantitate the amount of edema. There was a transmural increase of the T1 relaxation time of the central ischemic zone in groups I and II, although this increase was significantly greater in group II in both the subendocardium (group I = 707.8 +/- 12.5 msec, group II = 813.2 +/- 36.2 msec; p less than 0.01) and subepicardium (group I = 641.7 +/- 20.5 msec, group II = 760.5 +/- 34.7 msec; p less than 0.01). These increases were also observed in the T2 weighted relaxation time in the subendocardium (group I = 54.7 +/- 0.8 msec, group II = 78.7 +/- 6.3 msec; p less than 0.005) and subepicardium (group I = 54.0 +/- 1.4 msec, group II = 73.1 +/- 4.0 msec; p less than 0.001). Transmural differences were evident between the myocardial layers with increased T1 relaxation times (p less than 0.01) in the subendocardium in both groups. Similar increases were noted in the percent water content of the myocardium. Thus T1 and T2 relaxation times lengthened with an increase in myocardial water content following occlusion, and these relaxation times were augmented by reperfusion. We conclude that ischemia-induced edema occurs in a transmural distribution from subendocardium to subepicardium following occlusion, and this edema is further enhanced by reperfusion.

Animals↗

PubMed1991

Effect of coronary reocclusion after initial reperfusion on ventricular function and infarct size.

Reocclusion of a coronary artery after thrombolytic therapy occurs in approximately 12% to 33% of patients; however, there are few experimental data concerning reocclusion. Accordingly, to compare the effects of reocclusion versus sustained occlusion on the myocardium, a canine model (n = 12) of 2 h of left circumflex artery occlusion, 1 h of reperfusion and 1 h of reocclusion was studied. In a control group (n = 11), 3 h of circumflex artery occlusion was followed by 1 h of reperfusion. As a result, both groups had the same total duration of ischemia (3 h) and reperfusion (1 h). Hemodynamic measurements, radioactive microsphere injections and two-dimensional echocardiography were performed at baseline, occlusion and reperfusion for both groups and at the end of reocclusion for the experimental group. In vivo risk area was determined with Evans blue dye and infarct size with triphenyltetrazolium staining methods. Similar decreases in myocardial blood flow after coronary occlusion and similar reperfusion blood flows occurred in both groups. Despite intervening reperfusion in the reocclusion group, no significant difference was found in the infarct size/risk area ratio between the reocclusion and control groups (54.5 +/- 6.9% vs. 48.4 +/- 5.1%, respectively, p = NS). Two-dimensional echocardiography demonstrated a similar degree and extent (159 +/- 9 degrees vs. 153 +/- 12 degrees, p = NS) of left ventricular dysfunction with both the occlusion and reocclusion. In addition, there were no significant differences in global or regional left ventricular function between the two groups. However, reocclusion after reperfusion did produce a further deterioration in ischemic zone wall thickening (9.5 +/- 2.0% to 0.7 +/- 1.8%, p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1991

Intravascular ultrasound imaging of vascular responsiveness in isolated perfused canine arteries.

We investigated the feasibility of using intravascular ultrasound imaging to analyze vascular physiology in various arterial beds. Canine superficial femoral, external iliac, and common carotid arteries were harvested and suspended and perfused in a bath of oxygenated, heated, physiologic salt solution. A 6-Fr, 20-MHz ultrasound imaging catheter was inserted into the lumen of the arteries and serial images were acquired after bolus injections of either serotonin or normal saline into the extravascular bathing medium. Serotonin resulted in a significant time- and dose-dependent decrease in cross-sectional area in muscular femoral arteries (P less than .001): -5.2% with 10(-8) M serotonin, -15% with 10(-7) M, and -28% with 10(-6) M. Histologically transitional iliac arteries demonstrated less marked changes, while elastic carotid arteries demonstrated no significant changes. Our results indicate that intravascular ultrasound may be used to quantify and differentiate responses to vasoconstrictive agents in different vascular beds.

Animals↗

PubMed1991

The role of echocardiography in the evaluation of mechanical complications of acute myocardial infarction.

With the introduction of the coronary care unit and more effective therapy for primary life-threatening arrhythmias, cardiogenic shock and the mechanical complications of acute myocardial infarction are now responsible for the majority of in-hospital deaths. These mechanical complications, which include myocardial rupture of the left ventricular free wall, rupture of the ventricular septum, and rupture of the papillary muscle, are estimated to account for 25,000 fatalities yearly in the United States. Although the mechanism of myocardial rupture has not been clearly defined, there is increasing evidence that infarct expansion, which can be readily detected by two-dimensional echocardiography, may be an important pathophysiologic factor. The ready availability of echocardiography in the coronary care unit has made a major impact on the immediate diagnosis of mechanical complications in the hemodynamically compromised patient with acute myocardial infarction. In particular, two-dimensional and Doppler echocardiographic techniques have been extremely useful in the identification and localization of ventricular septal rupture. In addition, papillary muscle rupture can be readily diagnosed by Doppler approaches and is easily distinguished from ventricular septal rupture. In view of increasing evidence that early surgical intervention is indicated in these patients, these echocardiographic approaches offer the surgeon prompt diagnostic and anatomic information. Unfortunately, rupture of the free wall of the left ventricle often results in sudden death within minutes before echocardiographic evaluation can be attempted. Nevertheless, rapid echocardiographic diagnosis provides the patient with the possibility of potential life-saving resuscitative interventions before immediate surgery. Thus, over the past decade, echocardiography has become a vital tool in the diagnosis and evaluation of patients with mechanical complications of acute myocardial infarction. The development of Doppler techniques, color flow Doppler, and esophageal approaches should further enhance our diagnostic abilities and allow careful monitoring of patients before, during, and after surgical repair. It is hoped that with the improvements in echocardiographic evaluation of mechanical rupture and more rapid surgical intervention, future studies will demonstrate better surgical results with good long-term survival in patients with myocardial rupture.

Diagnosis, Differential↗

PubMed1990

Transient left ventricular filling abnormalities (diastolic stunning) after acute myocardial infarction.

A variety of experimental studies suggest that diastolic left ventricular (LV) function changes after acute myocardial infarction (AMI), but limited data exist on these changes in humans. To assess diastolic filling after AMI, 60 patients underwent Doppler echocardiographic examination within 24 hours of AMI. Of 54 patients who also underwent catheterization, 45 (83%) were successfully reperfused. A subgroup of 17 patients underwent a follow-up Doppler examination at 7 days after infarction, whereas 15 patients with stable exertional angina served as control subjects. There was no significant difference in age, gender, incidence of systemic hypertension or diabetes mellitus, heart rate, mean arterial pressure or severity of coronary artery disease between the infarct and control groups. The infarct group had a lower velocity time integral total (9.9 +/- 0.4 cm vs 12.0 +/- 0.9 cm, p less than 0.001), a lower velocity time integral E (5.8 +/- 0.3 cm vs 6.8 +/- 0.5 cm, p less than 0.01) and a lower velocity time integral 0.333 (3.5 +/- 0.4 cm vs 6.1 +/- 0.5 cm, p less than 0.01) than the control group. In addition, velocity time integral A/total was significantly greater in the infarction group (0.44 +/- 0.03 vs 0.35 +/- 0.04, p less than 0.01) compared to the control group. The follow-up subgroup showed an increase in velocity time integral total (p less than 0.01), velocity time integral E (p less than 0.05) and velocity time integral 0.333/total (p less than 0.05) over the first 7 days after infarction. The final recovery values at 7 days were not significantly different from those of the coronary artery disease group.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1990

Evaluation of myocardial viability following ischemic and reperfusion injury using phosphorus 31 nuclear magnetic resonance spectroscopy in vivo.

Recovery of myocardial high-energy phosphate (HEP) metabolism after coronary occlusion and reperfusion may vary with ischemic duration and may provide information about the extent of tissue viability. To evaluate the differences between varying durations of ischemia and to attempt to identify metabolic indexes of salvaged viable tissue, intact New Zealand white rabbits underwent either 30 (group 1; n = 8) or 60 (group 2; n = 8) minutes of coronary occlusion followed by reperfusion. HEP metabolism was evaluated with cardiac gated phosphorus 31 (31P) nuclear magnetic resonance (NMR) spectroscopy with a 2.0 T spectrometer. While similar HEP changes were observed during ischemia in both groups, differences in HEP recovery between groups were seen following reperfusion. Group 1 animals demonstrated a gradual decrease in inorganic phosphates (Pi) (p less than 0.05 versus group 2), an immediate recovery of phosphocreatine (PCr) (p = ns versus baseline), and a gradual increase of adenosine triphosphate (ATP) to pre-ischemic levels. Group 2 animals had elevated levels of Pi (p less than 0.05 versus baseline; p less than 0.05 versus group 1), slow recovery of PCr, and continued reduction of ATP (p less than 0.05 versus baseline; p less than 0.05 versus group 1). Group 1 rabbits had a greater extent of viable myocardium than group 2 (77.1 +/- 9.7% of risk area versus 39.4 +/- 9.4%; p less than 0.001). Significant correlations were found between PCr and Pi reperfusion values and myocardial viability (r = 0.59, p less than 0.05; r = 0.73, p less than 0.01, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1990

Augmentation of regional function in nonischemic myocardium during coronary occlusion measured with two-dimensional echocardiography.

Increased regional left ventricular function frequently occurs in the nonischemic myocardium after acute coronary occlusion. To further define the regional and global effects of this increased remote function in the ischemic left ventricle, 22 dogs were studied with two-dimensional echocardiography before and 1 h after left circumflex coronary artery occlusion. Two groups of dogs were identified with and without compensatory increased regional left ventricular function, defined as regional wall thickening in the nonischemic zone greater than 2 SD above baseline. After coronary occlusion, nonischemic wall thickening was 76 +/- 15% in the hyperfunction group (n = 11) and 45 +/- 14% in the nonhyperfunction group (n = 11) (p less than 0.001). Despite similar left ventricular end-diastolic cavity areas and equivalent degrees of ischemic wall thinning, dogs with increased left ventricular function in the nonischemic myocardium had a smaller extent of circumferential left ventricular dysfunction (136 +/- 33 versus 170 +/- 43 degrees, p less than 0.001) and a higher area ejection fraction (38 +/- 9% versus 27 +/- 6%, p less than 0.001). These functional differences occurred despite similar myocardial areas at risk by autoradiography (41 +/- 6% versus 37 +/- 12%, p = NS). The data suggest that increased left ventricular function in the nonischemic myocardium determines the global functional impact of acute coronary occlusion and, through interaction with adjacent myocardium, modifies the extent of circumferential left ventricular dysfunction.

Animals↗

PubMed1990

The effects of propranolol on regional cardiac metabolism during ischemia and reperfusion assessed by magnetic resonance spectroscopy.

Sixteen anesthetized New Zealand white rabbits were subjected to thoracotomy, and a reversible snare occluder was attached around a large branch of the left circumflex coronary artery. A 1.3 cm. diameter nuclear magnetic resonance (NMR) surface coil was placed adjacent to the myocardium perfused by this vessel. The animals were divided into two groups of eight animals each, treatment and control. The rabbits were studied using a 2.0 T magnetic resonance (MR) spectrometer, and baseline spectra were acquired. The treatment animals then received intravenous propranolol (1.5 mg/kg) and the control animals received an equal volume of saline. Spectra were then acquired during a 20-minute occlusion period and during subsequent reperfusion. Animals in both groups showed expected decreases in phosphocreatine and adenosine triphosphate and an increase in inorganic phosphate during occlusion; these changes reverted toward baseline values with reperfusion. There were no significant differences between the two groups. The myocardium became acidotic during occlusion in both groups, but significantly more so in the control animals: during the first 10 minutes of occlusion pH was 7.30 +/- 0.41 in the treatment group versus 6.55 +/- 0.24 for controls (p = 0.0005). During the second 10 minutes of occlusion pH was 7.05 +/- 0.65 in the treatment group versus 6.24 +/- 0.25 in controls (p = 0.0053). We conclude that attenuation of intracellular acidosis by propranolol during myocardial ischemia was evident by MR spectroscopy in this animal model.

Animals↗

PubMed1989

Importance of overweight in studies of left ventricular hypertrophy and diastolic function in mild systemic hypertension.

The relations of Metropolitan Life Insurance Co. Relative Weight values and blood pressure (BP) to minimal forearm vascular resistance, ventricular septal and posterior wall thickness, left ventricular (LV) mass index and cardiac diastolic function were assessed in 31 men, 37 +/- 2 (mean +/- standard error of the mean) years of age. Eighteen patients with untreated mild hypertension were compared with 13 normotensive control subjects of similar age and weight. The hypertensives had higher clinic (137 +/- 3/96 +/- 2 vs 121 +/- 4/81 +/- 3 mm Hg, p less than 0.001/less than 0.001) and home (p less than 0.001) BP. Despite higher BP, the hypertensives did not have significantly greater values than normotensives, respectively, for minimal forearm vascular resistance (2.20 +/- 0.12 vs 2.04 +/- 0.11 U), ventricular septal (9.9 +/- 0.5 vs 10.2 +/- 0.3 mm) and posterior wall thickness (10.2 +/- 0.4 vs 10.0 +/- 0.3 mm) or LV mass index (106 +/- 6 vs 107 +/- 6 g/m2). Furthermore, diastolic peak filling rate, an index of LV diastolic function, was virtually identical in the 2 groups (2.71 +/- 0.14 vs 2.69 +/- 0.07 liters/s, difference not significant). Correlates of peak filling rate included relative weight (r = -0.62, p less than 0.001), posterior wall thickness (r = -0.51, p less than 0.01) and age (r = -0.45, p less than 0.05). Relative weight also correlated significantly with posterior wall (r = 0.59, p less than 0.005), ventricular septal (r = 0.47, p less than 0.005) and LV mass index (r = 0.38, p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗