Literature DB >> 6372515

Anteroventral hypothalamus and hemorrhagic shock: cardiovascular and neuroendocrine responses.

G Feuerstein, A K Johnson, R L Zerbe, R Davis-Kramer, A I Faden.   

Abstract

The anteroventral third ventricle (AV3V) region was shown to be a site of central integration of sympathetic pressor pathways and central pressor and vasopressin (VP) release by angiotensin II (ANG II). Since the AV3V area seems to have an important role in the regulation of the three major pressor systems, we investigated the role of the AV3V in cardiovascular recovery after hemorrhage, a known stimulus for sympathetic, ANG II, and VP release. Conscious AV3V-lesioned (n = 19) and sham-operated rats (n = 14) underwent bleeding (40% of blood volume) through an arterial line. Mean blood pressure, heart rate, and plasma ANG II, VP, and catecholamines were monitored over 24 h. The exact site of lesion was determined by microscopic examination. The mean blood pressure and heart rate of both groups of rats were not different before or after hemorrhage. Plasma catecholamines, ANG II, and VP responses were also the same as were hematocrit and water consumption 24 h after the bleeding. Despite the lack of difference between control and lesioned animals with regard to cardiovascular, humoral, and neuroendocrine responses to hypovolemia, the AV3V-lesioned rats had a significantly higher early mortality rate. These data indicate that the AV3V may be an important region in recuperation and survival after hemorrhagic shock, but through mechanisms unrelated to activation of VP, renin-ANG II, or the sympathetic nervous system.

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Year:  1984        PMID: 6372515     DOI: 10.1152/ajpregu.1984.246.4.R551

Source DB:  PubMed          Journal:  Am J Physiol        ISSN: 0002-9513


  3 in total

1.  Redistribution of cardiac output after hypothalamic lesions and hemorrhage.

Authors:  S L Bealer; D W Busija
Journal:  Exp Brain Res       Date:  1987       Impact factor: 1.972

2.  Inhibiting the rabbit caudal ventrolateral medulla prevents baroreceptor-initiated secretion of vasopressin.

Authors:  W W Blessing; J O Willoughby
Journal:  J Physiol       Date:  1985-10       Impact factor: 5.182

3.  Controlled Hemorrhage Sensitizes Angiotensin II-Elicited Hypertension through Activation of the Brain Renin-Angiotensin System Independently of Endoplasmic Reticulum Stress.

Authors:  Guo-Biao Wu; Hui-Bo Du; Jia-Yi Zhai; Si Sun; Jun-Ling Cui; Yang Zhang; Zhen-Ao Zhao; Jian-Liang Wu; Alan Kim Johnson; Baojian Xue; Zi-Gang Zhao; Geng-Shen Zhang
Journal:  Oxid Med Cell Longev       Date:  2022-01-13       Impact factor: 6.543

  3 in total

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