The authors have counted circulating anuclear carcasses of endothelial cells by a new method in 105 patients with acute myocardial infarction and angina pectoris. In infarction cases as well as in severe angina a significant increase of endothelaemia was observed in duration of several days. No increase was observed in milder angina cases (type I--II).
Nicotine administered i.v. or p.o. in doses above 0.0125 mg/kg to the rat caused a highly significant increase in circulating anuclear carcasses of endothelial cells estimated by an original method. This effect of nicotine was completely prevented by a prior oral administration of the flavonoids hydroxyethylrutosides (HR) or Mono-7-HR.
Levels of haemostatic variables that may be involved in thrombogenesis have been compared in groups of men of similar mean age in communities at very low (Gambia), high (England and Czechoslovakia) or very high (Scotland and Finland) risk of ischaemic heart disease (IHD). There was a consistent gradient of higher factor VII levels with higher IHD risk and also suggestive gradients in the case of two other vitamin K dependent factors, factors II and X. Mean platelet counts were lower and mean fibrinolytic activity was greater in Gambian men than in European men. There was a suggestive though not entirely consistent association between mean fibrinogen levels and IHD risk in the groups from IHD-endemic countries. The results as a whole, and particularly those on factor VII, strengthen the case for the increasingly detailed epidemiological as well as laboratory investigation of the role of the haemostatic system in thrombogenesis and IHD.
A single intravenous injection of homocystine led to an increase in the number of circulating endothelial cells in the blood of rats. We observed also increased permeability of the lung capillaries, platelet sequestration and activation of the venostatic thrombosis. Endothelial injury is probably the key mechanism of thrombotic and atherosclerotic complications in homocystinuria, an inborn error of the amino acid metabolism.
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