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慢性酒精中毒和感染会改变心肌对异丙肾上腺素的反应。

Myocardial responses to isoproterenol are altered by chronic alcoholism and infection.

作者信息

McDonough K H, Causey K M

机构信息

Department of Physiology, Louisiana State University Medical Center, New Orleans 70112-1393.

出版信息

Am J Physiol. 1993 Feb;264(2 Pt 2):H357-63. doi: 10.1152/ajpheart.1993.264.2.H357.

DOI:10.1152/ajpheart.1993.264.2.H357
PMID:8447452
Abstract

Alcohol, consumed as 36% of the caloric intake for 8-10 wk, causes a potentiation of cardiac dysfunction induced by a second insult, sepsis. Because chronic alcoholism may attenuate the responsiveness of the myocardium to catecholamine stimulation, and because catecholamine support seems to be essential for the myocardium to generate an adequate cardiac output in sepsis, we hypothesized that the heart from the alcoholic septic rat would show a compromised inotropic responsiveness to catecholamines compared with the heart from the nonalcoholic septic rat. To test this hypothesis, rats were fed an ethanol-containing or control liquid diet for 8-10 wk and were then made septic with live Escherichia coli (10(10) E. coli) through a dorsal subcutaneous catheter. The next day, hearts were removed and perfused at a constant hydrostatic pressure, and a compliant balloon was placed in the left ventricule for measurement of pressure (LVP). Hearts were paced at 350-360 beats/min. Hearts were allowed to stabilize for 15 min, and then the response to a submaximal dose of isoproterenol (Iso) was measured. Hearts recovered for 30 min, at which time the response to a maximum dose of Iso was recorded. Basal (pre-Iso) LVP was lower in the control septic and alcoholic septic groups than in the control and alcohol groups. However, the maximum increase in LVP in response to Iso was greater in the two septic groups than in the two nonseptic groups. The peak LVP in response to Iso was similar in the control, septic, and alcoholic septic groups, and was significantly greater than in the alcohol group.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

以热量摄入的36%的酒精持续摄入8 - 10周,会增强由第二次损伤即脓毒症所诱发的心脏功能障碍。由于慢性酒精中毒可能会减弱心肌对儿茶酚胺刺激的反应性,并且由于儿茶酚胺支持似乎对于心肌在脓毒症中产生足够的心输出量至关重要,我们推测与非酒精性脓毒症大鼠的心脏相比,酒精性脓毒症大鼠的心脏对儿茶酚胺的变力反应性会受损。为了验证这一假设,将大鼠喂食含乙醇或对照液体饮食8 - 10周,然后通过背部皮下导管用活的大肠杆菌(10¹⁰大肠杆菌)使其发生脓毒症。第二天,取出心脏并在恒定静水压力下进行灌注,将一个顺应性球囊置于左心室内以测量压力(左心室压力,LVP)。心脏以350 - 360次/分钟的频率起搏。让心脏稳定15分钟,然后测量对次最大剂量异丙肾上腺素(Iso)的反应。使心脏恢复30分钟,此时记录对最大剂量Iso的反应。对照脓毒症组和酒精性脓毒症组的基础(异丙肾上腺素前)左心室压力低于对照组和酒精组。然而,两个脓毒症组对异丙肾上腺素反应时左心室压力的最大增加幅度大于两个非脓毒症组。对照组、脓毒症组和酒精性脓毒症组对异丙肾上腺素反应的左心室压力峰值相似,且显著高于酒精组。(摘要截短于250字)

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