Crespo S G, Schoffstall J M, Fuhs L R, Spivey W H
Department of Emergency Medicine, Medical College of Pennsylvania, Philadelphia 19129.
Ann Emerg Med. 1991 Mar;20(3):230-4. doi: 10.1016/s0196-0644(05)80928-x.
The objective of this study was to measure plasma catecholamine levels and the cardiovascular response before and after endotracheal administration of epinephrine in a swine cardiac arrest model.
Prospective, controlled laboratory investigation.
Twenty-one swine weighing 10 to 12 kg, anesthetized with ketamine and alpha-chloralose and ventilated with room air.
Ventricular fibrillation was induced with 90 V of 60 Hz current delivered to the right ventricle by transvenous pacemaker. Blood samples for epinephrine were drawn before arrest and every two minutes thereafter. At five minutes, external mechanical cardiac compressions were initiated. Nine animals received no further therapy and served as controls. Two groups of six animals received either 0.01 mg/kg or 0.1 mg/kg of epinephrine through the endotracheal tube at ten and 20 minutes. Blood samples were assayed for epinephrine.
Arterial blood pressure, lead II ECG, and plasma epinephrine.
Swine receiving epinephrine 0.01 mg/kg had an increase in epinephrine levels after drug administration, but these were not significantly different from control levels. The 0.1-mg/kg dose group had a significant increase in plasma epinephrine levels compared with controls and the 0.01-mg/kg dose group after receiving epinephrine at ten and 20 minutes. These increases were from 14 +/- 3 to 215 +/- 40 ng/mL (+/- SEM) at 12 minutes after arrest and from 151 +/- 56 to 402 +/- 80 ng/mL at 22 minutes after arrest.
These data suggest that standard dosing of epinephrine through the endotracheal tube during arrest does not produce significant increases in plasma catecholamines or blood pressure. Epinephrine 0.1 mg/kg produces a significant increase in plasma epinephrine levels, but it is not sufficient to produce a significant change in blood pressure.
本研究的目的是在猪心脏骤停模型中,测量气管内给予肾上腺素前后的血浆儿茶酚胺水平及心血管反应。
前瞻性对照实验室研究。
21头体重10至12千克的猪,用氯胺酮和α-氯醛糖麻醉,并用室内空气通气。
通过经静脉起搏器向右心室输送90伏60赫兹电流诱发心室颤动。在心脏骤停前及之后每隔两分钟采集肾上腺素血样。5分钟时开始进行体外机械心脏按压。9只动物未接受进一步治疗,作为对照组。两组各6只动物在10分钟和20分钟时通过气管导管分别接受0.01毫克/千克或0.1毫克/千克的肾上腺素。检测血样中的肾上腺素。
动脉血压、II导联心电图和血浆肾上腺素。
接受0.01毫克/千克肾上腺素的猪在给药后肾上腺素水平升高,但与对照水平无显著差异。0.1毫克/千克剂量组在10分钟和20分钟接受肾上腺素后,血浆肾上腺素水平与对照组和0.01毫克/千克剂量组相比显著升高。这些升高在心脏骤停后12分钟时从14±3纳克/毫升升至215±40纳克/毫升(±标准误),在心脏骤停后22分钟时从151±56纳克/毫升升至402±80纳克/毫升。
这些数据表明,心脏骤停期间通过气管导管给予标准剂量的肾上腺素不会使血浆儿茶酚胺或血压显著升高。0.1毫克/千克的肾上腺素可使血浆肾上腺素水平显著升高,但不足以使血压产生显著变化。