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[血管活性物质升压反应的血流动力学结构]

[Hemodynamic structure of pressor reactions to vasoactive substances].

作者信息

Samoĭlenko A V, Tkachenko B I, Orlov V A, Nichkov S, Shenfel'der G

出版信息

Fiziol Zh SSSR Im I M Sechenova. 1979 Jan;65(1):74-81.

PMID:437201
Abstract

In cats, similar changes of the blood pressure had different hemodynamic structures under the influence of catecholamines or angiotensin. Adrenalin was able to evoke a pressor response by means to either caridac or vascular factor. In the former case, the increase in the cardiac output was induced both by an increasing blood flow towards the heart and by an additive outflow of the blood from the minor to the major circulation; in the latter case, the increase in the general peripheral resistance entailed a decrease in the cardiac output in spite of the augmentation of the venous return which determined a delay of the blood in the minor circulation. The latter variant of interrelationships among hemodynamic parameters can occur under the influence of noradrenaline as well. A combined similarly rendered participation of the cardiac and the vascular factors in the increasing the blood pressure occurs under the influence of angiotensin and sometimes of noradrenaline. The participation of cardiac output in the pressor response may depend on hemodynamic shifts in the minor circulation which either limit or facilitate, or leave unchanged the rate of increment of the cardiac output.

摘要

在猫身上,在儿茶酚胺或血管紧张素的影响下,血压的类似变化具有不同的血流动力学结构。肾上腺素能够通过心脏或血管因素引发升压反应。在前一种情况下,心输出量的增加是由流向心脏的血流量增加以及从微循环到体循环的额外血液流出引起的;在后一种情况下,尽管静脉回流增加导致微循环中血液滞留,但全身外周阻力的增加导致心输出量减少。血流动力学参数之间的后一种相互关系变体在去甲肾上腺素的影响下也会出现。在血管紧张素以及有时在去甲肾上腺素的影响下,心脏和血管因素在血压升高中会以类似的方式共同参与。心输出量在升压反应中的参与可能取决于微循环中的血流动力学变化,这些变化要么限制、促进心输出量的增加速率,要么使其保持不变。

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