Fejes-Tóth G, Brinck-Johnsen T, Náray-Fejes-Tóth A
Dr. Margarete Fischer-Bosch Institute of Clinical Pharmacology, Stuttgart, Federal Republic of Germany.
Am J Physiol. 1988 May;254(5 Pt 2):H947-53. doi: 10.1152/ajpheart.1988.254.5.H947.
The effect of arginine vasopressin (AVP) pressor blockade on the response to graded hemorrhage was investigated on conscious, unstressed, freely moving rats. The parameters studied were mean arterial pressure (MAP), heart rate (HR), blood velocity in the ascending aorta (ABV), and plasma concentrations of AVP (pAVP), renin (PRC), corticosterone (pCS), and catecholamines. After the first hemorrhage (0.75% of body wt over 5 min), MAP remained unchanged while ABV declined and HR increased. The two subsequent hemorrhages brought about significant reduction in MAP, HR, and ABV. pAVP, pCS, and PRC increased gradually during the experiment, while plasma catecholamine levels remained unchanged except for epinephrine, which increased after the third hemorrhage. After pretreatment with the AVP-pressor antagonist, [d(CH2)5Tyr(Me)]AVP, the hemorrhage-induced cardiovascular changes were practically identical to those seen in control animals. Results with AVP blockade performed after the third hemorrhage were also negative. A pressor role of AVP after hypotensive hemorrhage could only be revealed in the presence of converting-enzyme inhibition and alpha-adrenergic blockade. In addition, [d(CH2)5Tyr(Me)]AVP did not modify the effect of hemorrhage on pCS and catecholamines and caused only a slight enhancement of the increase in PRC. It is concluded that conscious, nonstressed rats, if all compensatory mechanisms are allowed full expression, exhibit a normal cardiovascular compensatory response to hemorrhage in the absence of functional AVP pressor receptors.
在清醒、未受应激、自由活动的大鼠身上研究了精氨酸加压素（AVP）升压阻断对分级出血反应的影响。所研究的参数包括平均动脉压（MAP）、心率（HR）、升主动脉血流速度（ABV）以及AVP（pAVP）、肾素（PRC）、皮质酮（pCS）和儿茶酚胺的血浆浓度。第一次出血（5分钟内失血量为体重的0.75%）后，MAP保持不变，而ABV下降，HR增加。随后的两次出血导致MAP、HR和ABV显著降低。实验过程中pAVP、pCS和PRC逐渐升高，而血浆儿茶酚胺水平除肾上腺素在第三次出血后升高外其余保持不变。用AVP升压拮抗剂[d(CH2)5Tyr(Me)]AVP预处理后，出血诱导的心血管变化与对照动物所见基本相同。第三次出血后进行AVP阻断的结果也是阴性。只有在存在转化酶抑制和α-肾上腺素能阻断的情况下，降压性出血后AVP的升压作用才能显现出来。此外，[d(CH2)5Tyr(Me)]AVP并未改变出血对pCS和儿茶酚胺的影响，只是使PRC的升高略有增强。结论是，在没有功能性AVP升压受体的情况下，如果所有代偿机制都能充分发挥作用，清醒、未受应激的大鼠对出血会表现出正常的心血管代偿反应。
