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肾上腺素和去甲肾上腺素对开胸心肺复苏期间脑氧输送和消耗的影响。

Effects of epinephrine and norepinephrine on cerebral oxygen delivery and consumption during open-chest CPR.

作者信息

Lindner K H, Ahnefeld F W, Pfenninger E G, Schuermann W, Bowdler I M

机构信息

Universitaetsklinik fuer Anaesthesiologie, Klinikum der Universitaet Ulm, Federal Republic of Germany.

出版信息

Ann Emerg Med. 1990 Mar;19(3):249-54. doi: 10.1016/s0196-0644(05)82038-4.

Abstract

The effect of epinephrine and norepinephrine on cerebral oxygen delivery and consumption after five minutes of cardiopulmonary arrest and three minutes of open-chest cardiac massage was studied in 21 pigs. Norepinephrine, like epinephrine, has a marked alpha- and beta 1-sympathomimetic activity, but compared with epinephrine, the degree of beta 2-stimulation is weak. Epinephrine probably stimulates cerebral oxygen and glucose consumption by its beta 2-adrenergic effect. After three minutes of CPR, three groups of seven animals each blindly received either placebo (control group), 45 micrograms/kg epinephrine, or 45 micrograms/kg norepinephrine. During CPR but before drug administration, cerebral blood flow was 23 +/- 14 mL/min/100 g in the control group, 30 +/- 7 mL/min/100 g in the epinephrine group, and 30 +/- 11 mL/min/100 g in the norepinephrine group. At 90 seconds after epinephrine, cerebral blood flow increased to 54 +/- 14 mL/min/100 g and after norepinephrine, to 58 +/- 22 mL/min/100 g (P less than .05). Cerebral perfusion pressure for both drugs was significantly higher than the control group. Compared with mechanical measures alone, cerebral oxygen delivery rose from 4.3 +/- 1.2 to 7.4 +/- 1.7 mL/min/100 g after epinephrine and from 3.7 +/- 1.4 to 7.3 +/- 2.7 mL/min/100 g after norepinephrine (P less than .05). There was no increase in cerebral oxygen consumption after both catecholamines, and cerebral oxygen extraction ratio decreased. Cerebral glucose delivery increased in relation to glucose consumption, and extraction ratio did not change significantly after both catecholamines.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

在21头猪身上研究了心肺骤停5分钟及开胸心脏按压3分钟后肾上腺素和去甲肾上腺素对脑氧输送和消耗的影响。去甲肾上腺素与肾上腺素一样,具有显著的α和β1拟交感神经活性,但与肾上腺素相比,其β2刺激程度较弱。肾上腺素可能通过其β2肾上腺素能效应刺激脑氧和葡萄糖消耗。心肺复苏3分钟后,每组7只动物被随机分为三组,分别给予安慰剂(对照组)、45微克/千克肾上腺素或45微克/千克去甲肾上腺素。在心肺复苏期间但在给药前,对照组脑血流量为23±14毫升/分钟/100克,肾上腺素组为30±7毫升/分钟/100克,去甲肾上腺素组为30±11毫升/分钟/100克。给予肾上腺素后90秒,脑血流量增加至54±14毫升/分钟/100克,给予去甲肾上腺素后增加至58±22毫升/分钟/100克(P<0.05)。两种药物的脑灌注压均显著高于对照组。与单纯机械措施相比,给予肾上腺素后脑氧输送从4.3±1.2升至7.4±1.7毫升/分钟/100克,给予去甲肾上腺素后从3.7±1.4升至7.3±2.7毫升/分钟/100克(P<0.05)。两种儿茶酚胺给药后脑氧消耗均未增加,脑氧摄取率降低。脑葡萄糖输送相对于葡萄糖消耗增加,两种儿茶酚胺给药后摄取率无显著变化。(摘要截短于250字)

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