PubMed Health⌕ Search

Biomedical subjects

B H Dorman

Publications and source records attributed to B H Dorman.

At least 19 recordsLinked to original sources
PubMed1997

Potassium channel opener-augmented cardioplegia: protection of myocyte contractility with chronic left ventricular dysfunction.

BACKGROUND: An increased number of patients with preexisting left ventricular (LV) dysfunction and congestive heart failure (CHF) are undergoing cardiac surgery with a higher risk for decreased LV contractility after hyperkalemic cardioplegic arrest. Activation of adenosine triphosphate-sensitive potassium channels by potassium channel openers (PCO) within the myocyte appears to confer a protective effect in the setting of ischemia. Accordingly, the present study was designed to determine whether PCO supplementation during hyperkalemic cardioplegic arrest would provide protective effects on myocyte contractile function, particularly in the setting of CHF. METHODS AND RESULTS: LV myocytes were isolated from control pigs (n=7) and pigs with CHF (rapid pacing, 240 beats per minute; n=7) and then assigned to the following treatment groups: normothermia (cell culture media, 2 hours, 37 degrees C); cardioplegia (24 mEq/L K+, 2 hours, 4 degrees C; then 10 minutes of reperfusion); or PCO/cardioplegia (cardioplegia supplemented with 100 micromol/L of the PCO aprikalim). Myocyte velocity of shortening was reduced in both control (66+/-2 versus 33+/-1 microm/s) and CHFmyocytes (32+/-1 versus 22+/-1 microm/s) after hyperkalemic cardioplegic arrest (P<.05). Contractility after PCO cardioplegia was similar to normothermic values in control (57+/-2 microm/s) and CHF (33+/-1 microm/s) myocytes (P<.05). Intracellular free Ca2+ increased from normothermia during hyperkalemic cardioplegia in control (81+/-4 to 145+/-7 nmol/L) and CHF (262+/-30 to 823+/-55 nmol/L) myocytes (P<.05). PCO cardioplegia attenuated the intracellular increase in free Ca2+ during the cardioplegic interval in control (110+/-6 nmol/L) and CHF (383+22 nmol/L) myocytes (P<.05). CONCLUSIONS: PCO-augmented cardioplegic arrest preserved myocyte contractility and reduced the intracellular free Ca2+ release, which therefore may be of particular benefit in the setting of preexisting LV dysfunction.

Animals↗
PubMed1997

Preservation of myocyte contractile function after hyperthermic cardioplegic arrest by activation of ATP-sensitive potassium channels.

BACKGROUND: Left ventricular (LV) dysfunction can occur after hyperkalemic cardioplegic arrest and subsequent reperfusion and rewarming. Activation of adenosine triphosphate (ATP)-sensitive potassium (KATP) channels within the myocyte sarcolemma has been shown to be cardioprotective for myocardial reperfusion injury and ischemia and may play a contributory role in preconditioning for cardioplegic arrest. Accordingly, the present study tested the hypothesis that cardioplegic arrest and activation of KATP channels by a potassium channel opener (PCO) would attenuate alterations in ionic homeostasis and improve myocyte contractile function. METHODS AND RESULTS: Porcine LV myocytes were isolated and randomly assigned to the following treatment groups: normothermic control, incubation in cell culture media for 2 hours at 37 degrees C (n=60); hyperkalemic cardioplegia, incubation for 2 hours in hypothermic hyperkalemic cardioplegic solution (n=60); or PCO/cardioplegia, incubation in cardioplegic solution containing 100 micromol/L of the PCO aprikalim (n=60). Hyperkalemic cardioplegia and rewarming caused a significant reduction in myocyte velocity of shortening compared with normothermic control values (33+/-2 versus 66+/-2 microm/s, P<.05). Cardioplegic arrest with PCO supplementation significantly improved indices of myocyte contractile function when compared with hyperkalemic cardioplegia (58+/-4 microm/s, P<.05). Myocyte intracellular calcium increased during hyperkalemic cardioplegic arrest compared with baseline values (147+/-2 versus 85+/-2 nmol/L, P<.05). The increase in intracellular calcium was significantly reduced in myocytes exposed to the PCO-supplemented cardioplegic solution (109+/-4 nmol/L, P<.05). CONCLUSIONS: Cardioplegic arrest with simultaneous activation of KATP channels preserves myocyte contractile processes and attenuates the accumulation of intracellular calcium. These findings suggest that changes in intracellular calcium play a role in myocyte contractile dysfunction associated with cardioplegic arrest. Moreover, alternative strategies may exist for preservation of myocyte contractile function during cardioplegic arrest.

Animals↗
PubMed1997

Negative and selective effects of propofol on isolated swine myocyte contractile function in pacing-induced congestive heart failure.

BACKGROUND: Although propofol (2-6 di-isopropylphenol) is commonly used to induce and maintain anesthesia and sedation for surgery, systematic hypotension and reduced cardiac output can occur in patients with or without intrinsic cardiac disease. The effect of propofol on myocyte contractility after the development of congestive heart failure (CHF) remains unknown. This study tested the hypothesis that propofol would have direct effects on myocyte contractile function in both healthy and CHF cardiac myocyte preparations. METHODS: Isolated left ventricular (LV) myocyte contractile function (shortening velocity, micron/s) was examined in myocytes from five control pigs and in five pigs with pacing-induced CHF (240 beats/min, for 3 weeks) in the presence of propofol concentrations ranging from 1-6 micrograms/ml. In addition, myocyte contractility in response to beta-adrenergic receptor stimulation (isoproterenol, 10-50 nM) in the presence of propofol (3 micrograms/ml) was examined. RESULTS: Three weeks of pacing caused LV dysfunction consistent with CHF as evidenced by increased LV end-diastolic diameter (control 3.3 +/- 0.1 cm vs. CHF 5.6 +/- 0.2 cm; P < 0.05) and reduced LV fractional shortening (control 34 +/- 3% vs. CHF 12 +/- 2%, P < 0.05). Propofol (6 micrograms/ml) caused a concentration-dependent negative effect on velocity of shortening from baseline in both control (67 +/- 2 microns/s vs. 27 +/- 3 microns/s; P < 0.05) and CHF myocytes (29 +/- 1 microns/s vs. 15 +/- 1 microns/s; P < 0.05). Importantly, CHF myocytes were more sensitive than control myocytes to the negative effects of propofol on velocity of shortening at the lower concentration (1 microgram/ml). beta-adrenergic responsiveness was reduced by propofol (3 micrograms/ml) in control myocytes only. CONCLUSIONS: Propofol has a direct and negative effect on basal myocyte contractile processes in the setting of CHF, which is more pronounced than that on healthy myocytes at reduced propofol concentrations.

Adrenergic beta-Agonists↗
PubMed1996

Contributory mechanisms for the beneficial effects of myocyte preconditioning during cardioplegic arrest.

BACKGROUND: Preconditioning protects the myocardium from ischemia and may be a potent means of endogenous cardioprotection during cardioplegic arrest and rewarming. However, fundamental mechanisms that potentially contribute to the beneficial effects of preconditioning during cardioplegic arrest and rewarming remain unclear. Accordingly, the overall goal of the present study was to examine the potential mechanisms by which preconditioning protects myocyte contractile function during simulated cardioplegic arrest and rewarming. METHODS AND RESULTS: Left ventricular isolated porcine myocyte contractile function was examined with the use of videomicroscopy under three conditions: (1) normothermia, maintained in cell medium (37 degrees C) for 2 hours; (2) simulated cardioplegic arrest and rewarming, incubated in crystalloid cardioplegic solution (24 mEq/L K+, 4 degrees C) for 2 hours followed by normothermic reperfusion; and (3) preconditioning/cardioplegic arrest and rewarming, hypoxia (20 minutes) and reoxygenation (20 minutes) followed by simulated cardioplegic arrest and rewarming. Cardioplegic arrest and rewarming caused a decline in steady-state myocyte shortening velocity compared with normothermic controls (22.0 +/- 1.6 versus 57.2 +/- 2.6 microns/s, respectively, P < .05), which was significantly improved with preconditioning (36.1 1.7 microns/s, P < .05). In the next series of experiments, the influence of nonmyocyte cell populations with respect to preconditioning and cardioplegic arrest was examined. Endothelial or smooth muscle cell cultures were subjected to a period of hypoxia (20 minutes) and reoxygenation (20 minutes) and the eluent incubated with naive myocytes, which were then subjected to simulated cardioplegic arrest and rewarming. Pretreatment with the eluent from endothelial cultures followed by cardioplegic arrest and rewarming improved myocyte function compared with cardioplegia-alone values (31.7 +/- 2.2 versus 24.7 +/- 1.6 microns/s, respectively, P < .05), whereas smooth muscle culture eluent pretreatment resulted in no change (23.7 +/- 4.0 microns/s, P = .81). Molecular mechanisms for the protective effects of preconditioning on myocyte contractile processes with cardioplegic arrest and rewarming were examined in a final series of experiments. Adenosine-mediated pathways or ATP-sensitive potassium channels were activated by augmenting cardioplegic solutions with adenosine (200 mumol/L) or the potassium channel opener aprikalim (100 mumol/L), respectively. Both adenosine and aprikalim augmentation significantly improved myocyte function compared with cardioplegia-alone values (53.5 +/- 1.7, 57.6 +/- 2.0 versus 25.7 +/- 1.4 microns/s, respectively, P < .05). CONCLUSIONS: The unique findings from the present study demonstrated that preconditioning provides protective effects on myocyte contractile processes independent of nonmyocyte cell populations and that these effects are mediated in part through the activation of adenosine pathways or ATP-sensitive potassium channels. Thus, preconditioning adjuvant to cardioplegia may provide a novel means of protecting myocardial function after cardioplegic arrest and rewarming.

Adenosine↗
PubMed1996

Mechanisms of right ventricular dysfunction after pulmonary resection.

BACKGROUND: Significant right ventricular (RV) dysfunction as measured by increased end-diastolic volume and reduced ejection fraction has been documented in the postoperative period after pulmonary resection. We hypothesized that changes in RV contractile state or afterload may contribute to this RV pump dysfunction. METHODS: In part one of the study, RV preload was altered on postoperative day 2 (n = 6) by rapid infusion of Hespan to a total of 250, 500, and 1,000 mL. The relationship between RV stroke work and end-diastolic volume was plotted using linear regression. This preload recruitable stroke work relation had been previously validated as a load-insensitive index of RV contractility. The slopes of the preoperative relation (n = 35) and postoperative relation were compared. In part two of the study, RV afterload was reduced by continuous infusion of prostaglandin E1 (n = 6) through postoperative day 2 and RV pump function was assessed. RESULTS: Comparison of the slopes of the preload recruitable stroke work relation plotted preoperatively and on postoperative day 2 revealed no significant difference, indicating no change in RV contractile state. Infusion of prostaglandin E1 in the postoperative period (n = 6) significantly reduced pulmonary vascular resistance (3.67 +/- 0.19 versus baseline 5.72 +/- 0.19 dyne . s . cm-5/ m2; p < 0.05). However, RV ejection fraction remained significantly reduced (0.34 +/- 0.01 versus baseline 0.42 +/- 0.01; p < 0.05) and end-diastolic volume significantly increased (105 +/- 5 versus baseline 93 +/- 2 mL/m2; p < 0.05). Heart rate was increased compared with baseline throughout the postoperative period. CONCLUSIONS: The present study suggests that RV dysfunction after pulmonary resection is not caused by primary alterations in contractility or immediate changes in afterload. Better control of heart rate with minimal effect on inotropy may enhance RV pump function.

Alprostadil↗
PubMed1996

Direct effects of oxygenated crystalloid or blood cardioplegia on isolated myocyte contractile function.

UNLABELLED: The majority of myocardial protective techniques performed in the United States incorporate hypothermic, hyperkalemic blood or crystalloid cardioplegia. Oxygenated blood cardioplegia has not been compared with oxygenated crystalloid cardioplegia in an isolated myocyte model of hypothermic, hyperkalemic cardioplegic arrest in which direct measurements of contractile function and myocyte swelling can be made. Accordingly, isolated myocyte contractile function and myocyte profile surface area were examined after hypothermic arrest with oxygenated crystalloid or blood cardioplegia. METHODS: Isolated left ventricular pig myocytes were randomly assigned to undergo cardioplegic arrest for 2 hours at 4 degrees C. Either oxygenated crystalloid or blood cardioplegia was used. After 2 hours, myocytes were reperfused with standard cell medium at 37 degrees C and contractile function was examined. A control group of myocytes was maintained in cell medium at 37 degrees C for 2 hours. Myocyte velocity of shortening (micrometers per second) was examined at baseline and after beta-adrenergic stimulation (isoproterenol, 25 nmol/L). Velocity of shortening declined equally from baseline control values (65 +/- 2 micron n/sec) in the groups subjected to oxygenated crystalloid cardioplegia and blood cardioplegia (37 +/- 2 micron n/sec and 42 +/- 1 micron n/sec, respectively; p < 0.05). RESULTS: Although beta-adrenergic stimulation caused a significant increase in velocity of shortening in all myocyte groups, the increase was less pronounced in myocytes subjected to crystalloid cardioplegia (157 +/- 6 micron n/sec) and blood cardioplegia (159 +/- 6 micron n/sec) than in normothermic control myocytes (205 +/- microm/sec; p < 0.05). Myocyte profile surface area, an index of cell volume, was measured in all myocyte groups. Myocyte surface area increased equally after cardioplegic arrest and rewarming in both cardioplegia groups (crystalloid 4119 +/- 53 micron2; blood 3924 +/- 48 micron2); surface areas in both cardioplegia groups were significantly greater than in the normothermic control group (3158 +/- 39 micron2, p < 0.05). CONCLUSION: Equivalent effects of oxygenated crystalloid and blood cardioplegia were observed with respect to myocyte contractile function, inotropic responsiveness, and intracellular volume regulatory processes.

Animals↗
PubMed1996

Preservation of myocyte contractile function after hypothermic, hyperkalemic cardioplegic arrest with 2, 3-butanedione monoxime.

One proposed contributory mechanism for depressed ventricular performance after hypothermic, hyperkalemic cardioplegic arrest is a reduction in myocyte contractile function caused by alterations in intracellular calcium homeostasis. Because 2,3-butanedione monoxime decreases intracellular calcium transients, this study tested the hypothesis that 2,3-butanedione monoxime supplementation of the hyperkalemic cardioplegic solution could preserve isolated myocyte contractile function after hypothermic, hyperkalemic cardioplegic arrest. Myocytes were isolated from the left ventricles of six pigs. Magnitude and velocity of myocyte shortening were measured after 2 hours of incubation under normothermic conditions (37 degrees C, standard medium), hypothermic, hyperkalemic cardioplegic arrest (4 degrees C in Ringer's solution with 20 mEq potassium chloride and 20 mmol/L 2,3-butanedione monoxime). Because beta-adrenergic agonists are commonly employed after cardioplegic arrest, myocyte contractile function was examined in the presence of the beta-agonist isoproterenol (25 nmol/L). Hypothermic, hyperkalemic cardioplegic arrest and rewarming reduced the velocity (32%) and percentage of myocyte shortening (27%, p < 0.05). Supplementation with 2,3 butanedione monoxime normalized myocyte contractile function after hypothermic, hyperkalemic cardioplegic arrest. Although beta-adrenergic stimulation significantly increased myocyte contractile function under normothermic conditions and after hypothermic, hyperkalemic cardioplegic arrest, contractile function of myocytes exposed to beta-agonist after hypothermic, hyperkalemic cardioplegic arrest remained significantly reduced relative to the normothermic control group. Supplementation with 2,3-butanedione monoxime restored beta-adrenergic responsiveness of myocytes after hypothermic, hyperkalemic cardioplegic arrest. Thus, supplementation of a hyperkalemic cardioplegic solution with 2,3-butanedione monoxime had direct and beneficial effects on myocyte contractile function and beta-adrenergic responsiveness after cardioplegic arrest. A potential mechanism for the effects of 2,3-butanedione monoxime includes modulation of intracellular calcium transients or alterations in sensitivity to calcium. Supplementation with 2,3-butanedione monoxime may have clinical utility in improving myocardial contractile function after hypothermic, hyperkalemic cardioplegic arrest.

Animals↗
PubMed1996

Intravenous sedation for placement of automatic implantable cardioverter-defibrillators.

OBJECTIVE: To evaluate a change in anesthetic technique for transvenous placement of the automatic implantable cardioverter-defibrillator (ICD). DESIGN: Retrospective study. SETTING: A university hospital. PARTICIPANTS: Twenty-eight patients who underwent placement of ICDs. INTERVENTIONS: Thirteen patients had the ICD placed via the transvenous approach with general anesthesia (group GA). Fifteen patients had the ICD placed via the transvenous approach with intravenous sedation (group IV). MEASUREMENTS AND MAIN RESULTS: Intraoperative systolic and diastolic blood pressures were significantly higher in group IV compared with group GA. The ICD was successfully placed in all patients in both groups. There were no intraoperative complications noted in either group during induction of fibrillation and defibrillation, and there was no recall by any patient in either group. The average hospital stay was significantly less in group IV (1.8 days) compared with group GA (3.4 days). CONCLUSIONS: Intravenous sedation for the placement of ICDs is a safe and effective technique. Patients who had their ICD placed while receiving intravenous sedation experienced higher intraoperative blood pressures and were discharged from the hospital earlier than those patients who received general anesthesia.

Aged↗
PubMed1996

The direct effects of propofol on myocyte contractile function after hypothermic cardioplegic arrest.

Propofol is being used more often in cardiac surgery, particularly after hypothermic, hyperkalemic cardioplegic arrest (HHCA). The purpose of this study was to examine the effects of propofol on isolated myocyte contractile function under both normothermic conditions and after simulated HHCA and rewarming. Myocytes were isolated from the left ventricle of eight pigs. Myocyte contractile function was measured under both normothermic conditions and after simulated HHCA (incubation at 4 degrees C for 2 h in crystalloid cardioplegia; K+ = 24 mEq/L) using computer-assisted videomicroscopy in the presence of 2, 4, and 6 micrograms/mL propofol (11.2, 22.4, and 33.6 microM/L, respectively). Isoproterenol (25 nM) was then added and contractile function measurements repeated. Propofol caused significant dose-dependent reductions in myocyte velocity of shortening (baseline = 67 +/- 2 microns/s; propofol = 2 micrograms/mL, 45 +/- 4 microns/s; and propofol = 6 micrograms/mL, 27 +/- 3 microns/s; P < 0.05). HHCA and rewarming caused a significant reduction in myocyte velocity of shortening (29 +/- 0.9 microns/s, P < 0.05), with further significant dose-dependent reductions in contractile function after the addition of propofol. Propofol caused a decrease in beta-adrenergic responsiveness under normothermic conditions, but not after simulated HHCA. Results from the present study demonstrated for the first time that the reduction in isolated myocyte contractile function after simulated HHCA is further decreased by propofol administration.

Adrenergic beta-Agonists↗
PubMed1996

The effect of bupivacaine skull block on the hemodynamic response to craniotomy.

The placement of pointed cranial pins into the periosteum is a recognized acute noxious stimulation during intracranial surgery which can result in sudden increases in blood pressure and heart rate, causing increases in intracranial pressure. A skull block (blockade of the nerves that innervate the scalp, including the greater and lesser occipital nerves, the supraorbital and supratrochlear nerves, the auriculotemporal nerves, and the greater auricular nerves) may be effective in reducing hypertension and tachycardia. Twenty-one patients were allocated in a prospective, double-blind fashion to a control group or a bupivacaine group. After a standardized induction and 5 min prior to head pinning, a skull block was performed. Patients in the control group received a skull block of normal saline, while the bupivacaine group received a skull block with 0.5% bupivacaine. Systolic (SAP), diastolic (DAP), mean arterial pressure (MAP), heart rate (HR), and end-tidal isoflurane were recorded at the following times: 5 min after the induction of anesthesia, during performance of the skull block, during head pinning, and 5 min after head pinning. Significant increases in SAP of 40 +/- 6 mm Hg, DAP of 30 +/- 5 mm Hg, MAP of 32 +/- 6 mm Hg, and HR of 22 +/- 5 bpm occurred during head pinning in the control group, while remaining unchanged in the bupivacaine group. These results demonstrate that a skull block using 0.5% bupivacaine successfully blunts the hemodynamic response to head pinning.

Adolescent↗
PubMed1995

Protamine use during peripheral vascular surgery: a prospective randomized trial.

PURPOSE: One hundred twenty patients undergoing aortic reconstruction (40), infrainguinal bypass (49), and carotid endarterectomy (31) were prospectively enrolled into a double-blind randomized trial to investigate the utility of routine heparin reversal with protamine. METHODS: All patients underwent systemic heparinization with 90 U/kg body weight during operation and after revascularization were randomized to receive either protamine or saline solution for heparin reversal. Blood loss was measured throughout the surgical procedure, and indexes of coagulation and the requirement for blood and blood products were documented during operation and the first 24 hours after operation. RESULTS: Plasma heparin concentration, partial thromboplastin time, and activated clotting time were significantly higher (p < 0.05) in those receiving saline solution at 20 minutes and 1 hour after administration. Total surgical blood loss was not significantly different between study groups. No significant differences were found in blood product requirement, intravenous fluid administered, hematocrit, or wound hematomas between groups at 24 hours. In addition, no difference was seen in the surgeon's subjective intraoperative assessment of hemostasis after administration of either study drug. Furthermore, after study drug administration protamine was associated with a deleterious effect on subsequent intraoperative blood loss (318 +/- 33 ml vs 195 +/- 18 ml, p < 0.05). CONCLUSIONS: Although protamine effectively reverses heparin anticoagulation, its routine use after elective peripheral vascular surgical reconstruction does not appear to provide any clinical benefit.

Aged↗
PubMed1995

The direct and interactive effects of phosphodiesterase inhibition and beta-adrenergic stimulation on myocyte contractile function after hypothermic cardioplegic arrest.

The direct and interactive effects of phosphodiesterase inhibition (PDEI) and beta-adrenergic receptor (beta AR) stimulation on isolated myocyte contractile function were examined after hypothermic, hyperkalemic, cardioplegic arrest (HHCA) and under normothermic conditions. Left ventricular (LV) myocytes were isolated from porcine hearts and myocyte contractile function was measured under normothermic conditions (37 degrees C in standard media) and after HHCA (2 h at 4 degrees C in Ringer's solution with 24 mEq KCl) with subsequent rewarming. Myocytes were then randomly assigned to treatment with the beta AR agonist isoproterenol (25 nM), the phosphodiesterase inhibitor amrinone (50 microM), or a combination of these compounds and contractile function measurements repeated. Baseline myocyte contractile function was reduced by 32% after HHCA. Isoproternol alone increased myocyte contractile function more than 100% under both normothermic conditions and after HHCA, whereas amrinone alone significantly (60%) improved myocyte contractile function only after HHCA. Amrinone preincubation followed by isoproterenol improved contractile function after HHCA to a greater extent than all other treatment protocols. In contrast, combination treatment under normothermic conditions did not augment myocyte contractile function relative to isoproterenol alone. These findings suggest that amrinone has differential effects on contractile processes. Moreover, the marked improvement of contractile function after HHCA with PDEI pretreatment followed by beta AR stimulation may have implications in treatment strategies for improving myocardial function after cardiopulmonary bypass and provide insight into contractile dysfunction after HHCA.

Adrenergic beta-Agonists↗
PubMed1995

Myocyte contractile responsiveness after hypothermic, hyperkalemic cardioplegic arrest. Disparity between exogenous calcium and beta-adrenergic stimulation.

BACKGROUND: Acute left ventricular dysfunction is commonly encountered after hypothermic, hyperkalemic cardioplegic arrest (HHCA) and often requires inotropic intervention for successful separation from cardiopulmonary bypass. However, the basic mechanisms involved in depressed left ventricular function and the cellular basis for the differential effects of inotropic drugs after HHCA are unknown. Accordingly, the goal of this study was to determine the effects of calcium (Ca2+) and beta-adrenergic receptor agonists (beta AR) stimulation on isolated myocyte contractile function after HHCA. METHODS: Myocytes were isolated from the left ventricle of nine pigs and randomly assigned to one of the following treatment groups: (1) normothermic, control: incubation in oxygenated cell culture media for 2 h at 37 degrees C; and (2) cardioplegia: incubation in 4 degrees C crystalloid cardioplegia for 2 h, followed by rewarming. Steady-state myocyte contractile function was measured after pulse stimulation at baseline, in the presence of extracellular Ca2+ (3-10 mM), and in the presence of the beta AR agonist isoproterenol (2-100 nM). Myocyte profile surface area was measured for both normothermic myocytes and myocytes after HHCA. In a separate set of experiments, myocyte contractile function also was documented after 2 h of hypoxic conditions with both normothermic incubation and HHCA, in the presence and absence of beta AR stimulation. RESULTS: Baseline myocyte contractile function was significantly less in the cardioplegia group compared to control. Extracellular Ca2+ produced a dose-dependent significant increase in myocyte contractile function in the normothermic control group, whereas increased extracellular Ca2+ only minimally increased myocyte contractile function in the cardioplegia group. A dose-dependent, significant increase in myocyte contractile function was observed in both groups after beta AR stimulation by isoproterenol; however, myocyte contractile function in the cardioplegia group was decreased compared to the control group. Hypoxia under normothermic conditions significantly reduced myocyte contractile function, myocyte relaxation, and beta-adrenergic responsiveness. Hypoxia in combination with cardioplegic arrest compounded the negative effects on contractile processes but did not further impair beta-adrenergic responsiveness. Myocyte profile surface area was significantly increased after HHCA. CONCLUSIONS: The minimal improvement in myocyte contractile function after HHCA with increased extracellular Ca2+ suggests that Ca2+ depletion is not the primary mechanism for depressed myocyte contractility after HHCA. On the other hand, because beta AR administration improved myocyte contractile function after HHCA, the cellular basis for the effects of beta AR stimulation after HHCA is probably not increased myocyte Ca2+ but rather alternative mechanisms, such as changes in myofilament sensitivity to Ca2+. These results also suggest that the abnormalities in left ventricular function after HHCA result from the direct effects of hyperkalemic induced electromechanical uncoupling as well as relative hypoxic conditions.

Adrenergic beta-Agonists↗
PubMed1994

Postoperative hyperthermia in a patient having cortical brain resection.

When a profound fever occurs in a surgical patient, clinicians usually start thinking about the malignant hyperthermia syndrome. Simple consideration of the clinical situation, the patient's medical history, and a few rapid laboratory assessments are enough to direct appropriate treatment.

Adolescent↗
PubMed1994

Postoperative analgesia after major shoulder surgery with interscalene brachial plexus blockade: etidocaine versus bupivacaine.

Postoperative pain is commonly treated with significant doses of narcotics, occasionally resulting in side effects including nausea, pruritus, and respiratory depression. One potential advantage of regional anesthesia is profound postoperative analgesia that reduces exposure to potent narcotics. To evaluate the efficacy of two long-acting local anesthetics, bupivacaine and etidocaine, in providing pain relief after major shoulder surgery, we randomized 20 patients to receive either bupivacaine or etidocaine for brachial plexus block as the primary anesthetic for shoulder surgery. Surgeons, patients, and the acute pain service were blinded as to drug selection. After the patient was sedated, an interscalene block was placed with the use of a nerve stimulator to facilitate proper needle placement. Forty milliliters of either 0.5% bupivacaine or 0.75% etidocaine containing 5 micrograms/mL epinephrine was injected into the brachial plexus sheath. An additional 8 mL of local anesthetic was administered for superficial cervical plexus blockade. Intraoperative sedation was accomplished with an intravenous infusion of methohexital as needed. After surgery, patients received a standard patient-controlled analgesia protocol providing incremental doses of morphine. The degree of postoperative analgesia resulting from residual local anesthetic effect was expressed as the time until first morphine requirement and the total dose of morphine required during the first 24 hours postoperatively. We found no statistically significant intergroup differences either in time of initial use of morphine or in the total dose of morphine required in the first 24 hours. Both etidocaine and bupivacaine provide prolonged analgesia after major shoulder surgery when injected into the brachial plexus. Bupivacaine, however, possesses significant cardiotoxicity and has a relatively delayed onset in peripheral neural blockade. Etidocaine is less cardiotoxic and also has a more rapid onset of effect. Thus etidocaine may be a preferable agent for interscalene block for major shoulder surgery.

Aged↗
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↗