Schoffstall J M, Spivey W H, Davidheiser S, Fuhs L, Kirkpatrick R
Medical College of Pennsylvania, Department of Emergency Medicine/Division of Research, Philadelphia 19129.
Resuscitation. 1990 Jun;19(3):241-51. doi: 10.1016/0300-9572(90)90105-n.
The use of epinephrine in cardiac arrest remains an area of continuing controversy. This study was undertaken to characterize the effect of endogenous and exogenous epinephrine on plasma epinephrine levels, and the relationship between plasma epinephrine and norepinephrine and mean arterial pressure and diastolic arterial pressure. Nineteen young swine were anesthetized with ketamine and alpha-chloralose and instrumented with arterial and central venous lines. Ventricular fibrillation was induced by pacemaker. At 5 min post arrest cardiopulmonary resuscitation (CPR) was begun with a mechanical resuscitator. Animals were randomized to receive either saline placebo (n = 9), 0.01 mg/kg epinephrine (n = 5) or 0.1 mg/kg epinephrine (n = 5) via the central venous line. Plasma was drawn for high pressure liquid chromatographic analysis of catecholamines every 2 min. The resuscitation was carried on for 30 min after the arrest. Plasma epinephrine levels differed significantly between treated subjects and controls, as did mean arterial pressure and diastolic arterial pressure. There was a correlation between both mean arterial pressure and diastolic arterial pressure with plasma epinephrine and log epinephrine, but no correlation with plasma norepinephrine. The two doses of epinephrine did not differ in the degree to which they elevated the mean arterial pressure and diastolic pressure. We conclude that the endogenous catecholamine response to cardiac arrest while producing norepinephrine and epinephrine levels many times greater than those in the resting animal, is not sufficient to maintain blood pressure. There is a strong correlation between blood pressure and the log of the plasma epinephrine concentration, but epinephrine concentration alone does not solely account for changes in blood pressure during arrest.
肾上腺素在心脏骤停中的应用仍是一个存在持续争议的领域。本研究旨在描述内源性和外源性肾上腺素对血浆肾上腺素水平的影响,以及血浆肾上腺素与去甲肾上腺素、平均动脉压和舒张压之间的关系。19只幼猪用氯胺酮和α-氯醛糖麻醉,并插入动脉和中心静脉导管。通过起搏器诱发室颤。心脏骤停后5分钟开始用机械复苏器进行心肺复苏(CPR)。动物被随机分为通过中心静脉导管接受生理盐水安慰剂(n = 9)、0.01 mg/kg肾上腺素(n = 5)或0.1 mg/kg肾上腺素(n = 5)。每2分钟抽取血浆用于儿茶酚胺的高压液相色谱分析。心脏骤停后复苏持续30分钟。治疗组和对照组之间的血浆肾上腺素水平、平均动脉压和舒张压均有显著差异。平均动脉压和舒张压与血浆肾上腺素和肾上腺素对数之间存在相关性,但与血浆去甲肾上腺素无相关性。两种剂量的肾上腺素在升高平均动脉压和舒张压的程度上没有差异。我们得出结论,心脏骤停时内源性儿茶酚胺反应虽然产生的去甲肾上腺素和肾上腺素水平比静息动物高出许多倍,但不足以维持血压。血压与血浆肾上腺素浓度的对数之间存在很强的相关性,但仅肾上腺素浓度并不能完全解释心脏骤停期间血压的变化。