Thomas G R, Walder C E, Thiemermann C, Vane J R
William Harvey Research Institute, Saint Bartholomew's Hospital Medical College, London, England.
J Cardiovasc Pharmacol. 1990 Feb;15(2):211-7. doi: 10.1097/00005344-199002000-00006.
To identify those vascular beds that contribute to the elevated peripheral resistance (TPR) seen in spontaneously hypertensive rats (SHR) as compared to Wistar-Kyoto rats (WKY), the distribution of cardiac output, organ blood flow, and regional vascular resistance were measured using radiolabelled microspheres. WKY and SHR had similar heart rates, cardiac outputs, and cardiac stroke volumes, whereas SHR had significantly elevated TPR. This increased TPR was the cumulative effect of significant elevations in vascular resistance in the brain, testes, epididymides, gastrointestinal tract, pancreas/mesentery, skin, kidneys, and skeletal muscle. Only in the renal and skeletal muscle vasculature was this elevation in resistance associated with reduced blood flow. Haemodynamic responses to bradykinin [thought to act through a release of endothelium-derived relaxing factor (EDRF)] were similar in both WKY and SHR with the exception of the liver where no reduction of hepatic arterial resistance was seen in the SHR. We suggest that the increase in resistance in the renal and skeletal muscle vasculature is due to active vasoconstriction in these beds. This vasoconstriction diverts a significant proportion of the cardiac output through other vascular beds, especially the brain, liver, and coronary circulation. This will result in increased shear-stress and consequent damage to endothelial cells.
为了确定与Wistar-Kyoto大鼠（WKY）相比，自发性高血压大鼠（SHR）中导致外周阻力（TPR）升高的血管床，使用放射性标记微球测量了心输出量、器官血流量和局部血管阻力的分布。WKY和SHR的心率、心输出量和心搏量相似，而SHR的TPR显著升高。这种TPR的增加是大脑、睾丸、附睾、胃肠道、胰腺/肠系膜、皮肤、肾脏和骨骼肌血管阻力显著升高的累积效应。只有在肾和骨骼肌血管系统中，这种阻力升高才与血流量减少有关。WKY和SHR对缓激肽[被认为通过释放内皮衍生舒张因子（EDRF）起作用]的血流动力学反应相似，但肝脏除外，在SHR中未观察到肝动脉阻力降低。我们认为肾和骨骼肌血管系统中阻力的增加是由于这些血管床的主动血管收缩。这种血管收缩使很大一部分心输出量通过其他血管床，特别是大脑、肝脏和冠状动脉循环分流。这将导致剪切应力增加，进而损伤内皮细胞。
