By J. Knoll and K. Kelemen (Eds.)
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Additional info for Advances in Pharmacological Research and Practice. Proceedings of the 4th Congress of the Hungarian Pharmacological Society, Budapest, 1985
Treatment of essential hyperten sion with atenolol causes a highly significant reduction in LVH /Margaroli et al. 1985/. The lack of close correlation between the degree of hypertension and the extent of LVH suggests that other factors may determine the cardiac response to raised blood pressure. Cardiac hypertrophy in experimental hyperten sion is accentuated by adrenergic stimuli and may prevent its regression when pressure is normalised /Tarazi et al. 1982/. Attenuating the trophic influences of catecholamines on LVH may be a valuable, indirectly beneficial effect of chronic beta-blockade in reducing LVH, and secondarily reducing the predis position to sudden death.
The 15k fraction obtained by molecular sieving from the supernatant of rat peritoneal leukocytes incubated in the presence of dexamethasone, inhibited PLA2 in vitro, and, when it was given intravenously or intracisternally, a marked pro tection against fatal postocclusion arrhythmias or stroke was detected. Lipocortin injected subcutaneously into carotid ar tery ligated rats exerted no cerebroprotective effect, showing that it does not pass the blood brain barrier. These results suggest that the cardioprotective and cerebroprotective effect of glucocorticoids may be mediated via the formation and re lease of lipocortin-like substances.
Cellular disruption. / detergent lysophospho chloroquine/ of p l a t e l e t s /Lefer; Ca a c c u m u l a t i o n in m i t o c h o n d r i a /Moneada/, of gastric Schrör/ /Corr in intracellular and W i space kowsky/ The last part of my paper is dedicated to the action the highly effective prostanoid Pgl2. This latter will be analysed in detail by Dr. Udvary from our group in the symposium on Prostaglandins. Briefly we have found in earlier experiments that Pgl2 and its stable analogue 7-oxo-Pgl2 exerts a late antiischaemic effect in the dog model of angina expressed here as % protec tion from ST-segment elevation in the epicardial ECG.