Effects of atrial pacing on left ventricular performance in patients with heart disease.
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Biomedical subjects
Publications and source records attributed to A M Weissler.
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Anaerobically periused hearts from rats with experimentally induced hyperthyroidism exhibited accelerated deterioration of pacemaker activity and ventricular performance. The diminished anaerobic performance of hyperthyroid hearts was associated with decreased adenosine triphosphate (ATP) levels and a reduced rate of anaerobic glycolysis as reflected in decreased lactic acid production during 30 min of anoxic perfusion.Studies on whole heart homogenates demonstrated inhibition at the phosphofructokinase (PFK) step of the glycolytic pathway. Such inhibition was not demonstrated in the hyperthyroid heart cytosol. It is postulated that an inhibitor of PFK which resides dominantly in the particulate fraction is probably responsible for the diminished anaerobic glycolysis and performance of the hyperthyroid heart.
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Employing an isolated perfused rat heart preparation, we investigated the contribution of anaerobic metabolic energy to the performance, recoverability, and ultrastructure of the heart perfused at 32 degrees C in 5% albumin in Krebs-Ringer Bicarbonate solution. During exposure to anoxia for 30 min, inclusion in the perfusate of the anaerobic substrate, glucose, resulted in marked improvement in electrical and mechanical performance of the heart and in enhanced recovery during the subsequent period of reoxygenation. Lactate production was fivefold greater in the glucose-supported anoxic heart than in the anoxic heart without glucose. Electron microscope sections of the hearts exposed to anoxia in the absence of glucose revealed alterations in mitochondrial morphology and dilatation of the longitudinal tubules. These morphologic changes during anoxia were averted by inclusion of glucose in the perfusion fluid. The data are consistent with the hypothesis that anaerobic energy generation plays a significant role in preserving myocardial function and structure and in promoting recoverability of the anoxic mammalian heart.
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We have investigated the possibility that alterations in the duration of the systolic preejection period can be used to estimate adrenergic influences on the human left ventricle. The preejection period was determined from high speed, simultaneous recordings of the phonocardiogram, carotid pulse tracing, and electrocardiogram. The preejection period was shortened by isoproterenol, epinephrine, and moderate doses of norepinephrine-all of which activate beta adrenergic receptors-and by cedilanid-D. It was unaltered by changes in heart rate induced by atropine and right atrial electrical pacing. Beta adrenergic receptor blockade by propranolol abolished the shortening effects of the three catecholamines but did not inhibit that due to cedilanid-D. Vasoconstriction, both alpha adrenergic (epinephrine and norepinephrine after propranolol) and nonadrenergic (angiotensin), prolonged the preejection period. Most of the shortening of the preejection period by beta adrenergic receptor activating agents and cedilanid-D and all of the prolongation accompanying pharmacologic vasoconstriction occurred after the onset of the first heart sound, thereby excluding changes in electrical-mechanical delay as a major factor in the observed preejection period responses. Shortening of the preejection period by beta adrenergic activity induced with isoproterenol was dose-related. Increasing doses of propranolol produced parallel shifts to the right in the isoproterenol dose-response curve. In 37 normal resting subjects intravenous propranolol (10 mg) prolonged the preejection period an average of 10 (SE +/- 1) msec. In six patients with psychogenic sinus tachycardia and a patient with a pheochromocytoma the presence of excessive beta adrenergic influences on the left ventricle was demonstrated by the finding of an initially short preejection period which responded with an abnormally great prolongation to beta adrenergic receptor blockade.
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