Hellebrekers L J, Liard J F, Laborde A L, Greene A S, Cowley A W
Department of Physiology, Medical College of Wisconsin, Milwaukee 53226.
Am J Physiol. 1990 Oct;259(4 Pt 2):H1270-7. doi: 10.1152/ajpheart.1990.259.4.H1270.
We investigated pressure-dependent autoregulatory responses in mesenteric, iliac, and renal vascular beds of conscious dogs during intravenous infusion of angiotensin II, phenylephrine, or arginine vasopressin at rates which increased arterial pressure by 20-40 mmHg. The arteries supplying these beds were instrumented with an electromagnetic flow probe, a nonoccluding catheter, and an electromagnetic flow probe, a nonoccluding catheter, and an occluder cuff connected with a servo-amplifier, which enabled us to return perfusion pressure to control levels during infusion of the vasoconstrictor agents. We attempted to differentiate between the increase in vascular resistance due to the direct effect of the vasoconstrictor agent and the increase induced by an autoregulatory response induced by elevations of aortic perfusion pressure. We measured a strong degree of autoregulation in the renal vascular bed with a fractional compensation value close to 1. Moderate autoregulation occurred in the mesenteric vascular bed, where the compensation was 0.4-0.5 with angiotensin II and phenylephrine and between 0.74 and 0.94 with vasopressin. No autoregulatory capacity could be demonstrated in the hindlimb. The findings indicate that, under conditions of increased systemic blood pressure, both the renal and the mesenteric vascular beds contribute to the increase in total peripheral resistance by pressure-dependent vasoconstrictor responses.
我们研究了清醒犬在静脉输注血管紧张素II、去氧肾上腺素或精氨酸加压素期间,肠系膜、髂血管和肾血管床的压力依赖性自身调节反应,输注速率可使动脉压升高20 - 40 mmHg。为供应这些血管床的动脉安装了电磁流量探头、非阻塞性导管,以及与伺服放大器相连的电磁流量探头、非阻塞性导管和阻塞袖带,这使我们能够在输注血管收缩剂期间将灌注压力恢复到对照水平。我们试图区分血管收缩剂直接作用导致的血管阻力增加与主动脉灌注压升高引起的自身调节反应所诱导的血管阻力增加。我们在肾血管床中测量到了较强程度的自身调节,分数补偿值接近1。肠系膜血管床出现中度自身调节,使用血管紧张素II和去氧肾上腺素时补偿值为0.4 - 0.5,使用加压素时补偿值在0.74至0.94之间。在后肢未表现出自身调节能力。这些发现表明,在全身血压升高的情况下,肾血管床和肠系膜血管床均通过压力依赖性血管收缩反应导致总外周阻力增加。