Lindner K H, Strohmenger H U, Prengel A W, Ensinger H, Goertz A, Weichel T
Universitätsklinik für Anästhesiologie, Klinikum der Universität Ulm, Donau, FRG.
Crit Care Med. 1992 Jul;20(7):1020-6. doi: 10.1097/00003246-199207000-00020.
This study was designed to assess the effect of epinephrine during cardiopulmonary resuscitation (CPR) on left ventricular myocardial blood flow, systemic oxygen delivery and consumption, and on plasma glucose and lactate concentrations. Fourteen pigs were allocated to receive either 0.9% saline (n = 7), or 45 micrograms/kg epinephrine (n = 7) after 5 mins of ventricular fibrillation, and 3 mins of open-chest CPR. Left ventricular myocardial blood flow was measured with radiolabeled microspheres. Plasma catecholamine concentrations were measured by high-pressure liquid chromatography.
During open-chest CPR, mean (+/- SD) values of left ventricular myocardial blood flow before, 90 secs, and 5 mins following drug administration were 49 +/- 10, 46 +/- 12, 43 +/- 15 mL/min/100 g, respectively, in the control group, and 52 +/- 12, 118 +/- 21, 84 +/- 28 mL/min/100 g, respectively, in the epinephrine group (p less than .05 at 90 secs and 5 mins). At the same time points, mean (+/- SD) oxygen delivery indices were 7.7 +/- 3.0, 6.0 +/- 2.1, 6.5 +/- 2.7 mL/min/kg in the control group and 7.6 +/- 2.5, 5.3 +/- 2.1, 5.5 +/- 1.9 mL/min/kg in the epinephrine group (nonsignificant). Mean oxygen consumption indices were 5.8 +/- 2.4, 4.6 +/- 1.6, 5.2 +/- 2.6 mL/min/kg in the control group and 5.4 +/- 1.6, 4.2 +/- 1.6, 4.4 +/- 1.4 mL/min/kg in the epinephrine group (nonsignificant). During CPR and before epinephrine administration, arterial plasma epinephrine concentrations increased from prearrest values of 0.77 +/- 0.70 to 62.1 +/- 48.7 micrograms/L, and plasma norepinephrine concentrations increased from 0.28 +/- 0.32 to 104.3 +/- 57.1 micrograms/L. After administered epinephrine, there was an additional increase to 271 +/- 83 micrograms/L at 90 secs in arterial plasma epinephrine, but no important alteration in the plasma norepinephrine concentration. At no time point could we find a clinically important difference in plasma glucose or lactate concentrations between the two groups.
At a dose of 45 micrograms/kg, epinephrine caused an increase in left ventricular myocardial blood flow after a total of 8 mins of cardiac arrest, including 3 mins of CPR, while not altering systemic oxygen delivery and consumption, plasma glucose, or lactate concentrations.
本研究旨在评估心肺复苏（CPR）期间肾上腺素对左心室心肌血流、全身氧输送与消耗以及血浆葡萄糖和乳酸浓度的影响。14只猪在室颤5分钟及开胸CPR 3分钟后，被分为两组，分别接受0.9%生理盐水（n = 7）或45微克/千克肾上腺素（n = 7）。用放射性微球测量左心室心肌血流。通过高压液相色谱法测量血浆儿茶酚胺浓度。
在开胸CPR期间，对照组给药前、给药后90秒和5分钟时左心室心肌血流的平均值（±标准差）分别为49±10、46±12、43±15毫升/分钟/100克，肾上腺素组分别为52±12、118±21、84±28毫升/分钟/100克（90秒和5分钟时p<0.05）。在相同时间点，对照组平均（±标准差）氧输送指数分别为7.7±3.0、6.0±2.1、6.5±2.7毫升/分钟/千克，肾上腺素组分别为7.6±2.5、5.3±2.1、5.5±1.9毫升/分钟/千克（无显著差异）。对照组平均氧消耗指数分别为5.8±2.4、4.6±1.6、5.2±2.6毫升/分钟/千克，肾上腺素组分别为5.4±1.6、4.2±1.6、4.4±1.4毫升/分钟/千克（无显著差异）。在CPR期间且在给予肾上腺素之前，动脉血浆肾上腺素浓度从心脏骤停前的0.77±0.70微克/升增加至62.1±48.7微克/升，血浆去甲肾上腺素浓度从0.28±0.32微克/升增加至104.3±57.1微克/升。给予肾上腺素后，动脉血浆肾上腺素在90秒时进一步增加至271±83微克/升，但血浆去甲肾上腺素浓度无重要变化。在任何时间点，两组间血浆葡萄糖或乳酸浓度均未发现临床上的重要差异。
在心脏骤停共8分钟（包括3分钟CPR）后，给予45微克/千克剂量的肾上腺素可使左心室心肌血流增加，而不改变全身氧输送与消耗、血浆葡萄糖或乳酸浓度。
