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自发性高血压大鼠对急性低氧血症的血流动力学反应改变。

Altered hemodynamic responses to acute hypoxemia in spontaneously hypertensive rats.

作者信息

Walsh G M, Tsuchiya M, Cox A C, Tobia A J, Frohlich E D

出版信息

Am J Physiol. 1978 Mar;234(3):H275-9. doi: 10.1152/ajpheart.1978.234.3.H275.

Abstract

Conscious spontaneously hypertensive rats (SHR), 5--7 wk old, were studied hemodynamically by the direct Fick procedure to determine whether high total peripheral resistance (TPR) coexisted with increased oxygen consumption (QO2) at an early stage of hypertension development. Since under resting conditions cardiac output in SHR was not significantly different from normotensive controls, the elevated arterial pressure and QO2 were associated with increased TPR. Arterial hypoxemia was induced to reduce oxygen availability and to assess whether increased TPR in SHR could be reversed by this procedure. During hypoxemia, normotensive controls (WKY) responded with increased cardiac output and decreased arterial pressure and TPR. In contrast, arterial pressure and cardiac output fell in SHR; and the increased TPR persisted. QO2 fell in hypoxemic SHR demonstrating that the relationship between total body oxygen consumption and cardiac output was abnormal in young SHR, and that increased TPR in SHR was not dependent on resting levels of QO2 or oxygen availability. Although QO2 was elevated in SHR compared to age-matched WKY, this condition was not essential for maintained elevated vascular resistance.

摘要

对5至7周龄的清醒自发性高血压大鼠(SHR),采用直接Fick法进行血流动力学研究,以确定在高血压发展的早期阶段,高总外周阻力(TPR)是否与氧耗量(QO2)增加同时存在。由于在静息状态下,SHR的心输出量与正常血压对照大鼠无显著差异,因此动脉血压升高和QO2增加与TPR升高有关。诱导动脉低氧血症以减少氧供应,并评估该方法是否能逆转SHR中升高的TPR。在低氧血症期间,正常血压对照大鼠(WKY)的心输出量增加,动脉血压和TPR降低。相比之下,SHR的动脉血压和心输出量下降;而升高的TPR持续存在。低氧血症的SHR的QO2下降,表明幼龄SHR全身氧耗量与心输出量之间的关系异常,且SHR中升高的TPR不依赖于静息状态下的QO2水平或氧供应。尽管与年龄匹配的WKY相比,SHR的QO2升高,但这种情况对于维持血管阻力升高并非必不可少。

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