Hormonal responses to hemorrhage and their relationship to individual hemorrhagic shock susceptibility.

Endocrinologia experimentalis Pub Date : 1990-03-01
J Grässler, D Jezová, R Kvetnanský, D W Scheuch
{"title":"Hormonal responses to hemorrhage and their relationship to individual hemorrhagic shock susceptibility.","authors":"J Grässler,&nbsp;D Jezová,&nbsp;R Kvetnanský,&nbsp;D W Scheuch","doi":"","DOIUrl":null,"url":null,"abstract":"<p><p>The effect of differences in sympathoadrenomedullary and pituitary-adrenocortical responses of individual animals to 35% hemorrhage on severity of shock induction has been studied in unanesthetized unrestrained rats by measuring plasma concentrations of adrenaline (A), noradrenaline (NA), corticosterone (CS) and adrenocorticotropin (ACTH). The responses of A, CS and ACTH were related to the decrease of blood volume and mean arterial pressure (MAP), whereas plasma NA remained unchanged. Higher susceptibility to blood loss was characterized by more pronounced hemorrhage-induced increase in blood lactate concentration and plasma enzyme activities as well as lethal outcome of hemorrhagic shock. In animals with irreversible hemorrhagic shock, enhanced catecholamine secretion and reduced ACTH release was observed. Furthermore, a revealed direct correlation between A and blood lactate concentration and plasma enzyme activities (aspartate aminotransferase, isocitric dehydrogenase, creatine kinase, lipase and glutathione-S-transferase) may indicate its possible participation in the mechanism of shock induction. In contrast, an inverse relationship of plasma CS to the indicators of shock severity was demonstrated. In conclusion, non-optimal neuroendocrine regulation of cardiovascular adjustments to hemorrhage in shock-prone animals might cause an exaggerated compensatory activation of adrenomedullary catecholamine secretion, which in turn has been shown to exert deleterious vascular and metabolic effects. The mechanisms responsible for reduced ACTH secretion in shock-prone animals remain to be established.</p>","PeriodicalId":11547,"journal":{"name":"Endocrinologia experimentalis","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"1990-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Endocrinologia experimentalis","FirstCategoryId":"1085","ListUrlMain":"","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0

Abstract

The effect of differences in sympathoadrenomedullary and pituitary-adrenocortical responses of individual animals to 35% hemorrhage on severity of shock induction has been studied in unanesthetized unrestrained rats by measuring plasma concentrations of adrenaline (A), noradrenaline (NA), corticosterone (CS) and adrenocorticotropin (ACTH). The responses of A, CS and ACTH were related to the decrease of blood volume and mean arterial pressure (MAP), whereas plasma NA remained unchanged. Higher susceptibility to blood loss was characterized by more pronounced hemorrhage-induced increase in blood lactate concentration and plasma enzyme activities as well as lethal outcome of hemorrhagic shock. In animals with irreversible hemorrhagic shock, enhanced catecholamine secretion and reduced ACTH release was observed. Furthermore, a revealed direct correlation between A and blood lactate concentration and plasma enzyme activities (aspartate aminotransferase, isocitric dehydrogenase, creatine kinase, lipase and glutathione-S-transferase) may indicate its possible participation in the mechanism of shock induction. In contrast, an inverse relationship of plasma CS to the indicators of shock severity was demonstrated. In conclusion, non-optimal neuroendocrine regulation of cardiovascular adjustments to hemorrhage in shock-prone animals might cause an exaggerated compensatory activation of adrenomedullary catecholamine secretion, which in turn has been shown to exert deleterious vascular and metabolic effects. The mechanisms responsible for reduced ACTH secretion in shock-prone animals remain to be established.

分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
对出血的激素反应及其与个体失血性休克易感性的关系。
在未麻醉的大鼠中,通过测定血浆中肾上腺素(A)、去甲肾上腺素(NA)、皮质酮(CS)和促肾上腺皮质激素(ACTH)的浓度,研究了个体动物对35%出血的交感病理肾上腺髓质和垂体-肾上腺皮质反应的差异对休克诱导程度的影响。A、CS和ACTH的反应与血容量和平均动脉压(MAP)的降低有关,而血浆NA保持不变。失血易感性较高的特点是出血引起的血乳酸浓度和血浆酶活性的明显增加,以及失血性休克的致命结局。在不可逆失血性休克动物中,观察到儿茶酚胺分泌增强,ACTH释放减少。此外,a与血乳酸浓度和血浆酶活性(天冬氨酸转氨酶、异柠檬酸脱氢酶、肌酸激酶、脂肪酶和谷胱甘肽s转移酶)之间的直接相关可能表明其可能参与休克诱导机制。相反,血浆CS与休克严重程度指标呈反比关系。综上所述,休克易感动物对心血管出血的非最佳神经内分泌调节可能会导致肾上腺髓质儿茶酚胺分泌的过度代偿激活,而这反过来又会对血管和代谢产生有害的影响。休克易感动物ACTH分泌减少的机制仍有待确定。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 去求助
来源期刊
自引率
0.00%
发文量
0
期刊最新文献
Intraglandular colloid induced nuclear proliferation of murine thymic cells as determined by flow cytometry. Effect of catecholamines and FSH on progesterone secretion by pig granulosa cells. Liver thiol content under varying glucoregulatory states in rats. Effect of varying glucosinolate and iodine intake via rapeseed meal diets on serum thyroid hormone level and total iodine in the thyroid in growing pigs. Nuclear binding of thyroid hormones and activity of malic enzyme and ornithine decarboxylase in rat liver during postnatal development.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1