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犬内毒素休克期间小脑的升压效应观察。

An observed pressor effect of the cerebellum during endotoxin shock in the dog.

作者信息

Janssen H F, Lutherer L O, Barnes C D

出版信息

Am J Physiol. 1981 Mar;240(3):H368-74. doi: 10.1152/ajpheart.1981.240.3.H368.

Abstract

The current study investigates the possibility that the cerebellum may be involved in the regulation of mean arterial pressure (MAP) during endotoxin shock in the anesthetized dog. The effect of intravenously injected Escherichia coli endotoxin on MAP in the cerebellectomized dog was compared to that observed in the intact animal. Even though removal of the cerebellum did not significantly affect MAP in a control group, the cerebellectomized animal (unlike the intact animal) was unable to recover from the initial hypotension typically seen immediately following an intravenous endotoxin injection. Previous investigators have demonstrated that stimulation of fastigial nuclei in the cerebellum increases MAP via beta-adrenergic activation of the renin-angiotensin system. Captopril (SQ 14,225, an angiotensin I-converting enzyme inhibitor) was used to determine whether this system could be responsible for the maintenance of MAP during endotoxin shock. When continuously infused into the intact dog given endotoxin, captopril suppressed MAP to a level similar to that of the cerebellectomized group. A similar response pattern to endotoxin was also observed in animals with a spinal transection at C2.

摘要

本研究探讨了小脑可能参与麻醉犬内毒素休克期间平均动脉压(MAP)调节的可能性。将静脉注射大肠杆菌内毒素对去小脑犬MAP的影响与完整动物中观察到的影响进行了比较。尽管切除小脑对对照组的MAP没有显著影响,但去小脑动物(与完整动物不同)无法从静脉注射内毒素后立即出现的初始低血压中恢复。先前的研究人员已经证明,刺激小脑中的顶核通过肾素-血管紧张素系统的β-肾上腺素能激活来增加MAP。使用卡托普利(SQ 14,225,一种血管紧张素I转换酶抑制剂)来确定该系统是否可能负责内毒素休克期间MAP的维持。当持续输注到给予内毒素的完整犬体内时,卡托普利将MAP抑制到与去小脑组相似的水平。在C2水平进行脊髓横断的动物中也观察到了对内毒素的类似反应模式。

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