Reduction of postoperative hypothermia with a new warming device: a prospective randomized study in off-pump coronary artery surgery.

Hypothermia has been used for decades in cardiac surgery to limit the ischemic insult to the heart. With the diffusion of off-pump coronary artery surgery, the practice of arresting and cooling the heart has been abandoned. At University of Miami Miller School of Medicine, we tested a new warming device by performing a prospective study in which 50 patients were randomized to either the use of the Kimberly-Clark warming system or to standard methods of control of body temperature. The two groups were compared in terms of core body temperature (CBT), intra- and postoperative blood loss, blood products transfusions, extubation time, intensive care unit (ICU) and hospital length of stay and incidence of infections. Five patients in the control group and 0 patients in the study group dropped their CBT below 35 degrees C during the operation (P<0.01). Total blood loss, measured in terms of cell-saver and chest tube drainage, was 27 % and 14 % less for the study group (P<0.01). Hospital length of stay was 1.2 day less in the study group (P<0.01). The Kimberly-Clark Patient Warming System allowed for better control of core body temperature during off pump coronary artery bypass surgery compared to traditional techniques. This translated in less intra and postoperative blood loss and shorter hospital length of stay. Other advantages, such as decreased blood-products transfusions, decreased incidence of infections, decreased ICU length of stay and overall reduction of costs might be evident on larger study groups.

Cardioplegic arrest in pigs. Effects of glucose-containing solutions.

A clinically used cardioplegic solution was evaluated in the laboratory in an attempt to elucidate the value of glucose in maintaining the glycogen and energy stores of the myocardium during aortic cross-clamping. In one group of animals the cardioplegic solution contained glucose; in the other group it did not. Energy stores were determined in full-thickness biopsies of left ventricular myocardium taken prior to bypass, at 60 minutes of cardioplegic arrest, and after 20 minutes of reperfusion. At the end of cardioplegic arrest, glycogen levels were slightly higher than control values, with no differences between the groups. Creatine phosphate (CP) and adenosine triphosphate (ATP) fell by 69% to 73% and 43% to 55%, respectively, from the control values, but there were no statistical differences between these groups. At the end of reperfusion, glycogen and CP stores had returned to control but ATP concentration remained below control values in both groups. These results indicate that glucose is of no value either to maintain myocardial glycogen or to influence the changes in CP and ATP during cardioplegic arrest. The dissociation between the complete and partial restoration of CP and ATP stores to control levels during reperfusion suggests either that ATP consumption is greater than the energy transfer between CP and ADP:ATP systems or that the energy transfer is defective under these experimental conditions.

Surgical treatment of symptomatic cervical venous hum.

A 28-year-old woman presented with pulsating tinnitus in the right ear and a venous hum heard over the right internal jugular vein. Maneuvers which abolished the hum also eliminated the tinnitus. Permanent symptomatic relief was achieved by ligation of the right internal jugular vein.

Prospective analysis of valvular replacement without venting the left ventricle.

The present study is a prospective analysis of a series of consecutive valve replacement and combined (valvular plus coronary artery) operations performed without left ventricular decompression. Results indicate that left ventricular venting (direct or indirect) is unnecessary provided that cardioplegic arrest is used, that the venous line is positioned in the right atrium, and that left-sided pressures are monitored. Left ventricular distention, as measured by left ventricular pressure recording, did not occur; air embolism, as determined clinically and by electroencephalographic (EEG) monitoring, was not encountered. The routine use of a left ventricular vent has been abandoned in most intracardiac operations at our center.

Spontaneous ventricular fibrillation occurring immediately after institution of cardiopulmonary bypass: possible clinical implications.

Twenty-four patients developed spontaneous ventricular fibrillation (SVF), for no apparent reasons, immediately after the institution of cardiopulmonary bypass (CPB) and prior to aortic cross-clamping and cardioplegic arrest. These were compared to 76 similar patients who remained in normal sinus rhythm (NSR). The following observations were made: (1) SVF occurred more frequently in patients undergoing urgent coronary bypass and having unstable or crescendo angina with severe triple coronary artery disease and/or left main coronary artery stenosis; (2) in nonvented hearts the mean left atrial pressure increased to levels above 28 mm Hg during SVF and prior to cardioplegic arrest; (3) at the end of CPB, arrhythmias and episodes of ventricular fibrillation were common (48% SVF versus 8% NSR); (4) the overall myocardial infarction rate was 37% SVF versus 4% NSR; and (5) the mortality rates were 25% SVF versus 1.3% NSR. It is postulated that the occurrence of SVF at the start of CPB may be indicative of serious derangements in myocardial cellular metabolism and/or function and may have clinical and prognostic implications.

The hemodynamic effects of intra-aortic versus intravenous administration of protamine for reversal of heparin in pigs.

The hemodynamic effects of intra-aortic (IA) versus intravenous (IV) administration of protamine for reversal of heparin were studied in pigs. The animals were anesthetized with sodium thiopental, nitrous oxide, oxygen, and halothane. Twenty minutes after heparinization (3 mg/kg) the following hemodynamic parameters were measured: heart rate, arterial pressure, pulmonary artery pressure (PAP), left ventricular end-diastolic pressure, and cardiac output. Protamine sulfate (3 mg/kg) was injected over 30 seconds IV in Group I (five pigs) and into the ascending aorta (IA) in Group II (five pigs). After injection, the above measurements were repeated at 1.0, 2.5, 5, and 15 minutes. The hemodynamic effects of intravenous protamine (3 mg/kg) without prior heparinization were studied in Group III (four pigs). Groups I and II experienced a decrease in cardiac output (Group I, 14%; Group II, 29%) and a marked increase in PAP (Group I, 78%; Group II, 79%) and pulmonary vascular resistance (PVR) (Group I, 174%; Group II, 559%) which peaked at 1 minute after protamine injection (p less than 0.05). Cardiac output, PAP, and PVR returned to baseline within 15 minutes. Heart rate, arterial pressure, left ventricular end-diastolic pressure, and systemic vascular resistance (SVR) were unchanged. No hemodynamic abnormalities occurred in animals injected with protamine alone (Group III). It is concluded that IV or IA administration of protamine causes marked hemodynamic changes in heparinized pigs. This does not confirm a recent clinical study reporting stable hemodynamics after IA administration of protamine. The lack of circulatory effects of protamine in unheparinized pigs suggests that a protamine-heparin interaction may be involved.

Glucose substrate in myocardial protection.

Glucose-insulin-potassium (GIK) was infused preoperatively in 30 patients scheduled for coronary artery operation. Before cardiopulmonary bypass (CPB) each patient received an intravenous infusion of 50% glucose. Myocardial protection was achieved with a cardioplegic solution containing glucose. A similar group of 30 patients received an equal volume of NaCl infused preoperatively and before CPB, and their cardioplegic solution contained no glucose. Clinically and by hemodynamic evaluation postoperatively one could not separate the two groups. Glycogen grading of the myocardium prior to bypass demonstrated no difference in glycogen levels in patients receiving glucose and those receiving NaCl. However, at the end of cardioplegic arrest only the group receiving glucose maintained normal grading of myocardial glycogen.

Toward a better understanding of the hemodynamic effects of protamine and heparin interaction.

Hemodynamic changes have been documented during protamine infusion into heparinized but not unheparinized pigs and suggest that a protamine-heparin interaction might be responsible. This hypothesis was tested in four groups of pigs by varying the dosage and order of administration of these two drugs: Group I (n = 9) received heparin (3 mg/kg) followed by protamine (3 mg/kg); Group II (n = 9) received protamine (3 mg/kg) followed by heparin (3 mg/kg); Group III (n = 9) received protamine (25 mg/kg) followed by heparin (3 mg/kg); and Group IV (n = 16) received protamine-heparin complex (protamine 3 mg/kg and heparin 3 mg/kg mixed immediately prior to injection). Systemic and pulmonary arterial pressures, systemic and pulmonary vascular resistances, left ventricular end-diastolic pressure, central venous pressure, cardiac output, and heart rate were measured before and at 1.0, 2.5, 5.0, and 15 minutes after protamine, heparin, or protamine-heparin complex infusions. Immediately following protamine infusion, Group I pigs exhibited transiently but significantly increased pulmonary artery pressure, pulmonary vascular resistance, systemic vascular resistance, and central venous pressure and decreased cardiac output with (Group Ib, n = 5) or without (Group Ia, n = 4) systemic hypotension. The fact that no hemodynamic changes occurred in Group II confirms that infusion of clinical doses of protamine produces no hemodynamic changes in unheparinized pigs. Protamine alone in high doses (Group III) produced hemodynamic changes similar to clinical-dose protamine reversal of heparin (Group I). This effect suggests that the presence of heparin in the circulation lowers the threshold for protamine-mediated hemodynamic responses. Infusion of heparin (3 mg/kg) into pigs 15 minutes after treatment with high (25 mg/kg) (Group III) but not clinical (3 mg/kg) (Group II) doses of protamine produced hemodynamic effects similar to clinical-dose protamine reversal of heparin (Group I), suggesting that a protamine-heparin interaction may be responsible. These results also suggest a rapid inactivation in vivo of clinical doses (3 mg/kg) (Group II) of infused protamine. Protamine-heparin complex formed in vitro (Group IV) also produced hemodynamic changes similar to clinical-dose protamine reversal of heparin (Group I), suggesting that formation of this complex in vivo may be the protamine-heparin interaction responsible. Protamine-heparin complex may well be a useful tool in further elucidating the full effects of protamine reversal of heparin.

Acute respiratory insufficiency from an aneurysm of the descending thoracic aorta.

A 70-year-old woman presented with life-threatening acute respiratory insufficiency resulting from tracheobronchial compression by a large calcified expanding aneurysm confined to the descending thoracic aorta. This combination has not previously been reported. Successful surgical correction was carried out. This report describes in detail the presentation, diagnosis, and steps involved in the management of this entity.

Hypertension after coronary operation. Can it be prevented by pulsatile perfusion?

Nonpulsatile perfusion during cardiopulmonary bypass (CPB) has been implicated as a causative factor of postoperative hypertension. In a consecutive series, patients undergoing coronary bypass were selected for perfusion with either nonpulsatile flow (American Optical roller pump) or pulsatile flow (Desjardin's modification of the roller pump). The incidence of postoperative hypertension and the levels of peripheral renin were noted. No differences could be observed in renin activity, with either modality of perfusion, before CPB, after 30 minutes of stable CPB, or 2 hours postoperatively. Hypertension, necessitating treatment, occurred in 60% of the patients having pulsatile and 68% of those having nonpulsatile perfusion (p less than 0.05). Although pulsatile CPB would appear to be more physiological than nonpulsatile perfusion, this method of creating pulsatile flow does not appear to eliminate postoperative hypertension.

Hemolysis during pulsatile perfusion: clinical evaluation of a new device.

The degree of hemolysis occurring during cardiopulmonary bypass was evaluated in two groups of patients undergoing pulsatile and nonpulsatile perfusion. Results indicate that, with a newly developed method of creating pulsatile flow, both groups of patients compared favorably and had approximately the same degree of hemolysis. Because of its simplicity, low cost, reliability, and limited hemolytic activity, this pulsatile device warrants further clinical evaluation.

Pulmonary blood flow. A potential factor in the pathogenesis of pulmonary edema.

The purpose of this study is to examine the hemodynamics of the pulmonary circulation and the potential role of pulmonary blood flow in the pathogenesis of cardiogenic pulmonary edema. To do so, the pulmonary circulation was isolated and controlled such that, within a closed circuit, pulmonary blood flow and left atrial pressure (LAP) could be regulated independently: the first by a constant flow pump, the second by a variable height reservoir. The effect of pulmonary blood flow on pulmonary artery pressure and intravascular blood volume was then determined at different LAPs. Contrary to our expectations, the results indicate that (1) pulmonary vascular resistance does not change appreciably as flow increases, (2) the microcirculation comprises the major capacitance vessels of the lung, and (3) increased pulmonary flow in the normal lung causes little change in intravascular pulmonary blood volume, whereas, by contrast, major changes in pulmonary blood volume occur as LAP rises. Next, the effect of pulmonary blood flow on edema formation in the lungs was examined. Below a critical level of LAP (15 mm Hg in these experiments), pulmonary blood flow up to 5 L/min did not produce pulmonary edema. Above this level, however, such an effect was clear. Thus, at an LAP of 20 mm Hg, edema did not develop if pulmonary flow was low (0.7 L/min) but did if flow was increased to 2 L/min. As well, if the LAP was 17.5 mm Hg and pulmonary flow 3.5 L/min, severe pulmonary edema also resulted.

Pulmonary artery balloon counterpulsation in the management of right heart failure during left heart bypass.

Pulmonary artery balloon counterpulsation was instituted in 10 pigs when right ventricular failure limited cardiac output. Global myocardial depression was produced by infusion of propranolol, and the left ventricle was fully supported by left heart bypass. A stable model of failure was achieved in six pigs. Following application of pulmonary artery balloon counterpulsation right atrial pressure decreased from 18.2 +/- 2.1 to 15.9 +/- 2.5 mm Hg (p less than 0.05). Cardiac output increased from 416 +/- 94 to 758 +/- 127 ml/min (p less than 0.001). Right ventricular stroke work increased from 0.29 +/- 0.07 to 0.65 +/- 0.12 gm X m. (p less than 0.05). There was no cardiac output before or after institution of balloon counterpulsation in four pigs studied during ventricular fibrillation or asystole. We conclude that pulmonary artery balloon counterpulsation improved cardiac output and right ventricular stroke work in a model of right ventricular failure where the pulmonary circulation was unaltered and the left ventricle supported by left heart bypass. Balloon counterpulsation was not effective during ventricular fibrillation or asystole. Pulmonary artery balloon counterpulsation should be considered when right ventricular failure limits cardiac output during left heart bypass.

Protection of the hypertrophied pig myocardium. A comparison of crystalloid, blood, and Fluosol-DA cardioplegia during prolonged aortic clamping.

The myocardial protective effects of crystalloid, blood, and Fluosol-DA-20% cardioplegia were compared by subjecting hypertrophied pig hearts to 3 hours of hypothermic (10 degrees to 15 degrees C), hyperkalemic (20 mEq/L) cardioplegic arrest and 1 hour of normothermic reperfusion. Left ventricular hypertrophy was created in piglets by banding of the ascending aorta, with increase of the left ventricular weight-body weight ratio from 3.01 +/- 0.2 gm/kg (control adult pigs) to 5.50 +/- 0.2 gm/kg (p less than 0.001). An in vivo isolated heart preparation was established in 39 grown banded pigs, which were divided into three groups to receive aerated crystalloid (oxygen tension 141 +/- 4 mm Hg), oxygenated blood (oxygen tension 584 +/- 41 mm Hg), or oxygenated Fluosol-DA-20% (oxygen tension 586 +/- 25 mm Hg) cardioplegic solutions. The use of crystalloid cardioplegia was associated with the following: a low cardioplegia-coronary sinus oxygen content difference (0.6 +/- 0.1 vol%), progressive depletion of myocardial creatine phosphate and adenosine triphosphate during cardioplegic arrest, minimal recovery of developed pressure (16% +/- 8%) and its first derivative (12% +/- 7%), and marked structural deterioration during reperfusion. Enhanced oxygen uptake during cardioplegic infusions was observed with blood cardioplegia (5.0 +/- 0.3 vol%), along with excellent preservation of high-energy phosphate stores and significantly improved postischemic left ventricular performance (developed pressure, 54% +/- 4%; first derivative of left ventricular pressure, 50% +/- 5%). The best results were obtained with Fluosol-DA-20% cardioplegia. This produced a high cardioplegia-coronary sinus oxygen content difference (5.8 +/- 0.1 vol%), effectively sustained myocardial creatine phosphate and adenosine triphosphate concentrations during the extended interval of arrest, and ensured the greatest hemodynamic recovery (developed pressure, 81% +/- 6%, first derivative of left ventricular pressure, 80% +/- 10%) and the least adverse morphologic alterations during reperfusion. It is concluded that oxygenated Fluosol-DA-20% cardioplegia is superior to oxygenated blood and especially aerated crystalloid cardioplegia in protecting the hypertrophied pig myocardium during prolonged aortic clamping.

Arch versus femoral artery perfusion during cardiopulmonary bypass.

Aortic arch perfusion is favored by most cardiac surgeons. Perfusion via the femoral artery is still used sporadically at reoperations for aneurysms of the ascending aorta, or for the institution of partial pump support in very sick patients prior to opening of the chest. Our over-all experience indicates that surgical complications occurred primarily in the group of patients perfused via the femoral artery. On the other hand, serious disturbance in cerebral perfusion, as determined by electroencephalogram (EEG) monitoring, occurred in 7 percent of the patients perfused via the arch and 3 percent of those perfused via the femoral artery, a difference that was not statistically significant. We continue to advocate aortic arch cannulation and EEG monitoring during cardiopulmonary bypass procedures.

Monitoring of electroencephalogram during open-heart surgery. A prospective analysis of 118 cases.

The electroencephalogram (EEG) was prospectively analyzed in 118 consecutive open-heart procedures. In 96 patients (81%) the records were normal whereas in 22 patients (19%) the EEG showed slow wave activity and decreased electrical voltage. In 16 of these patients the EEG abnormality was transient or only of mild degree. In 10 of this group of patients the abnormality occurred with the institution of total cardiopulmonary bypass (CPB) and returned to normal within 2 minutes. In four other patients the abnormalities were mild, persisted to the end of the CPB, and then returned to normal; in two patients the EEG abnormalities developed in the last half of CPB and then returned to normal. In the remaining six patients the EEG was grossly abnormal. In one of these patients the abnormality was secondary to a previous stroke. In five patients, however, the EEG alerted the surgeon to an otherwise unsuspected poor cerebral blood flow. A serious neurologic insult was probably prevented by identifying and correcting the mechanical cause.

Coronary artery bypass grafting in patients with poor ventricular function. Cardiovascular Surgeons of the University of Toronto.

Although patients with severe ventricular dysfunction have improved long-term survival times after coronary bypass procedures, operative morbidity and mortality rates remain high. This study was designed to identify the contemporary risk factors for isolated coronary artery bypass grafting in this high-risk subgroup. Between January 1982 and December 1990, a total of 12,471 patients underwent isolated coronary artery bypass grafting. The 9445 patients with preoperative ejection fractions greater than 40% had a lower operative mortality rate (2.3%) than that of the 2539 patients with ejection fractions between 20% and 40% (4.8%) and that of the 487 patients with ejection fractions less than 20% (9.8%; p less than 0.001). However, patients with ejection fractions of less than 20% were demographically distinct from those with higher ejection fractions. This group was older, with fewer women, a higher frequency of left main stenosis, and more frequent requirement of urgent operation for unstable angina. The risk factors for operative death also varied with preoperative ejection fraction. The traditionally accepted risk factors--urgency of operation, left main coronary artery stenosis, reoperation, sex, and age--were predictive of risk of operative death for patients with ejection fractions greater than 40%. The risk of operative death for patients with ejection fractions between 20% and 40% was predicted by urgency of operation, reoperation, sex, myocardial protection, and age. The only predictor of risk of operative death for patients with ejection fractions less than 20% was urgency of operation. Patients undergoing isolated coronary artery bypass grafting who have severe ventricular dysfunction are therefore a highly selected, high-risk subgroup of patients who risk depends on the urgency of operation. Strategies to improve the results in these patients should be focused on patient selection, improvement of myocardial protection, and more aggressive preoperative treatment of myocardial ischemia.

Cerebral protection during moderate hypothermic circulatory arrest: histopathology and magnetic resonance spectroscopy of brain energetics and intracellular pH in pigs.

OBJECTIVE: We evaluated the effect of antegrade and retrograde brain perfusion during moderate hypothermic circulatory arrest at 28 degrees C. METHODS: Phosphorus 31-magnetic resonance spectroscopy was used to follow brain energy metabolites and intracellular pH in pigs during 2 hours of ischemia and 1 hour of reperfusion. Histopathologic analysis of brain tissue fixed at the end of the experimental protocol was performed. Fourteen pigs were divided into two experimental groups subjected to antegrade (n = 6) or retrograde (n = 8) brain perfusion. Anesthesia (n = 8) and hypothermic cardiopulmonary bypass groups (15 degrees C, n = 8) served as control subjects. In the antegrade and retrograde brain perfusion groups, the initial bypass flow rate was 60 to 100 ml x kg(-1) x min(-1). In the antegrade group, the brain was perfused through the carotid arteries at a flow rate of 180 to 210 ml x min(-1) during circulatory arrest at 28 degrees C. In the retrograde group, the brain was perfused through the superior vena cava at a flow rate of 300 to 500 ml x min(-1) during circulatory arrest at 28 degrees C. RESULTS: The intracellular pH was 7.1 +/- 0.1 and 7.2 +/- 0.1 in the anesthesia and hypothermic bypass groups, respectively. Brain intracellular pH and high-energy metabolites (adenosine triphosphate, phosphocreatine) did not change during the course of the 3.5-hour study. In the antegrade group, adenosine triphosphate and intracellular pH were unchanged throughout the protocol. In the retrograde perfusion group, the intracellular pH level decreased to 6.4 +/- 0.1, and adenosine triphosphate and phosphocreatine levels decreased within the first 30 minutes of circulatory arrest and remained at low levels until the end of reperfusion. High-energy phosphates did not return to their initial levels during reperfusion. Histopathologic analysis of nine regions of the brain showed good preservation of cell structure in the anesthesia, hypothermic bypass, and antegrade perfusion groups. The retrograde perfusion group showed changes in all the regions examined. CONCLUSIONS: The study shows that moderate hypothermic circulatory arrest at 28 degrees C with antegrade brain perfusion during circulatory arrest protects the brain but that retrograde cerebral perfusion at 28 degrees C does not protect the brain.

Assessment of retrograde cardioplegia with magnetic resonance imaging and localized 31P spectroscopy in isolated pig hearts.

OBJECTIVE: This study was done to determine whether retrograde delivery of cardioplegic solution provides uniform blood flow to the myocardium supplied by an occluded coronary artery and whether it maintains myocardial energy levels beyond the coronary occlusion. METHODS: Isolated pig hearts were used. A hydraulic occluder was placed at the origin of the left anterior descending coronary artery. The perfusion pressure for retrograde delivery of cardioplegic solution was controlled at 40 to 50 mm Hg. Magnetic resonance imaging and localized 31P magnetic resonance spectroscopy were used to assess myocardial perfusion and energy metabolism, respectively. RESULTS: Magnetic resonance perfusion images (n = 7) showed that the perfusion defect that occurred during antegrade delivery of cardioplegic solution (as a result of the occlusion of the left anterior descending coronary artery) resolved during retrograde delivery of cardioplegic solution. Retrograde perfusion delivered similar amounts of flow to the jeopardized myocardium as it did to other areas of the myocardium. However, the distribution of cardioplegic solution by the retrograde route was heterogeneous (cloudlike) across both ventricular walls. 31P magnetic resonance spectra showed that the ischemic changes induced by occlusion of the left anterior descending artery during antegrade perfusion were greatly alleviated by retrograde perfusion; however, it took longer for retrograde cardioplegia (n = 7, 17.08 minutes) to restore the levels of inorganic phosphate/phosphocreatine relative to the effect of releasing the left anterior descending artery occluder during antegrade delivery of cardioplegic solution (n = 7, 5.3 minutes). CONCLUSIONS: First, retrograde delivery of cardioplegic solution provides sufficient flow to the myocardium beyond a coronary occlusion to maintain near normal levels of energy metabolites, and second, the efficacy of the retrograde route of cardioplegic solution delivery (in terms of distribution of the solution and rate of myocardial energy recovery) is significantly lower than that of the antegrade route.

Aspartate/glutamate-enriched blood does not improve myocardial energy metabolism during ischemia-reperfusion: a 31P magnetic resonance spectroscopic study in isolated pig hearts.

OBJECTIVE: Our objective was to test the effects of exogenous L-aspartate and L-glutamate on myocardial energy metabolism during ischemia-reperfusion. METHODS: Phosphorus 31-magnetic resonance spectroscopy was used to observe cellular energetics and intracellular pH in isolated pig hearts perfused with blood (group A, n = 8) or blood enriched with 13 mmol/L each of L-aspartate and L-glutamate (group B, n = 6). The hearts were subjected to 30 minutes of total normothermic ischemia and then reperfused for 40 minutes. Two hearts from each group were inotropically stimulated by titration with calcium after normokalemic reperfusion. Left ventricular function was measured with the use of a compliant balloon and oxygen consumption was calculated. RESULTS: Magnetic resonance spectroscopy showed no decrease in the rate of energy decline during ischemia for group B versus group A. No significant differences were observed between the two groups in terms of myocardial function, oxygen consumption, or the rate or extent of high-energy phosphate recovery after normokalemic reperfusion or inotropic stimulation. Inotropic stimulation of postischemic hearts, however, led to dramatic improvement in myocardial function in both groups (p < 0.05 for all parameters) and significant improvement in oxygen consumption (p = 0.01). CONCLUSIONS: In a normal, isolated, blood-perfused pig heart subjected to 30 minutes of total normothermic ischemia, (1) enrichment of the perfusate with aspartate/glutamate before and after ischemia affects neither myocardial energy metabolism during ischemia-reperfusion nor postischemic recovery of myocardial function or oxygen consumption and (2) inotropic stimulation can recruit significant postischemic function and sufficient aerobic respiration to support it, irrespective of aspartate/glutamate enrichment.