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血管紧张素II刺激清醒犬的呼吸,并拮抗压力感受器抑制。

Angiotensin II stimulates respiration in awake dogs and antagonizes baroreceptor inhibition.

作者信息

Ohtake P J, Jennings D B

机构信息

Department of Physiology, Queen's University, Kingston, Ontario, Canada.

出版信息

Respir Physiol. 1993 Mar;91(2-3):335-51. doi: 10.1016/0034-5687(93)90110-v.

DOI:10.1016/0034-5687(93)90110-v
PMID:8469855
Abstract

The effects of intravenous infusions of physiologic doses of angiotensin II (AII) on expired ventilation (VE) and acid-base balance were determined in awake dogs. A control infusion of saline was followed by AII infusion, initially with mean arterial pressure (MAP) raised 15%, and then with MAP at control levels by concurrent infusion of sodium nitroprusside (SNP). To control for SNP, the protocol was repeated using arginine vasopressin (AVP). Ventilatory responses to CO2 (VRC) were measured at the end of these protocols and separately with MAP elevated during infusion of AII. With AVP, increased MAP inhibited VE, heart rate (HR) and metabolism. However, with MAP elevated during AII infusion, stimulation by AII opposed baroreceptor reflexes and these variables, as well as plasma AVP, did not change. When MAP was lowered to control during AII infusion all variables increased. With AII, PaCO2 followed VE changes, decreasing 3 Torr with MAP at control levels; however, [H+] remained constant due to a decrease in arterial strong ion difference. The stimulatory effects of AII were not due to SNP; SNP did not stimulate VE during AVP infusion. The slope of the VRC was unaltered by AII infusion or MAP; however, AVP reduced the VRC slope. Physiological increases in AII stimulate VE and other systems at normal MAP and maintain several regulatory systems at control levels during baroreceptor inhibition.

摘要

在清醒犬中测定了静脉输注生理剂量的血管紧张素II(AII)对呼出通气量(VE)和酸碱平衡的影响。先输注生理盐水作为对照,随后输注AII,最初使平均动脉压(MAP)升高15%,然后通过同时输注硝普钠(SNP)使MAP维持在对照水平。为了对照SNP的影响,使用精氨酸加压素(AVP)重复该方案。在这些方案结束时以及在输注AII期间MAP升高时分别测量对二氧化碳的通气反应(VRC)。使用AVP时,MAP升高会抑制VE、心率(HR)和代谢。然而,在输注AII期间MAP升高时,AII的刺激作用对抗压力感受器反射,并且这些变量以及血浆AVP均未改变。当在输注AII期间将MAP降至对照水平时,所有变量均增加。使用AII时,动脉血二氧化碳分压(PaCO2)随VE变化,在MAP处于对照水平时降低3托;然而,由于动脉强离子差减小,[H⁺]保持恒定。AII的刺激作用并非由于SNP;在输注AVP期间SNP不会刺激VE。AII输注或MAP均未改变VRC的斜率;然而,AVP降低了VRC斜率。生理水平的AII升高在正常MAP时刺激VE和其他系统,并在压力感受器抑制期间将多个调节系统维持在对照水平。

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