Protective effect of diltiazem on ischaemic heart muscle

Protective effect of diltiazem on ischaemic heart muscle

101 PROTECTIVE EFFECT OF DILTIAZEM ON ISCHAEMIC HEART MUSCLE. Alice Zamanis, Jean Verdetti and Jog1 de Leiris. Laboratoire de Physiologie animale, Uni...

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101 PROTECTIVE EFFECT OF DILTIAZEM ON ISCHAEMIC HEART MUSCLE. Alice Zamanis, Jean Verdetti and Jog1 de Leiris. Laboratoire de Physiologie animale, Universite Scientifique et Medicale, Grenoble, France. The ability of diltiazem to limit the extent of myocardial necrosis was studied in rat 48 hours after left coronary artery ligation. Myocardial infarct size was estimated by planimetry of histologic sections of serial slices of ventricular mass. Each section was stained for succinodehydrogenase activity. Diltiazem (30-100 ug.kg-l.min-l) was infused intravenously for 20 min before and 60 min after ligation. Diltiazem-treated hearts showed a significant reduction in the volume of myocardial necrosis. However the topography of the protection was complex. Mean arterial blood pressure and heart rate were significantly lower in diltiazem-treated rats. 48 hours after ligation diltiazemtreated rats exhibited significantly higher cardiac content of ATP and creatine phosphate than did untreated rats. This ability ischaemia

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EFFECT OF RIBOSE ON ADENINE NUCLEOTIDE(AN) METABOLISM IN RAT HEARTS WITH EXPERIMENTALMYOCARDIALINFARCTION. H.-G.Zimmer, H.Ibel and G.Korb, Department of Physiology, University of Munich and Institute of Pathology, General Hospital Weiden, Germany. Ribose has been shown to potentiate the enhancement of AN biosynthesis in hearts of isoproterenol-treated rats thus preventing the decrease of the ATP level and reducing the incidence of focal myocardial cell lesions (Zimmer et al., Science 207, 319,198O). The present studies were performed to elucidate whether ribose may also have an effect in hearts with infarction which was produced by ligation of the descending branch of the left coronary artery. Thereafter, the rats received continuous'i.v. infusion of 0.9% NaCl or ribose (200 mg/kg/h) for 24 and 48 hours, respectively. AN biosynthesis was then measured in the noninfarcted part of the heart (septum and right ventricle) which was devoid of any necrosis and mesenchymal infiltration. Ribose did augment the increase in AN biosynthesis (nmoles/g/h) occurring in the noninfarcted myocardium both after 24 hours (31.5 + 5.3, n=6; sham-operated controls: 14.9 + 1.4, n=4; ribose: 51.5 + 6.4, n=4) and after 48 hours (24.8 + 4.2, n=4; Tham-operated controls: 6.6 + 1.4, n=3; ribose: 48.2 + 8.0,-n=6). The decline of the ATP content (pmoies/g) observed in the enFire infarcted hearts after 48 hours (2.4 + 0.18, n=6; sham-operated controls: 4.4 + 0.15, n=5) was less pronouncedwhen ribose was administered (3.2 + 0.20, n=8). Thus, ribose further stimulates AN biosynthesis in the nor&farcted myocardium thus leading to an elevation of the ATP level which may have a beneficial effect.