Titlebook: Arteriosclerosis; New Insights into Pa H. Just,W. Hort,A. M. Zeiher Conference proceedings 1994 Dr. Dietrich Steinkopff Verlag GmbH & Co. K

变化无常

河流

Extracellular matrix degrading metalloproteinases in the pathogenesis of arteriosclerosis,ncentration-dependent manner, Ro 31–4724 also inhibited outgrowth. Rabbit aortic smooth muscle cells were further shown to release MMPs, namely a 95 and a 72 kDa gelatinases that were inhibited by Ro 31–4724 and Ro 31–7467. The evidence suggests that degradation of basement membrane by gelatinase is

奇怪

Vascular renin-angiotensin-system, endothelial function and atherosclerosis?,ion of elastic arteries upregulates the local renin-angiotensin system in these arteries and thereby downregulates nitric oxide releasability. Enhanced local synthesis of the trophic factor angiotensin-II and reduced releasability of the antitrophic factor nitric oxide appear to cooperate in the tro

Indent

Endothelial dysfunction in atherosclerosis,review, evidence for these alterations will be considered, potential interventions for restoring endothelium-dependent relaxations examined, and the possible impact of endothelial dysfunction in atherosclerosis considered.

Hemoptysis

New determinants of the uptake of atherogenic plasma proteins by arteries,ectly supports the evidence that LDL leaves the plasma by transcytosis through the endothelial cells..In anesthetized rabbits and in conscious rats the uptake of LDL, methylated to prevent its removal by high-affinity receptors (m-LDL), is significantly increased by noradrenaline and by adrenaline a

演绎

Assessment of endothelial modulation of coronary vasomotor tone: Insights into a fundamental functilopment of atherosclerosis, and impaired endothelial vasodilation is the predominant mechanism underlying inappropriate vasoconstriction in atherosclerosis. However, endothelial vasodilator dysfunction is not only confined to atherosclerotic epicardial vessels, but may also extend into the coronary

议程

男生戴手铐

Therapeutic approaches to the control of coronary atherosclerosis,h lower plasma cholesterol provide one approach. Another approach is to use calcium antagonists which not only lower blood pressure, but also directly interfere with some of the metabolic events involved in lesion formation.