Liard J F, Dériaz O, Schelling P, Thibonnier M
Am J Physiol. 1982 Nov;243(5):H663-9. doi: 10.1152/ajpheart.1982.243.5.H663.
To better understand the role of arginine vasopressin in cardiovascular regulation, we measured in unanesthetized dogs regional blood flows with radioactive microspheres before and during 1-h vasopressin infusions that increased the vasopressin concentration of plasma by 11 +/- 0.6 pg/ml. Cardiac output measured by an electromagnetic flowmeter decreased by 13%. Blood flows to the skeletal muscle and skin, the areas most affected, decreased by 30.8 and 34.3%, respectively. In the same group of dogs a period of 48-h water restriction increased plasma vasopressin by 6.9 +/- 1.3 pg/ml and reduced cardiac output by 14.4%. Skeletal muscle blood flow decreased by 32.8%, a pattern strikingly similar to that following vasopressin infusion. Obvious differences between vasopressin infusion and dehydration were also noted, in particular in the skin and splanchnic areas. However, the possibility that vasopressin contributed to the cardiovascular adjustments to dehydration must be considered. The use of an antagonist of the vascular effects of vasopressin, [1-deaminopenicillamine, 2-(O-methyl)tyrosine]arginine-vasopressin ([dPTyr(Me)]AVP), did not permit us to clarify this issue, because this analogue given alone exerted pronounced systemic and regional cardiovascular effects that resembled those of vasopressin.
为了更好地理解精氨酸血管加压素在心血管调节中的作用，我们在未麻醉的犬类动物中，于输注血管加压素前及输注血管加压素1小时期间，使用放射性微球测量局部血流，输注血管加压素使血浆血管加压素浓度升高了11±0.6 pg/ml。通过电磁流量计测得的心输出量下降了13%。受影响最大的骨骼肌和皮肤区域的血流分别下降了30.8%和34.3%。在同一组犬类动物中，48小时的限水期使血浆血管加压素升高了6.9±1.3 pg/ml，并使心输出量降低了14.4%。骨骼肌血流下降了32.8%，这一模式与输注血管加压素后极为相似。血管加压素输注与脱水之间也存在明显差异，尤其是在皮肤和内脏区域。然而，必须考虑血管加压素在脱水导致的心血管调节中发挥作用的可能性。使用血管加压素血管效应的拮抗剂[1-脱氨青霉胺，2-(O-甲基)酪氨酸]精氨酸血管加压素([dPTyr(Me)]AVP)并不能使我们阐明这一问题，因为单独给予这种类似物会产生明显的全身和局部心血管效应，与血管加压素的效应相似。
