Coronary vascular hyperpermeability and angiotensin II.

H K Reddy, H Sigusch, G Zhou, S C Tyagi, J S Janicki, K T Weber
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Abstract

Elevations in plasma angiotensin II (AngII) are associated with evidence of vascular hyperpermeability expressed as efflux of plasma macromolecules into the perivascular and interstitial space. This exudative response is followed by a series of fibrogenic events that lead to a perivascular fibrosis of involved vessels. Mediators of hyperpermeability and fibrogenesis are unknown. In dogs receiving intravenous AngII, hemodynamic factors (i.e., arterial hypertension or coronary venoconstriction) were discounted as being responsible for the rise in cardiac lymph-to-plasma protein ratio. Accordingly, we investigated the relationship between AngII-induced coronary hyperpermeability and the release of prostaglandin E2 (PGE2) and activation of the basement membrane degrading matrix metalloproteinase, gelatinase/type IV collagenase. In dogs, cardiac lymph was monitored over the course of a 90-minute intravenous infusion of either AngII (0.2 to 0.3 micrograms/kg/min; n = 8) or saline solution (n = 6). Lymph was examined at 30-minute intervals for the following: total protein (Lowry's method), albumin (sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE)), plasma fibronectin (SDS-PAGE and enzyme-linked immunosorbent assay); PGE2 (radioimmunoassay) and gelatinase/type IV collagenase (zymography). In comparison with baseline we found a consistent rise in lymph flow (p = 0.02), total protein (p = 0.02), albumin, fibronectin, PGE2 (p = 0.03), and gelatinase/type IV collagenase (p = 0.019), which began after 30 minutes of AngII infusion. Similar trends were not observed in dogs receiving saline solution alone. We therefore conclude that AngII-induced coronary vascular hyperpermeability is associated with an early release of PGE2 and gelatinase.

冠状动脉血管高渗透性和血管紧张素II。
血浆血管紧张素II (AngII)的升高与血管高通透性有关,表现为血浆大分子向血管周围和间隙的外排。这种渗出反应之后是一系列的纤维化事件,导致受损伤血管的血管周围纤维化。高渗透性和纤维形成的介质尚不清楚。在接受静脉注射AngII的狗中,血流动力学因素(即动脉高血压或冠状动脉静脉收缩)被认为是导致心脏淋巴-血浆蛋白比率上升的原因。因此,我们研究了血管内皮诱导的冠状动脉高通透性与前列腺素E2 (PGE2)的释放和基底膜降解基质金属蛋白酶、明胶酶/ IV型胶原酶的激活之间的关系。在狗身上,在90分钟的静脉输注AngII(0.2至0.3微克/千克/分钟;n = 8)或生理盐水溶液(n = 6)。每隔30分钟检测一次淋巴:总蛋白(Lowry法)、白蛋白(十二烷基硫酸钠-聚丙烯酰胺凝胶电泳(SDS-PAGE))、血浆纤维连接蛋白(SDS-PAGE和酶联免疫吸附法);PGE2(放射免疫测定)和明胶酶/ IV型胶原酶(酶谱分析)。与基线相比,我们发现在AngII输注30分钟后,淋巴流量(p = 0.02)、总蛋白(p = 0.02)、白蛋白、纤维连接蛋白、PGE2 (p = 0.03)和明胶酶/ IV型胶原酶(p = 0.019)持续上升。在单独接受生理盐水的狗身上没有观察到类似的趋势。因此,我们得出结论,血管i诱导的冠状血管高通透性与PGE2和明胶酶的早期释放有关。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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