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Biomedical subjects

V L Gott

Publications and source records attributed to V L Gott.

At least 73 records · Page 4Linked to original sources
PubMed1983

Improved myocardial preservation during global ischemia by continuous retrograde coronary sinus perfusion.

To investigate whether retrograde continuous low-pressure perfusion of the coronary sinus could deliver cardioplegic solutions with oxygen and substrate beyond stenoses and result in improved myocardial preservation, we subjected 41 canine hearts to 90 minutes of ischemia with an occlusion on the circumflex coronary artery. There were four groups: Group I, antegrade (aortic root) crystalloid cardioplegia every 30 minutes during ischemia; Group II, antegrade plus topical cooling; Group III, continuous retrograde perfusion; Group IV, same as Group III, with an oxygenated perfluorocarbon. All solutions had a PO2 of 400 to 500 mm Hg. Intramyocardial oxygen and carbon dioxide tensions (PO2 and PCO2) and mean myocardial temperatures were monitored during ischemia, and left ventricular (LV) function was assessed before ischemia and after reperfusion. After global ischemia, the circumflex occlusion was released and the hearts reperfused. Following 60 minutes of reperfusion, isovolumic developed pressure returned to 36% +/- 4% and 41% +/- 5% of preischemic levels, respectively, in Groups I and II. By contrast, Groups III and IV (retrograde perfusion) had a significantly greater percent of recovery (78% +/- 5% and 73% +/- 5%). Circumflex area intramyocardial PO2 fell 20 and 25 mm Hg below preischemic levels in Groups I and II during ischemia, whereas in Group III, intramyocardial PO2 in the circumflex region remained near preischemic levels, and in Group IV, it rose 19 mm Hg. Mean myocardial temperature during ischemia in the circumflex area was significantly higher in Group I than in Groups II, III, and IV. Peak intramyocardial PCO2 in the circumflex region was significantly less in the retrogradely perfused hearts. Retrograde coronary sinus perfusion resulted in significant improvement in recovery of LV function, uniform myocardial cooling, normal intramyocardial PO2, and less intramyocardial PCO2 accumulation, despite the presence of a total circumflex coronary artery occlusion.

Animals↗
PubMed1983

Left ventricular aneurysmectomy. Factors influencing postoperative results.

One hundred consecutive patients who underwent resection of aneurysms of the left ventricle were reviewed. Eighty-four of these patients had resection or plication of an aneurysm of the anterior left ventricular wall either alone or in combination with coronary artery bypass grafting. In 27 patients who had little or no congestive heart failure, the primary indication for operation was disabling angina pectoris. In them the early mortality was 4% and late mortality, 4%. In nine other patients the primary indication for operation was life-threatening ventricular arrhythmias. In this group the early mortality was 56% and late mortality, 0%. Severe congestive heart failure was the primary indication for aneurysmectomy in 48 patients. In these patients the early mortality was 21% and late mortality, 34%. When the primary indication for operation was severe congestive heart failure, overall survival and postoperative results were best in patients in whom the nonaneurysmal left ventricle had good function preoperatively and was supplied by coronary arteries either unobstructed or favorable for bypass grafting; results were poorest in those patients with three-vessel coronary artery disease who had impaired motion of the lateral left ventricular wall and distal lateral wall vessels that were unfavorable for bypass grafting. It is concluded that patients with left ventricular aneurysms form a heterogeneous group in which the prognosis varies markedly. The probability of a good postoperative result can be predicted by careful preoperative analysis of a patient's symptoms, ventricular function, and coronary artery anatomy.

Adult↗
PubMed1983

Enhanced myocardial protection with verapamil prior to postischemic reflow.

Reperfusion of the heart after induced myocardial ischemia may be associated with severe myocardial damage, characterized by massive calcium influx and accumulation in the heart cells. The present study was undertaken to investigate whether verapamil, a slow channel calcium blocker, administered prior to reperfusion, might reduce this reflow injury without causing depression of heart function. Thirty-two isolated, perfused rabbit hearts were subjected either to 45 minutes of normothermic or 150 minutes of hypothermic global ischemia. Half of the heart in each group received verapaMil immediately prior to reperfusion, while the remaining hearts received no verapamil. Following ischemia and 60 minutes of reperfusion, left ventricular (LV) contractivity was superior in both groups of verapamil-treated hearts, compared to control hearts (LV developed pressure [DP] in normothermic hearts 63 +/- 6% of preischemic DP for verapamil-treated hearts versus 46 +/- 6% of preischemic DP for control hearts; in the hypothermic group, 65 +/- 8% of preischemic DP for verapamil-treated hearts versus 33 +/- 10% DP for control hearts). Postischemic LV compliance also was significantly improved in the verapamil-treated hearts through the period of reperfusion, compared to control hearts. No differences were noted in coronary flow, myocardial water content, or the onset of electromechanical activity between the verapamil and control hearts, but there was significantly improved ultrastructural preservation in both verapamil groups. These data demonstrate that verapamil, when administered just prior to reperfusion, results in improved recovery of myocardial function and excellent cellular preservation, presumably for reducing calcium influx into myocardial cells.

Animals↗
PubMed1982

Optimal myocardial protection with fluosol cardioplegia.

An oxygenated perfluorocarbon cardioplegic solution was examined, utilizing a blood-perfused canine model. Twenty-one animals were divided into three equal groups, and each animal received Fluosol cardioplegia at one of three infusion temperatures: 20 degrees C, or 4 degrees C. All hearts underwent 90 minutes of ischemia, during which time 150 ml of the cardioplegic solution was infused every 30 minutes. Myocardial oxygen and carbon dioxide tensions (PmO2 and PmCO2) were monitored continually using mass spectrometry, and myocardial oxygen consumption was calculated with each cardioplegic injection. The mean increase in PmO2 was 7.1 +/- 0.9 mm Hg with 20 degrees C Fluosol infusions, 31.1 +/- 4.7 mm Hg with 10 degrees C Fluosol injections, and 22.2 +/- 4.7 mm Hg with infusions of 4 degrees C Fluosol. Average myocardial oxygen consumptioN, expressed as cubic centimeters of oxygen per 100 gm of left ventricle (wet weight), was 21.2 +/- 0.5 with 20 degrees C Fluosol, 22.8 +/- 1.3 for 10 degrees C Fluosol, and 19.6 +/- 1.0 for 4 degrees C Fluosol. Mean myocardial temperatures with infusions of 20 degrees C, 10 degrees C, and 4 degrees C solutions were 21.4 +/- 0.1 degree C, 16.9 +/- 0.4 degree C, and 15.9 +/- 0.5 degree C, respectively. After 45 minutes of reperfusion, maximum rate of rise of left ventricular pressure, expressed as percentage of preischemic control, was 70.9 +/- 3.9% for 20 degrees C Fluosol, 90.9 +/- 3.2% for 10 degrees C Fluosol, and 90.4 +/- 2.3% for 4 degrees C Fluosol (p less than 0.005, 20 degrees C versus 10 degrees C, 4 degrees C Fluosol). In addition, the 10 degrees C and 4 degrees C Fluosol hearts had essentially normal structure by light and electron microscopy. These data demonstrate tht Fluosol cardioplegia results in near optimal myocardial protection when infused at cold temperatures (4 degrees C to 10 degree C). The increases intramyocardial oxygen and myocardial oxygen consumption with each injection demonstrate that there is enhanced oxygen delivery and utilization, which may account for the improved functional recovery observed in these hearts.

Animals↗
PubMed1982

Implantation of the automatic defibrillator: the subxiphoid approach.

The automatic implantable defibrillator is an electronic device capable of diagnosing and correcting malignant venticular arrhythmias. While major thoracic surgery was required in the original 24 implants, a new technique for implanting the device has been developed. The first subxiphoid implantations have been accomplished with the defibrillatory function successfully tested intraoperatively. The advantages and indications of the subxiphoid technique are reviewed.

Arrhythmias, Cardiac↗
PubMed1982

Mechanisms of ischemic myocardial cell damage assessed by phosphorus-31 nuclear magnetic resonance.

Phosphorus-31 nuclear magnetic resonance (31P NMR) can estimate tissue intracellular pH as well as the content of high-energy phosphate metabolites in isolated perfused hearts. We used 31P NMR to examine mechanisms associated with the recovery of ventricular function in hearts subjected to global ischemia and reperfusion, with special emphasis on intracellular pH, a previously unreported variable. Single-dose and multiple-dose administration of a hyperkalemic cardioplegic solution were compared with hypothermia alone in 18 isolated perfused rabbit hearts. Hearts in group 1 were subjected to 24 degrees C hypothermia during 60 minutes of global ischemia; group 2 hearts received a single injection of 37-mM KCL cardioplegic solution at 10 degrees C at the onset of ischemia; and group 3 hearts received a similar initial cardioplegic injection followed by two subsequent 24 degrees C injections at 20-minute intervals during the ischemic period. Using an intraventricular balloon, maximal dP/dt provided a quantitative index of left ventricular performance before and after ischemia. Return of ventricular function expressed as a percentage of control was 54 +/- 11% for group 1, 84 +/- 6% for group 2, and 101 +/- 18% for group 3. Differences in the rate of development of intracellular acidosis were noted during the 60-minute ischemic period. Intracellular pH fell to 6.09 +/- 0.12 in group 1, 6.31 +/- 0.09 in group 2, an 6.79 +/- 0.03 in group 3. In all three groups intracellular pH returned to control (pH 7.20) within 10 minutes of reflow. The metabolic correlates of functional recovery appeared to be the tissue content of ATP at the end of ischemia and after reflow. ATP content at the end of ischemia was 22 +/- 2% of control in group 1 hearts, 31 +/- 4% in group 2 and 64 +/- 2% in group 3. After 45 minutes of reperfusion, ATP levels recovered to 33 +/- 9% of control in group 1, to 71 +/- 9% in group 2 and to 86 +/- 6% in group 3. Although there were no differences between groups in the content of creatine phosphate after 60 minutes of ischemia, the rates of creatine phosphate decline were dissimilar. Further, during the early reflow period, a marked overshoot in tissue creatine phosphate was detected, especially in groups 1 and 2. Histologic damage assessed by light microscopy correlated with the metabolic data, confirming that multidose cardioplegia provided the best preservation of cellular morphology. These results demonstrate that the magnitude of intracellular acidosis and the associated increase in inorganic phosphate correlate inversely with recovery of postischemic ventricular structure and function. ATP, but not creatine phosphate, content correlates with return of contractile performance after reperfusion. The overshoot in creatine phosphate during early reperfusion might impede optimal restoration of ATP content and, as a result, optimal recovery of cell functions.

Adenosine Triphosphate↗
PubMed1982

Failure of blood cardioplegia to protect myocardium at lower temperatures.

To assess the effect of temperature, oxygenated blood and crystalloid cardioplegic solutions (CPs) at infusion temperatures of 20 degrees C, 10 degrees C and 4 degrees C were compared. The amount of potassium in each CP was 25 mEq/l. There were six study groups with seven canine hearts in each group, all of which were subjected to 90 minutes of global ischemia at 20 degrees C, 10 degrees C or 4 degrees C, followed by 45 minutes of normothermic reperfusion. During ischemia, either blood or crystalloid CP was given every 30 minutes. With each infusion, any change in myocardial oxygen tension was recorded using mass spectrometry, and oxygen consumption (MVO2) was calculated. Left ventricular (LV) function was assessed before and after ischemia in all hearts by measuring isovolumic developed pressure using an intraventricular balloon. Injection of 20 degrees C blood CP resulted in a mean increase in intramyocardial oxygen tension (PO2) of 7 mm Hg. At 10 degrees C or 4 degrees C, blood CP infusions did not cause a significant increase in intramyocardial PO2, while with crystalloid CP, intramyocardial PO2 did not increase at any of the three infusion temperatures. The mean MVO2 with each blood CP injection, expressed as ml O2/100 g LV wet weight, was 16.5 +/- 0.8 for 20 degrees C blood, 4.1 +/- 0.3 for 10 degrees C blood and 3.5 +/- 0.4 for 4 degrees C blood (p less than 0.001, 20 degrees C blood vs 10 degrees C and 4 degrees C blood). MVO2 with each crystalloid CP injection was 0.9 +/- 0.1 for 20 degrees C CP, 0.8 +/- 0.1 for 10 degrees C CP, and 0.7 +/- 0.1 for 4 degrees C CP. Recovery of developed pressure after 45 minutes of reperfusion, expressed as a percentage of preischemic control, was 76.0 +/- 3.4% or 20 degrees C blood CP, 65.6 +/- 2.3% for 10 degrees C blood CP, and 54.0 +/- 2.7% for 4 degrees C blood CP (p less than 0.05, 20 degrees C blood CP vs 10 degrees C and 4 degrees C blood CP). Recovery of developed pressure, also expressed as a percentage of preischemic control, was 56.6 +/- 1.4% for 20 degrees C crystalloid CP, 72.9 +/- 3.0% for 10 degrees C crystalloid CP, and 72.0 +/- 2.3% for 4 degrees C crystalloid CP (p less than 0.05, 20 degrees C crystalloid CP vs 10 degrees C and 4 degrees C crystalloid CP). These data show that blood CP is most effective when infused at 20 degrees C. The use of 10 degrees C blood CP enhanced myocardial cooling, but was of no additional benefit, presumably because there was little oxygen delivery. Blood CP at 4 degrees C resulted in significantly poorer preservation of LV function. Crystalloid CP infused at either 4 degrees C or 10 degrees C was as effective as 20 degrees C blood CP, despite the absence of oxygen use by hearts treated with crystalloid CP.

Animals↗
PubMed1982

Assessment of myocardial protection during global ischemia with myocardial gas tension monitoring.

Intramyocardial gas tension monitoring with mass spectrometry allows for the continuous assessment of myocardial metabolic activity during prolonged global ischemia. With aortic cross-clamping there is a rapid decrease in intramyocardial oxygen tension (PmO2) and a steady increase in carbon dioxide tension (PmCO2). In laboratory studies the extent to which myocardial metabolic activity is reduced has correlated with the degree of myocardial protection being afforded. In the present study the metabolic consequences of single-dose versus multiple-dose infusions of a hyperkalemic cardioplegic solution were compared in 23 patients undergoing aortic valve replacement (AVR) for severe aortic stenosis. Group I (n = 13) had single-dose cardioplegia during AVR, while group II (n = 10) had multiple-dose cardioplegia. The preoperative status and the surgical procedures were identical except for two multiple-dose patients who also underwent single coronary bypass grafting. In group I the PmCO2 rose steadily and at cross-clamp release was 182 +/- 20 mm Hg, while in group II the PmCO2 rose only to 77 +/- 8 mm Hg (P less than 0.01). During reperfusion the peak PmCO2 in group I was 219 +/- 22 mm Hg versus 111 +/- 5 mm Hg in group II (P less than 0.01). After operation six patients in group I required pharmacologic support, and two other patients died of low cardiac output. In contrast, only one patient in group II required inotropic support, and there were no deaths. The significantly lower PmCO2 values with multiple-dose cardioplegia suggest both reduced metabolic activity and washout of metabolic end products, with resultant improved myocardial protection, evidenced by less postoperative left ventricular dysfunction.

Adult↗
PubMed1982

Reduced oxygen consumption with effective left ventricular venting during postischemic reperfusion.

The effect of left ventricular (LV) venting on myocardial oxygen consumption (MVO2) during reperfusion after hypothermic cardioplegic arrest was tested using 29 dogs placed on cardiopulmonary bypass (CPB). During the first 20 minutes of reperfusion after 45 minutes of 20 degrees C arrest, group 1 (n = 10) had total venting with the LV systolic pressure (LVSP) maintained at 0 mm Hg. Group 2 (n = 10) had partial venting with the LVSP at 41.6 +/- 1.4 mm Hg (one-half perfusion pressure), while in group 3 (n = 9), the LVSP was kept just below CPB perfusion pressure (76.6 +/- 3.1 mm Hg) by occlusion of the LV vent. Next, there were 10 minutes of partial bypass (CPB flow reduced by 50%) followed by cessation of CPB. MVO2 expressed as ml O2/100 g LV/min (wet weight) during the first 20 minutes of reperfusion was 2.66 +/- 0.33 for group 1, 2.40 +/- 0.36 for group 2 and 4.62 +/- 0.53 for group 3 (p less than 0.05 vs groups 1 and 2). There were no significant differences in MVO2 in any of the groups during partial CPB compared with the period without CPB. These results demonstrate that effective LV venting reduces MVO2 during reperfusion after hypothermic ischemic arrest. However, there was no reduction in MVO2 during partial CPB compared with the initial period without CPB. Thus, volume loading of the left ventricle during reperfusion by failing to vent leads to increased myocardial oxygen demand, which may be detrimental in hearts that have sustained significant ischemia or when revascularization is incomplete.

Animals↗
PubMed1981

Diagnosis and management of postoperative pericardial effusions and late cardiac tamponade following open-heart surgery.

The clinical and laboratory findings of 28 patients identified as having late pericardial effusions were examined. Eleven of these patients were asymptomatic; 9 patients had moderate symptoms including fatigue, malaise, weight gain, and dyspnea on exertion, and 8 patients with similar symptoms had evidence of cardiac tamponade. Ten patients underwent right heart catheterization in the intensive care unit; normal hemodynamics were confirmed in 4 and cardiac tamponade in 6 patients. Pericardiocentesis was effective in decompressing cardiac tamponade in 7 of 8 patients. One patient required operative subxiphoid drainage after unsuccessful pericardiocentesis. In addition, 5 patients with moderate clinical symptoms and pericardial effusions, who did not have cardiac tamponade, underwent pericardiocentesis because of a need for chronic anticoagulant therapy. The remaining patients were managed successfully by observation, discontinuation of warfarin when possible, fluid restriction, and diuretic therapy. All but 1 patient was symptomatically improved. A diagnostic and therapeutic schema is presented as an aid to early recognition of this troublesome and potentially lethal complication.

Adult↗
PubMed1981

Clinical and hemodynamic evaluation of the 19 mm Björk-Shiley aortic valve prosthesis.

Between November, 1973, and March, 1980, 43 patients underwent isolated aortic valve replacement with 19 mm Björk-Shiley prostheses at the Johns Hopkins Hospital. There were 4 male and 39 female patients ranging from 12 to 75 years old (mean, 54.5 years). Average weight was 62 +/- 2 kg and average body surface area, 1.64 +/- 0.3 m2. Five patients died within thirty days of operation; however, since 1975, hospital mortality has been 5.9%. The 38 survivors have been followed up for as long as 85 months (mean, 40 months). There were 4 late deaths, and actuarial survival in patients discharged from the hospital was 81% at five years. All long-term survivors were in New York Heart Association Functional Class I (29 patients) or Class II (5 patients). Preoperative and postoperative echocardiograms in 17 patients demonstrated significant decreases in mean left ventricular wall thickness (12.9 +/- 1.8 mm vs 10.3 +/- 1.4 mm; p less than 0.001) and in left ventricular mass (262 +/- 95 gm vs 188 +/- 50 gm; p less than 0.02). Postoperative cardiac catheterization data were obtained from an additional 24 patients undergoing aortic valve replacement with the 19 mm Björk-Shiley prosthesis at the National Heart Institute. Average peak systolic gradient at rest was 16 mm Hg (range, 0 to 45 mm Hg) and was found to be directly related to body surface area (r = 0.60, p less than 0.002). Average effective valve orifice area was 1.06 cm2 (range, 0.63 to 2.02 cm2). For patients with small aortic roots, aortic valve replacement with the 19 mm Björk-Shiley valve is a satisfactory and, perhaps, preferable alternative to aortic annuloplasty to accommodate larger sized prostheses.

Actuarial Analysis↗
PubMed1981

The harmful effects of ventricular distention during postischemic reperfusion.

To assess the effects of left ventricular distention during the early reperfusion period following ischemic arrest, 16 canine heart preparations were subjected to 45 minutes of hypothermic (27 degree C) cardioplegic arrest and normothermic reperfusion. Isovolumic left ventricular developed pressure and rate of rise of left ventricular pressure (dp/dt) were measured with an intraventricular balloon; endocardial/epicardial flow ratios were determined with microspheres; and myocardial gas tensions were monitored with mass spectrometry. During early reperfusion, Group 1 hearts (n = 8) were not distended (end-diastolic pressure = 0). Group 2 hearts (n = 8) were subjected to an enddiastolic pressure of 20 mm Hg for the initial 15 minutes of reperfusion. Group 2 hearts demonstrated impaired subendocardial blood flow after 5 minutes of reflow (0.75 +/- 0.06 vs 0.96 +/- 0.04, endocardial/epicardial flow rates, Group 2 vs Group 1) and persistent elevation of intramyocardial carbon dioxide (CO2) tension (68 +/- 4 vs 51 +/- 4 mm Hg, Group 2 vs Group 1). In addition, postischemic ventricular function was significantly worse in Group 2 hearts (60 +/- 7 vs 79 +/- 3% of control dP/dt, Group 2 vs Group 1, and 53 +/- 6 vs 81 +/- 5% of control left ventricular developed pressure, Group 2 vs Group 1). These data demonstrate that even mild distention during early reperfusion can result in reduced subendocardial perfusion and delayed washout of tissue CO2. Although myocardial blood flow and CO2 tension subsequently returned to normal in the distended hearts, left ventricular performance remained significantly depressed. This injury can occur clinically in nonvented hearts prior to the resumption of effective ventricular contraction.

Animals↗
PubMed1981

Mechanism of elevated left ventricular end-diastolic pressure after ischemic arrest and reperfusion.

The effects of ischemic arrest and reperfusion on isovolumic end-diastolic pressure, diastolic pressure-volume curves, and indices of ventricular relaxation and contractility were studied in an isolated feline heart preparation. In hearts subjected to 60 min of normothermic (37 degrees C) ischemic arrest, isovolumic developed pressure, and dP/dtmax during reperfusion returned to only approximately 60% of prearrest control levels. Isovolumic end-diastolic pressure (Ped) increased 37.0 +/- 4.3 mmHg and the time constant of ventricular relaxation was prolonged. Hearts maintained at 27 degrees C hypothermia during the 60-min ischemic period demonstrated improved contractile performance (approximately 100% of control), less elevation of Ped (21.4 +/- 4.5 mmHg), and no significant increase in the time constant of relaxation. In both groups of hearts, postarrest end-diastolic pressure-volume curves were shifted up and to the left, whereas indices of ventricular stiffness and muscle stiffness remained unchanged. These data suggest that the rise in isovolumic end-diastolic pressure observed after 1 h of ischemic arrest and reperfusion is the result of an upward and to the left shift of the entire diastolic pressure-volume relationship of the left ventricle. This shift does not appear to be related to diminished contractile performance or incomplete relaxation. Furthermore, the shift is not due to a change in muscle compliance, but to a reduction in the unstressed volume of the ventricle, which most likely results from myocardial contracture and edema.

Animals↗
PubMed1981

Reversal of experimental pulmonary hypertension with sodium nitroprusside.

Pulmonary vascular resistance may be elevated by the use of vasoconstrictive agents or by alveolar hypoxia. The present study was designed to determine the precise vasoconstrictive effects of the two inotropic agents, dopamine and epinephrine, as well as the effects of alveolar hypoxia on the pulmonary vascular system. In addition, the vasoactive effects of a known vasodilator, nitroprusside, were studied. A canine pulmonary lobar preparation was isolated in situ with its pulmonary artery and bronchus selectively cannulated in order to maintain a constant lobar pulmonary blood flow and in order to vary the inspired oxygen concentration from 95% to 0%. Pulmonary vascular pressures were determined by direct measurements and pulmonary vascular resistance units (PVRU) were calculated. Dopamine, epinephrine, and nitroprusside were infused into the isolated pulmonary artery singly and in combination, and the inspired oxygen concentration was varied during each drug infusion. The results of the study demonstrate that dopamine, epinephrine, and alveolar hypoxia all significantly elevate pulmonary vascular resistance. When these two drugs are used together in the presence of hypoxia, the effect on pulmonary resistance is additive. Furthermore, nitroprusside prevents the elevation of pulmonary vascular resistance caused by alveolar hypoxia, and when used with dopamine or epinephrine in the presence of hypoxia, nitroprusside reduces pulmonary vascular resistance toward normal.

Animals↗
PubMed1981

Superiority of perfluorocarbon cardioplegia over blood or crystalloid cardioplegia.

Oxygenated Fluosol-43 cardioplegia (CP), a perfluorocarbon with high oxygen solubility, was compared with crystalloid and oxygenated blood cardioplegia. Potassium in each CP was 25 mEq/l. Thirty perfused rabbit hearts in three groups of 10 hearts each underwent 100 minutes of global ischemia at 20 degrees C, followed by 45 minutes of reperfusion at 37 degrees C. During ischemia, CP was given every 20 minutes. With each CP injection, increases in myocardial oxygen tension were recorded using mass spectrometry and oxygen consumption (MVO2) was calculated. Left ventricular function was assessed before and after ischemia by measuring isovolumic developed pressure and dP/dt with an intraventricular balloon. Intramyocardial PO2 increased by 19.6 +/- 1.8 mm Hg in the Fluosol CP group, 0.4 +/- 0.1 mm Hg in the crystalloid CP group and 1.5 +/- 0.3 mm Hg in the blood CP group (p less than 0.001, Fluosol CP vs crystalloid CP and blood CP). MVO2 with each CP injection, expressed as ml O2/100 g dry weight, was 203.8 +/- 7.0 for Fluosol CP, 20.4 +/- 1.2 for crystalloid CP and 39.2 +/- 4.3 for blood CP (p less than 0.001 Fluosol CP vs crystalloid CP and blood CP). Recovery of maximal dP/dt after 45 minutes of reperfusion, expressed as a percentage of preischemic control, was 75.6 +/- 4.0% for Fluosol CP, 60.9 +/- 5.5% for crystalloid CP and 53.4 +/- 3.7% for blood CP (p less than 0.02 Fluosol CP vs blood CP and crystalloid CP). These data clearly show that the use of Fluosol cardioplegic solution enhanced oxygen delivery and use compared with blood and crystalloid cardioplegic solutions. The marked increase in intramyocardial oxygen and MVO2 with each injection of Fluosol CP shows that there is effective aerobic metabolic activity during ischemia, which may explain the improved functional recovery. The failure of blood CP to afford similar protection can be explained by a decreased oxygen release from hemoglobin due to the leftward shift of the oxygen-hemoglobin dissociation curve with hypothermia.

Animals↗