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Biomedical subjects

C S Apstein

Publications and source records attributed to C S Apstein.

123 records · Page 7Linked to original sources
PubMed1978

Acute cardiac ischemia and reperfusion: contractility, relaxation, and glycolysis.

The mechanical and metabolic effects of 3 min of complete global ischemia and 25 min of reperfusion were studied in the isolated rat heart. The decrease in contracile function was biphasic; a rapid 50% decline occurred in the first 10 s of ischemia, after which contractile function transiently stabilized and then fell at a slower rate. During reperfusion, recovery of relaxation was impaired relative to recovery of contractile function. A second period of ischemia and reflow produced changes in contractility, relaxation, and lactate production virtually identical to the initial one. In the absence of glycolytic blockade, tissue lactate accumulation developed, no contracture occurred, the pacing threshold did not increase, and reperfusion after 3 min of ischemia resulted in complete recovery of contractile function. Glycolytic blockade with 0.1 mM iodoacetate (IAA) prevented ischemic lactate production, accelerated the fall in contractility, caused irreversible contracture after 30 s of ischemia, an irreversible increase in pacing threshold within 3 min of ischemia, and poor recovery of contractile function with reperfusion. Thus during the first 3 min of severe ischemia, glycolysis exerted a net beneficial effect on myocardial function despite significant tissue lactate accumulation.

Animals↗
PubMed1977

Left ventricular performance and graft patency after coronary artery-saphenous vein bypass surgery: early and late follow-up.

Left ventircular performance and graft patency were studied postoperatively at 2 weeks in 19 patients, and at 9 months in 15 patients. At early follow-up, left ventricular ejection fraction and mean rate of circumferential shortening were unchanged for the group as a whole, but were slightly improved in patients who had had a moderately abnormal preoperative ejection fraction of 0.30 to 0.60. At late follow-up, 10 of 14 patients had occluded at least one graft or the proximal segment of the grafted coronary artery and had an associated decrease in ventricular function. The risk of graft occlusion was greater if the preoperative ejection fraction was decreased; seven of 10 patients with a preoperative EF of less than 0.60 suffered one or more graft occlusions, but only three of 16 patients with a preoperative EF greater than 0.60 had a postoperative graft occlusion (p is less than 0.05). The results suggest that bypass graft surgery is not generally indicated as a measure to improve ventricular function in patients with ischemic heart disease.

Angina Pectoris↗
PubMed1977

Graded global ischemia and reperfusion. Cardiac function and lactate metabolism.

The effect of global ischemia of different degrees of severity and reperfusion was studied in the isolated working rat heart. Four degrees of ischemia were induced by reducing the control total coronary flow of 8 ml/min to 0, 0.04, 0.4, or 0.8 ml/min for 30 minutes, after which the coronary flow was returned to the control level. After severe ischemia (0 and 0.04 ml/min ischemic coronary flow groups), recovery of contractility was to less than 30% of the control, pre-ischemic value of ventricular developed pressure and dP/dt, and irreversible cardiac contracture and an increased pacing threshold occurred. After moderate ischemia (0.4 and 0.8 ml/min ischemic coronary flow groups), contractile function recovered completely, ischemic contracture was rapidly reversible and the pacing threshold did not increase. The moderately ischemic groups were able to function at a stable, low level of contractility for the 30 minute ischemic period, whereas the severely ischemic groups had no contractile activity. The amount of calculated tissue lactate accumulation correlated with the occurrence of irreversible ischemic injury; the severely ischemic groups which failed to recover with reperfusion accumulated 3-5 times as much lactate as the moderately ischemic groups which recovered completely. The results suggest that relatively small differences in the severity of the ischemic condition can markedly affect the degree of tissue injury.

Animals↗
PubMed1976

Experimental myocardial infarction. XIII. Sequential changes in left ventricular pressure-length relationships in the acute phase.

Diastolic pressure-length relationships of an ischemic region of the canine left ventricle were measured over a six-hour period following left anterior descending coronary artery ligation, and their evolution was compared with the extent of systolic aneurysmal bulging. Normalized ischemic segment length excursion, which after coronary artery ligation may be taken as a measure of systolic aneurysmal bulging, increased during the first hour after ligation but thereafter declined toward control values. Concurrently, reciprocal changes were demonstrated in the slope of the end-diastolic pressure-length curves obtained during transient pressure loading of the left ventricle. These data show that the magnitude of acute systolic aneurysmal bulging followed experimental coronary artery ligation is determined not only by loss of contractile function, but also by changes in passive pressure-length relationships of the myocardium. Moreover, the results indicate that development of akinesis in experimental ischemia, heretofore demonstrated only in the chronic phase of infarction, may begin within hours of the onset of myocardial ischemia.

Acute Disease↗
PubMed1975

Factors influencing tolerance of cardiac muscle to hypoxia.

The effects of isoproterenol, glucose, and pH on the responses of isolated rat cardiac muscle to hypoxia (95% N2, 5% CO2) were examined while the muscles were contracting isometrically 12 times a minute at 28 degrees C. In the presence of 5.5 mM glucose, 10(-5) M isoproterenol and alkaline pH (7.8) improved the performance of cardiac muscle during early hypoxia. This was followed by a premature decline in developed tension, and contracture appeared. Recovery of function following reoxygenation with 95% O2 and 5% CO2 after a 60-min period of hypoxia was poor. Acid pH (6.8) resulted in an early decline of mechanical activity during hypoxia; but contracture did not appear, and full recovery of developed tension was seen upon reoxygenation after 60 min of hypoxia. When 22 mM glucose was used as substrate, the early responses to hypoxia were not altered; but late performance was improved, contracture did not appear, and full recovery after 60 min of hypoxia was seen. If additional glucose was added to the bath after 30 min of hypoxia (concentration 22 mM), little effect on developed tension was evident; but contracture diminished and recovery after 60 min of hypoxia was improved. Addition of 22 mM glucose allowed isoproterenol to exert its inotropic effect in the absence of late deleterious changes. The data support the concept that factors tending to increase the utilization of limited stores of anaerobic substrate during hypoxia facilitate deterioration. By increasing exogenous glucose, the support of inotropic activity without late adverse effects appears possible, and recovery is improved upon reoxygenation.

Acidosis↗
PubMedDate not supplied

A model of anoxic preconditioning in the isolated rat cardiac myocyte. Importance of adenosine and insulin.

OBJECTIVE: Ischemic or hypoxic preconditioning has been shown, in multicellular preparations, to reduce post-ischemic injury. In the present study, we attempted to develop a model of preconditioning in isolated rat myocytes in order to facilitate investigation into the mechanism of preconditioning. METHODS: The protective effect of a short period (10 min) of anoxia and reoxygenation against a subsequent longer period of anoxia was studied in single, electrically stimulated (0.2 Hz, 37 degrees C) adult rat cardiac myocytes. The control group received only the long period of anoxia. Three protocols were tested: Protocol 1 in which octanoate was the only substrate; Protocol 2 in which only glucose was present during all normoxic phases and during the preconditioning anoxia and octanoate alone during the prolonged period of anoxia and; Protocol 3 in which protocol 2 was repeated with the addition of adenosine (100 microM) and insulin (15 microU/ml) during the prolonged anoxic period. The end-point of assessment was loss of cell morphology, i.e., hypercontracture (death) or relengthening (survival) on reoxygenation following the prolonged anoxic period. Membrane integrity was also examined at the end of each protocol by observing if the cells excluded trypan blue. RESULTS: No protective effect of preconditioning on cell survival was observed in protocols 1 or 2. In contrast, in protocol 3, a significant protection was observed in the preconditioned versus control group (58% vs 27% survival respectively; p < 0.001). However, in the absence of preconditioning, adenosine and insulin provided no additional protection in the control group. No significant differences in trypan blue exclusion were observed between the groups in any protocol. CONCLUSIONS: These results suggest that preconditioning cannot protect against a subsequent period of anoxia where the accumulation of metabolic products, e.g., adenosine is prevented. However, that protection can be re-instated by the presence of adenosine and insulin during the period of prolonged anoxia. Furthermore, this study suggests that the preconditioning by anoxia may induce a change in the A1-receptor or its second messenger system such that adenosine is able to provide protection.

Adenosine↗