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Biomedical subjects

J T Flaherty

Publications and source records attributed to J T Flaherty.

At least 55 records · Page 3Linked to original sources
PubMed1985

Results of a randomized prospective trial of intraaortic balloon counterpulsation and intravenous nitroglycerin in patients with acute myocardial infarction.

A randomized prospective clinical trial compared combined treatment with intraaortic balloon pumping and intravenous nitroglycerin for 4 to 5 days with routine clinical management in 20 patients with extensive myocardium at risk for infarction as evidenced by a thallium defect score of 7.0 units or greater. No significant differences in mortality or clinical outcome were observed between the 10 patients receiving the combined treatment and the 10 receiving routine management. In 14 patients two-dimensional echocardiograms obtained 6 to 24 hours after the onset of symptoms and at follow-up 6 to 16 days later (after completion of combined intraaortic balloon pumping plus nitroglycerin therapy) were analyzed to determine whether infarct segment or noninfarct segment lengths were affected by therapy. Among these 14 patients, 5 (3 receiving the combined therapy and 2 receiving routine management) demonstrated an increase in infarct segment length of greater than 1.0 cm. Mean infarct segment length increased 0.30 +/- 0.44 cm in patients receiving the combined therapy and 0.29 +/- 0.36 cm in patients on routine management (p = NS). In contrast, noninfarct segment length increased greater than 1.0 cm (mean increase 1.20 +/- 0.39) in five of seven patients on routine management but in none of 7 patients receiving intraaortic balloon pumping plus nitroglycerin therapy (mean decrease 0.22 +/- 0.20 cm) (p less than 0.05). No significant differences were noted in left ventricular ejection fraction, as measured by gated blood pool scintigraphy, or thallium perfusion defect score in a comparison of day 1 (pretreatment) with day 4 thallium or day 7 to 14 gated blood pool scintigrams. Thus, in patients with extensive myocardium at risk, it is unlikely that a reduction in mortality or a significant improvement in myocardial perfusion or ventricular function can be obtained by early intervention with intraaortic balloon pumping in combination with nitroglycerin. Although this combined therapy failed to prevent infarct segment lengthening (infarct expansion), the combined afterload-lowering effects of intraaortic balloon pumping and nitroglycerin did appear to prevent dilation or remodeling of noninfarcted segments during the first 2 weeks after acute myocardial infarction.

Adult↗
PubMed1984

Unstable angina. Rational approach to management.

Unstable angina can be defined by the development of chest pain at rest, usually with reversible S-T segment changes. It has been found in patients in whom angina developed at rest in the cardiac catheterization laboratory that a decrease in coronary sinus oxygen saturation preceded changes in left ventricular relaxation and contractility that preceded the development of chest pain and/or electrocardiographic changes. Increases in heart rate and/or blood pressure followed, rather than preceded, these ischemic episodes. These findings suggest that a decrease in oxygen supply, rather than an increase in oxygen demand, is the cause of episodes of angina at rest. Although principles of treatment of effort angina have emphasized the reduction of myocardial oxygen demand, treatment of rest angina should logically emphasize therapies that improve oxygen supply. A stepwise approach to the treatment of patients admitted to the Coronary Care Unit with unstable angina is proposed. The initial step consists of replacing oral and/or transcutaneous nitrates with an intravenous infusion of nitroglycerin while maintaining beta-blockers and calcium blockers at their previous doses. Nitroglycerin dilates coronary arteries and intercoronary collateral channels in addition to reducing preload and afterload. Intravenous administration allows faster titration to an effective dose and also more rapid reversal of hemodynamic effects, if the patient's status changes. The second step would consist of maintaining the nitroglycerin infusion and beta-blockers and adding or increasing the dose of calcium channel blockers. Slow channel calcium blockers dilate coronary arteries and prevent or reverse coronary spasm in addition to reducing afterload. The third step consists of adding or increasing the dose of beta-blockers in subgroups of patients with resting tachycardia and/or arterial hypertension. The fourth and final step would be to employ intra-aortic balloon counterpulsation therapy and/or to perform urgent coronary angiography. In patients with suitable coronary anatomy, angiography could be followed by percutaneous transluminal angioplasty or coronary artery bypass surgery.

Adrenergic beta-Antagonists↗
PubMed1984

Progression and resolution of myocardial reflow injury.

The development of and recovery from a severe yet nonlethal myocardial injury following hyperkalemic cardioplegia and prolonged hypothermic global ischemia was examined over 14 days in a rat model of heterotopic intraabdominal cardiac isograft transplantation. Mitochondrial enzymatic markers of myocardial ischemic injury and light microscopic signs of damage were examined. Eighteen hearts were arrested in situ using hyperkalemic cardioplegia and subjected to a mean of 38 min of ischemia at 20 degrees C as transplantation was achieved. No changes in mitochondrial creatine kinase (CKm) activity, mitochondrial malate dehydrogenase (MDHm) activity, their ratio, or morphologic evidence of injury were found during 8 days of reperfusion. In a second group of 66 hearts, the duration of hypothermic cardioplegic ischemia was extended by 120 min before transplantation. Neither unreperfused hearts nor hearts reperfused for only 1 hr demonstrated significant depression of enzyme activities or microscopic evidence of injury. However, after 1 day of reperfusion, CKm and MDHm activities were depressed to 36 and 44% of control levels (P less than 0.05). These activities had returned to control levels by 2 days of reperfusion and remained stable for 12 days thereafter. Light microscopic analysis revealed cellular injury to be maximal at 1 to 2 days of reperfusion with gradual improvement noted over the following 12 days. These observations suggest the existence of a mitochondrial injury following prolonged cardioplegic arrest and hypothermic global ischemia that is maximal after 24 hr of reperfusion but shows evidence of improvement thereafter. These findings justify aggressive support of the poorly functioning heart for the first few days after prolonged global ischemia.

Animals↗
PubMed1984

Identification and control of noncoronary collateral blood flow.

To identify the source of noncoronary collateral myocardial blood flow and to establish methods to control it during induced ischemia, 29 dogs were placed on cardiopulmonary bypass. The right and left ventricles were vented, vent flows were measured volumetrically, and intracavitary left ventricular (LV) pressures were monitored. After induction of ischemia by aortic cross-clamping and infusion of cardioplegic solution, six different microspheres 7 to 10 microns in diameter were injected into the aorta at six different times to measure myocardial blood flow during the following interventions:vent drainage of the right or left ventricle or both, proximal ligation of both coronary arteries, severance of the proximal pulmonary artery or the ascending aorta or both, and ligation of the bronchial arteries. Without effective LV venting, LV intracavitary pressure rose to 7.0 +/- 0.1 mm Hg (mean +/- standard error of the mean) and myocardial blood flow in the anterior left ventricle was 2.3 +/- 1.3 ml/100 gm/min. When the LV vent was opened, vent flow was 35.9 +/- 3.5 ml/min and myocardial blood flow fell to 0.3 +/- 0.2 ml/100 gm/min. Right ventricular (RV) vent flow was absent except when the LV vent was occluded, and this RV vent flow was abolished by ligating the coronary arteries. With bronchial artery ligation, LV vent flow ceased and myocardial blood flow was virtually absent. These studies demonstrate that myocardial blood flow does occur during induced ischemia, but that the source of this blood flow is primarily through systemic-pulmonary channels. True noncoronary collateral myocardial blood flow was virtually nonexistent.

Animals↗
PubMed1984

Immediate improvement of dysfunctional myocardial segments after coronary revascularization: detection by intraoperative transesophageal echocardiography.

To ascertain the immediate effects of coronary artery bypass grafting on regional myocardial function, intraoperative transesophageal two-dimensional echocardiograms were obtained in 20 patients using a 3.5 MHz phased array transducer at the tip of a flexible gastroscope. Cross-sectional images of the left ventricle were obtained at multiple levels before skin incision and were repeated serially before and immediately after cardiopulmonary bypass. Using a computer-aided contouring system, percent systolic wall thickening was determined for eight anatomic segments in each patient at similar loading conditions (four each at mitral and papillary muscle levels). Of the 152 segments analyzed, systolic wall thickening improved from a prerevascularization mean value (+/- SEM) of 42.7 +/- 2.9% to a postrevascularization mean value of 51.6 +/- 2.6% (p less than 0.001). Thickening improved most in those segments with the worst preoperative function (p less than 0.001). Chest wall echocardiograms obtained 8.4 +/- 2.3 days after operation showed no deterioration or further improvement in segmental motion compared with transesophageal echocardiograms obtained after revascularization. Thus: regional myocardial function frequently improves immediately after bypass grafting, with increases in regional thickening being most marked in those segments demonstrating the most severe preoperative dysfunction, and this improvement appears to be sustained; and in some patients, chronic subclinical ischemic dysfunction is present which can be improved by revascularization.

Aged↗
PubMed1984

Maintenance of aerobic metabolism during global ischemia with perfluorocarbon cardioplegia improves myocardial preservation.

We used phosphorus-31 nuclear magnetic resonance to test the ability of a perfluorocarbon blood substitute that has been shown in previous studies to improve oxygen delivery to hypothermic myocardium to maintain aerobic high-energy phosphate metabolism during total global ischemia. Twenty-three isolated perfused rabbit hearts were subjected to 180 min of hypothermic (23 degrees C) global ischemia followed by 45 min of normothermic reperfusion. Hearts received multiple doses of a cardioplegic solution that contained either oxygenated perfluorocarbon (Fluosol O2), nonoxygenated perfluorocarbon (Fluosol N2), or standard crystalloid hyperkalemic cardioplegic solution (STD-KCl) at 30 min intervals. Recovery of isovolumic left ventricular developed pressure (LVDP) was used to assess preservation of contractile function. Recovery of LVDP was 84 +/- 19% of preischemic control values with Fluosol O2, 68 +/- 16% with Fluosol N2, and 67 +/- 17% with STD-KCl (p = .058 vs Fluosol N2 and p = .056 vs STD-KCl). During 3 hr of ischemia intracellular pH (pHi) fell to 6.68 +/- 0.20 with STD-KCl and to 6.71 +/- 0.14 with Fluosol N2 but remained above 7.00 throughout the ischemic period with Fluosol O2 (p less than .0001 vs Fluosol N2 or STD-KCl). Myocardial ATP content was better preserved at 107 +/- 14% of control values with Fluosol O2 compared to 60 +/- 18% of control with Fluosol N2 and 75 +/- 21% of control with STD-KCl (p less than .001 vs Fluosol N2, p = .002 vs STD-KCl). Phosphocreatine (PCr) was also better preserved with Fluosol O2.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphate↗
PubMed1984

Localization of regional myocardial ischemia by recording of monophasic action potentials.

Identification of regional myocardial ischemia by TQ-ST segment mapping, while commonly used, is relatively imprecise and nonspecific. In 41 open-chest dogs we examined whether monophasic action potentials (MAPs) recorded from the myocardial surface by means of a new contact-electrode technique could be used to more precisely and specifically index regional myocardial ischemia. After ligation of the left anterior descending coronary artery (LAD), epicardial and endocardial MAPs from the ischemic region demonstrated shortening of plateau duration followed by a progressive loss in amplitude to 48 +/- 8% and in maximum upstroke velocity (dV/dtmax) to 9 +/- 2% of control (n = 7). Regional hyperkalemia produced by intracoronary injection of potassium chloride also resulted in regional decreases in duration, amplitude, and dV/dtmax of the MAP. Similar to previously reported effects on transmembrane action potentials, ischemia- or hyperkalemia-induced loss in MAP amplitude was due to decreases in both diastolic (negative) and systolic (positive) potential and paralleled TQ segment depression and "true" ST segment elevation in unipolar direct current-coupled electrograms recorded from an adjacent site. In eight canine hearts we compared the abilities of MAP recordings and TQ-ST segment measurements in defining a region of myocardial ischemia. Transmural ischemia with a sharp flow border was produced by LAD ligation and distal embolization with dental rubber. One hour later simultaneous MAP and TQ-ST mapping was performed in each dog at 45 to 65 epicardial sites inside and outside the ischemic region. TQ-ST voltage was significantly increased 10 to 20 mm outside the visible cyanotic border, reaching a maximum just inside the border and decreasing progressively toward the center of the ischemic region to values not significantly different from those from sites 10 mm outside the ischemic border. In contrast, MAP amplitude and dV/dtmax were normal up to 5 to 10 mm outside the cyanotic border, decreased sharply across a lateral transition zone of only 8 mm to 8.7 +/- 2.3% and 4.3 +/- 0.9% of control, respectively, at sites 4 to 6 mm inside the border, and were uniformly abnormal across the entire ischemic region. Recordings made 3 hr after LAD ligation revealed an overall decline in the magnitude of TQ-ST, making definition of the ischemic border by TQ-ST even less precise, whereas the differences between MAPs from normal and ischemic myocardium had become even more pronounced than after 1 hr. Thus, unlike TQ-ST segment measurements, MAP recordings uniquely define ischemic and nonischemic sites and more precisely localize the border of an ischemic region.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗
PubMed1984

Parenteral nitroglycerin: clinical usefulness and limitations.

It would appear that nitroglycerin, which has been the time-honored therapy for angina pectoris, has a much broader therapeutic scope. Since the Food and Drug Administration has only recently released intravenous nitroglycerin for general clinical use, other clinical applications may develop in the future. Intravenous nitroglycerin appears to provide predictable and rapid lowering of left ventricular filling pressure and mean arterial pressure in patients with ischemic heart disease. The ability to increase cardiac output appears to be greatest in those patients with severe left ventricular failure. However, anti-ischemic effects are evident in all hemodynamic subgroups. Compared with sodium nitroprusside, nitroglycerin appears to have more favorable effects on intercoronary collateral flow, pulmonary artery pressure, and intrapulmonary shunting. In the perioperative setting, nitroglycerin appears to be as effective an afterload-lowering agent as nitroprusside in the majority of patients. In view of its more favorable effects on coronary collateral resistance, nitroglycerin may be preferable to nitroprusside for many such afterload-lowering applications, especially in patients with significant obstructive coronary disease. With greater clinical use, intravenous nitroglycerin will undoubtedly prove to be a valuable new tool for the management of patients with ischemic heart disease.

Angina Pectoris↗
PubMed1984

Propranolol-induced postoperative hypertension following coronary artery bypass grafting.

Fifteen patients receiving propranolol preoperatively and undergoing coronary artery bypass grafting had serum propranolol levels determined preoperatively and at several times early postoperatively. In addition, the patients' hemodynamic parameters and postoperative sodium nitroprusside dose requirements were monitored. All patients had significant multivessel disease and normal left ventricular function. Preoperative serum propranolol levels ranged from 16 to 243 ng/ml, with a mean level of 92 +/- 17 ng/ml; propranolol measured at the end of bypass ranged from 0 to 92 ng/ml, with a mean level of 23 +/- 7 ng/ml. Fourteen patients (93%) had hypertension postoperatively and required intravenous sodium nitroprusside to maintain mean blood pressure at or below 90 mm Hg. According to linear regression analysis, the severity of the postoperative hypertension or, specifically, the nitroprusside dose requirements, correlated significantly with the patients' serum propranolol levels postoperatively (correlation coefficient, R = 0.76, with p less than 0.001). The one normotensive patient had no detectable serum propranolol at any time postoperatively. No correlation was noted between the patient's preoperative serum propranolol levels and the need for nitroprusside therapy postoperatively. These results demonstrate that there is a significant relationship between residual propranolol and the development of hypertension postoperatively.

Adult↗
PubMed1983

Comparison of intravenous nitroglycerin and sodium nitroprusside in acute myocardial infarction.

Initial studies from our institution demonstrated beneficial anti-ischemic effects of short-term infusion of intravenous nitroglycerin in patients with acute myocardial infarction. At lower doses, nitroglycerin was shown to be principally a venodilator; at higher doses, a mixed venous and arterial dilating effect was demonstrated. The acute hemodynamic effects of nitroglycerin varied in the presence or absence of left ventricular failure; patients with the most severe degree of left ventricular dysfunction had the most beneficial hemodynamic effect. Similar differential effects have been demonstrated for nitroprusside in other studies. A comparison of the arterial vasodilating potency of nitroglycerin and nitroprusside in patients in whom acute hypertension develops following coronary artery bypass surgery revealed that equal lowering of arterial pressure and systemic vascular resistance could be demonstrated in 85 percent of the patients with comparable infusion rates. Review of previous clinical and laboratory studies in animals, in which the effects of nitroglycerin and nitroprusside were compared, in most cases revealed opposite effects on intercoronary collateral flow and, thereby, opposite effects on the severity of regional ischemia. Our recently completed randomized placebo-controlled clinical trial employing a 48-hour infusion of nitroglycerin demonstrated a higher incidence of significant improvement in abnormalities noted on scintigraphy when nitroglycerin treatment was initiated within 10 hours of the onset of symptoms. Beneficial effects of early nitroglycerin treatment have also been demonstrated in previous clinical trials. In similar studies, which utilized nitroprusside infusions in patients with acute myocardial infarction, some investigators found an increase in short-term mortality with early nitroprusside treatment whereas others found benefit. The uniformly favorable results of the clinical trials that utilized intravenous nitroglycerin, although not necessarily supporting its routine use in all patients, would support a preference for nitroglycerin over nitroprusside for the treatment of congestive heart failure and/or acute hypertension complicating acute myocardial infarction.

Aged↗
PubMed1983

A randomized clinical trial of intravenous nitroglycerin in patients with acute myocardial infarction: benefits of early treatment.

A prospective randomized clinical trial of intravenous nitroglycerin administered for 48 hours following acute infarction was undertaken to determine whether clinical improvement and/or preservation of ischemic myocardium could be demonstrated. One hundred four patients were randomized to receive either nitroglycerin or placebo infusion. Nitroglycerin infusion was titrated to lower mean arterial pressure 10% using non-invasive monitoring. Early nitroglycerin treatment, defined as treatment initiated less than 10 hours after symptom onset, resulted in a lower incidence of new congestive heart failure, myocardial infarct extension, and/or early death from pump failure (15%) compared to late nitroglycerin treatment (50%, p = 0.008) or early placebo treatment (48%, p = 0.01). Improvement in ejection fraction of greater than or equal to 10% was demonstrated in 7 of 20 (35%) early nitroglycerin treated patients compared to 6, 11 and 0% of patients in the three other subgroups, respectively (p = 0.004). Similarly, thallium-201 perfusion scintigrams showed a greater than 75% improvement in defect score in 23 (48%) patients receiving nitroglycerin within 10 hours compared to 14%, 33% and 0% respectively, in the remaining subgroups (p = 0.035). However, before routine administration of nitroglycerin can be recommended for all patients with acute infarction, larger clinical trials will be required.

Clinical Trials as Topic↗
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

Improved myocardial protection with perfluorocarbon cardioplegia.

An oxygenated perfluorocarbon solution containing 25 mEq/L potassium has been investigated as a potentially useful cardioplegic solution to be administered to patients undergoing prolonged induced global myocardial ischemia during open-heart surgical procedures. Experimental studies have demonstrated that, compared to simply crystalloid and cold-blood cardioplegic solutions, an oxygenated perfluorocarbon cardioplegic solution administered at low temperatures can deliver oxygen to the ischemic heart and that this available oxygen is utilized by the heart. In an experimental study in which a Fluosol-43 solution was compared to both crystalloid and oxygenated-blood cardioplegia, Fluosol-43-treated hearts demonstrated better recovery of left ventricular function following postischemic reperfusion.

Animals↗
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

Nifedipine in unstable angina: a double-blind, randomized trial.

We assessed the efficacy of adding nifedipine to the conventional treatment of unstable angina in 138 patients in a prospective, double-blind, randomized, placebo-controlled trial. There was no difference between the two groups in the dose of conventional antianginal medication or in age, prior myocardial infarction, ejection fraction, or other risk factors. Failure of medical treatment (defined as sudden death, myocardial infarction, or bypass surgery within four months) occurred in 43 of 70 patients given placebo and in 30 of 68 given nifedipine. Kaplan-Meier survival-curve analysis of the number and time dependence of treatment failures demonstrated a benefit of nifedipine over placebo (P = 0.03). The benefit was particularly marked in patients with ST-segment elevation during angina (P = 0.02). Side effects (transient hypotension or diarrhea) required withdrawal of the drug from four patients given nifedipine and from one given placebo. We conclude that the addition of nifedipine to conventional therapy is safe and effective in unstable angina.

Adult↗
PubMed1982

Use of an isolated heart model to test the utilization of substrates for inclusion in cardioplegic solutions.

Previous studies from our laboratory utilized an isolated isovolumic Langendorff heart preparation to study myocardial metabolism and preservation of left ventricular function following global ischemia and reperfusion. The present study employed a similar preparation to assess the utilization of various glycolytic substrates by monitoring the level of left ventricular developed pressure. Twenty-one rabbit hearts were perfused with an oxygenated but substrate-free Krebs-Ringer-bicarbonate solution in order to deplete the hearts of endogeneous substrate stores. Following a brief period of anoxic, substrate-free perfusion, hearts were perfused with one of seven test substrates under anaerobic, then aerobic conditions. Under anaerobic conditions only perfusion of glucose resulted in a measurable increase in ventricular function which was still less than 20% of control. Under aerobic conditions, provision of glucose, pyruvate, or the combination of alpha-glycerol phosphate and pyruvate resulted in significant increases in contractile function which were 40-70% of control. These results obtained in normal hearts will provide a base line for future studies of the metabolism of postischemic hearts which may have altered cell membrane permeability and/or enzymatic activity.

Animals↗