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正常血压和自发性高血压大鼠在脊髓毁损前后的动脉血压、心输出量和全身阻力。

Arterial pressure, cardiac output and systemic resistance before and after pithing in normotensive and spontaneously hypertensive rats.

作者信息

Albrecht I, Hallbäck M, Julius S, Lundgren Y, Stage L, Weiss L, Folkow B

出版信息

Acta Physiol Scand. 1975 Jul;94(3):378-85. doi: 10.1111/j.1748-1716.1975.tb05897.x.

DOI:10.1111/j.1748-1716.1975.tb05897.x
PMID:1101646
Abstract

After complete cardiovascular denervation mean arterial pressure (MAP) falls to almost equally low levels in spontaneously hypertensive rats (SHR) and normotensive control rats (NCR). This has earlier been suggested to indicate a dominance of neurogenic mechanisms in established SHR hypertension. -- In the present study, total peripheral resistance (TPR) remains, however, some 35 per cent higher in adult SHR than in NCR after pithing while cardiac output (CO), and stroke volume, is 35 per cent lower in SHR. These opposite differences in TPR and CO after denervation, resulting in equal MAP levels in SHR and NCR, seem rather to be a consequence of the rapidly established structural adaptation that affects all SHR high-pressure cardiovascular sections. Thus, the SHR precapillary resistance vessels display thickened walls and luminal narrowing, which keeps TPR higher than in NCR even during maximal vasodilatation. Due to hypertrophy, the SHR left ventricle exhibits a reduced myocardial stretch for a given filling pressure and stroke volume is consequently reduced more than in NCR after complete denervation. -- Paradoxically, therefore, rather than reflecting any dominance of neurogenic mechanisms in established SHR hypertension the MAP equalization in SHR and NCR after cardiovascular denervation emphasizes the hemodynamic importance of cardiovascular structural changes present in hypertension.

摘要

在完全去除心血管神经支配后,自发性高血压大鼠(SHR)和正常血压对照大鼠(NCR)的平均动脉压(MAP)降至几乎相同的低水平。此前有人认为,这表明在已形成的SHR高血压中神经源性机制占主导地位。——然而,在本研究中,成年SHR在脊髓毁损后总外周阻力(TPR)仍比NCR高约35%,而心输出量(CO)和每搏输出量在SHR中则低35%。去神经支配后TPR和CO的这些相反差异,导致SHR和NCR中的MAP水平相等,这似乎是影响所有SHR高压心血管节段的快速建立的结构适应的结果。因此,SHR的毛细血管前阻力血管显示出壁增厚和管腔狭窄,这使得即使在最大血管舒张时TPR也高于NCR。由于肥大,SHR左心室在给定的充盈压下心肌拉伸减少,因此在完全去神经支配后每搏输出量比NCR减少得更多。——因此,矛盾的是,心血管去神经支配后SHR和NCR中的MAP平衡并非反映已形成的SHR高血压中神经源性机制的任何主导地位,而是强调了高血压中存在的心血管结构变化的血流动力学重要性。

相似文献

1
Arterial pressure, cardiac output and systemic resistance before and after pithing in normotensive and spontaneously hypertensive rats.正常血压和自发性高血压大鼠在脊髓毁损前后的动脉血压、心输出量和全身阻力。
Acta Physiol Scand. 1975 Jul;94(3):378-85. doi: 10.1111/j.1748-1716.1975.tb05897.x.
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Structural and functional adaptation in the rat myocardium and coronary vascular bed caused by changes in pressure and volume load.压力和容量负荷变化引起的大鼠心肌和冠状血管床的结构与功能适应性改变。
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Research on Experimental Hypertension in Prague (1966-2009).布拉格实验性高血压研究(1966-2009)。
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2
Hypertension-induced remodelling: on the interactions of cardiac risk factors.高血压诱导的重塑:关于心脏危险因素的相互作用
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