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实验性低血容量性休克时血流动力学和代谢变化的连续模式。I. 对急性出血的反应。

Sequential patterns of haemodynamic and metabolic changes in experimental hypovolaemic shock. I. Responses to acute haemorrhage.

作者信息

Pardy B J, Dudley H A

出版信息

Br J Surg. 1979 Feb;66(2):84-8. doi: 10.1002/bjs.1800660204.

Abstract

Little is known about cardiorespiratory changes during the development of hypovolaemia. This study attempts to provide such information and compares the period of bleeding with that of established hypovolaemia. Eleven anaesthetized and ventilated greyhounds were bled and analyses of cardiopulmonary function made at fixed intervals both during and after haemorrhage. Six sequential patterns of cardiopulmonary and metabolic change were recognized. It was apparent that bleeding caused the first three phases of change, recovery from the effects of bleeding the next two and steady hypovolaemia the last. The event of bleeding is the main factor that elevates total peripheral resistance and reduces tissue perfusion with consequent lowering of oxygen consumption and alkalosis secondary to impaired carbon dioxide production; when bleeding ceases these changes partially reverse in a manner characteristic of that induced by the reinfusion of shed blood; and hypovolaemia per se has a relatively weak influence. These findings provide an explanation for disparities in previous published reports and have obvious clinical implications.

摘要

关于低血容量发展过程中的心肺变化,人们了解甚少。本研究试图提供此类信息,并比较出血期与已确立的低血容量期。对11只麻醉并通气的灵缇犬进行放血,并在出血期间和出血后每隔固定时间对心肺功能进行分析。识别出六种心肺和代谢变化的连续模式。显然,出血导致了前三个变化阶段,接下来的两个阶段是从出血影响中恢复,最后一个阶段是持续的低血容量。出血事件是升高总外周阻力和减少组织灌注的主要因素,随之降低氧消耗,并因二氧化碳生成受损继发碱中毒;出血停止后,这些变化会以回输 shed blood 所诱导的特征性方式部分逆转;而低血容量本身的影响相对较弱。这些发现解释了先前发表报告中的差异,并具有明显的临床意义。

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本文引用的文献

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Mechanism of pressor response to 1-norepinephrine during hemorrhagic shock.
Circ Res. 1957 Mar;5(2):153-6. doi: 10.1161/01.res.5.2.153.
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pH and blood-gas analysis. Methods of measurement and sources of error using electrode systems.
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Changes in (a-A)CO2 difference and pulmonary artery pressure in anesthetized man.
J Appl Physiol. 1966 Jul;21(4):1299-305. doi: 10.1152/jappl.1966.21.4.1299.

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