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[急性高铁血红蛋白血症大鼠微循环变化的机制]

[Mechanisms of changes of microcirculation in rats under acute methemoglobinemia].

作者信息

Rozova K V, Sydoriak N H

出版信息

Fiziol Zh (1994). 2014;60(5):43-51.

Abstract

It was investigated the features of microcirculation and mechanisms it's conditioned, under acute administration of sodium nitrite in 5 mg of dry substance per 100 g of body weight. It was shown that acute administration of sodium nitrite leads to the development of methemoglobinemia, arterial and venous hypoxemia, and severe tissue hypoxia. Increase in the diffusion path O2 at methemoglobinemia is caused due to significant hyperhydratation of lung air-blood barrier and its individual layers, and is accompanied by a decrease in both components of the diffusion capacity of the lungs for oxygen: its membrane and blood components. It was revealed that the administration of sodium nitrite has a double effect, leading to inactivation of hemoglobin, as well as to microcirculatory disturbances associated primarily with changes in the regulation of vascular tone. In this initial perfusion per unit volume of tissue per time unit intrinsic for the organism defines a set of mechanisms which are responsible for changes in tissue blood flow under methemoglobinemia.

摘要

研究了在每100克体重急性给予5毫克干物质亚硝酸钠的情况下微循环的特征及其调节机制。结果表明,急性给予亚硝酸钠会导致高铁血红蛋白血症、动脉和静脉低氧血症以及严重的组织缺氧。高铁血红蛋白血症时氧扩散路径增加是由于肺气血屏障及其各层的显著过度水化所致,并伴有肺对氧扩散能力的两个组成部分(其膜和血液成分)的降低。研究发现,亚硝酸钠的给药具有双重作用,导致血红蛋白失活,以及主要与血管张力调节变化相关的微循环紊乱。在这种情况下,单位时间内单位体积组织的初始灌注为机体固有,它定义了一组负责高铁血红蛋白血症时组织血流变化的机制。

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