Role of arginine vasopressin and angiotensin II in cardiovascular responses to combined acute hypoxemia and hypercapnic acidosis in conscious dogs.
Role of arginine vasopressin and angiotensin II in cardiovascular responses to combined acute hypoxemia and hypercapnic acidosis in conscious dogs.
复制标题
精氨酸加压素和血管紧张素 II 在清醒狗对急性低氧血症和高碳酸血症联合酸中毒的心血管反应中的作用。
DOI：
10.1172/jci111427
复制
发表时间：
1984
期刊：
影响因子：
--
通讯作者：
Carey,RM
中科院分区：
文献类型：
--
作者：
RoseJr,CE;GodineJr,RL;Rose,KY;Anderson,RJ;Carey,RM
在合并低氧血症和高碳酸血症酸中毒时，循环血管紧张素和血管加压素升高与循环变化的生理关系尚不清楚。为了评估血管紧张素II和血管加压素的作用，研究了7只未麻醉的雌性杂种狗，控制钠摄入量（80 meq/24 h X 4 d），在急性低氧血症和高碳酸血症合并酸中毒（PaO2, 36 +/- 1 mmHg, PaCO2, 55 +/- 2 mmHg, pH = 7.16 +/- 0.04） 40 min时，在以下条件下：(a)完整状态下单独输注载药；(b)通过输注d，l-心得安阻断β -肾上腺素能（1.0 mg/kg, 0.5 mg/kg / h）；抗利尿激素拮抗剂d-(CH2)5Tyr（甲基）精氨酸-抗利尿激素（10微克/千克）；(d)通过额外输注1-肌氨酸，8-丙氨酸血管紧张素II（2.0微克/千克每分钟）同时抑制血管加压素和血管紧张素II。由于总外周阻力下降，在车辆联合血气紊乱期间平均动脉压升高似乎与心输出量增加有关。在合并低氧血症和高碳酸血症酸中毒时，β -肾上腺素能阻断可消除总外周抵抗的下降，并减少心输出量的上升，但全身升压反应不变。此外，合并血气紊乱时平均动脉压的升高与单用抗利尿激素抗逆性药物没有变化。相反，在合并低氧血症和高碳酸中毒期间同时使用抗利尿激素和血管紧张素II抑制剂，尽管心输出量增加，但由于总外周抵抗更明显地下降，导致全身降压反应消失。在血管加压素和血管紧张素II阻断联合血气紊乱时，循环儿茶酚胺增加，提示在低氧血症和高碳酸血症联合酸中毒的最后30分钟，全身升压反应的消除与交感神经系统活性的降低无关。这些研究表明，血管加压素和血管紧张素II是急性低氧血症和高碳酸血症合并酸中毒时全身性降压反应的主要因素。
The physiological relationship of increased circulating angiotensin II and vasopressin to circulatory changes during combined hypoxemia and hypercapnic acidosis is unclear. To evaluate the role(s) of angiotensin II and vasopressin, seven unanesthetized female mongrel dogs with controlled sodium intake (80 meq/24 h X 4 d) were studied during 40 min of combined acute hypoxemia and hypercapnic acidosis (PaO2, 36 +/- 1 mmHg; PaCO2, 55 +/- 2 mmHg; pH = 7.16 +/- 0.04) under the following conditions: (a) intact state with infusion of vehicles alone; (b) beta-adrenergic blockade with infusion of d,l-propranolol (1.0 mg/kg bolus, 0.5 mg/kg per h); of the vasopressin pressor antagonist d-(CH2)5Tyr(methyl)arginine-vasopressin (10 micrograms/kg); and (d) simultaneous vasopressin pressor and angiotensin II inhibition with the additional infusion of 1-sarcosine, 8-alanine angiotensin II (2.0 micrograms/kg per min). The rise in mean arterial pressure during the combined blood-gas derangement with vehicles appeared to be related to increased cardiac output, since total peripheral resistance fell. Beta-adrenergic blockade abolished the fall in total peripheral resistance and diminished the rise in cardiac output during combined hypoxemia and hypercapnic acidosis, but the systemic pressor response was unchanged. In addition, the rise in mean arterial pressure during the combined blood-gas derangement was unaltered with vasopressin pressor antagonism alone. In contrast, the simultaneous administration of the vasopressin pressor and angiotensin II inhibitors during combined hypoxemia and hypercapnic acidosis resulted in the abrogation of the overall systemic pressor response despite increased cardiac output, owing to a more pronounced fall in total peripheral resistance. Circulating catecholamines were increased during the combined blood-gas derangement with vasopressin pressor and angiotensin II blockade, suggesting that the abolition of the systemic pressor response in the last 30 min of combined hypoxemia and hypercapnic acidosis was not related to diminished activity of the sympathetic nervous system. These studies show that vasopressin and angiotensin II are major contributors to the systemic pressor response during combined acute hypoxemia and hypercapnic acidosis.