EPINEPHRINE DOSAGE EFFECTS ON CEREBRAL AND MYOCARDIAL BLOOD-FLOW IN AN INFANT SWINE MODEL OF CARDIOPULMONARY-RESUSCITATION
EPINEPHRINE DOSAGE EFFECTS ON CEREBRAL AND MYOCARDIAL BLOOD-FLOW IN AN INFANT SWINE MODEL OF CARDIOPULMONARY-RESUSCITATION
复制标题
DOI：
10.1097/00000542-199112000-00017
复制
发表时间：
1991-12-01
期刊：
影响因子：
8.8
通讯作者：
TRAYSTMAN, RJ
中科院分区：
文献类型：
--
作者：
BERKOWITZ, ID;GERVAIS, H;TRAYSTMAN, RJ
尽管在心肺复苏（CPR）过程中肾上腺素增加了脑血流量（CBF）和左心室血流量（LVBF），但在长时间心肺复苏过程中，高剂量肾上腺素对LVBF和CBF以及脑氧摄取的影响尚未得到研究。在猪婴儿心肺复苏模型中，我们确定对数增量肾上腺素剂量是否会增加LVBF和CBF以及脑氧摄取。我们比较了肾上腺素和肾上腺素能激动剂苯肾上腺素的反应。五组（n = 6）戊巴比妥麻醉仔猪（3.5-5.6 kg）接受持续肾上腺素输注（0、1、10和100 μ g.kg-1）进行心肺复苏术。Min-1)或苯肾上腺素输注（40 μ g.kg-1 Min-1）。在心肺复苏术期间，对照组血浆肾上腺素浓度增加了10-100倍，并以逐步的方式使浓度在100 μ g.kg-1时增加了10(4)以上。Min-1肾上腺素组。未输注肾上腺素的对照组，心肺复苏5 min时LVBF降至< 10 ml.min-1.100 g-1。肾上腺素的剂量分别是10毫克和100毫克。min-1时，5 min时LVBF分别为75 +/- 19和44 +/- 15 ml.min-1.100 g-1，均显著高于对照组。随着心肺复苏术时间的延长，LVBF仍显著高于对照组，但仅为10 μ g.kg-1。肾上腺素的Min-1。与对照组相比，苯肾上腺素也增加了心肺复苏术10分钟的LVBF。所有剂量的肾上腺素和苯肾上腺素在心肺复苏20分钟内维持CBF接近骤停前值。长时间心肺复苏术，10和100毫克/公斤。min-1肾上腺素导致CBF明显高于对照组。与对照组相比，增加肾上腺素剂量并没有统计学意义上增加脑氧摄取或降低脑氧提取分数，尽管产生了更高的脑血流。在这个未成熟的动物CPR模型中，10mu -g.kg-1。min-1肾上腺素是最大化CBF和LVBF的最佳剂量，其剂量大大超过目前人类婴儿心肺复苏术推荐的肾上腺素剂量。此外，短期心肺复苏术，40 μ g.kg-1。min-1苯肾上腺素将CBF和LVBF增加到类似于高剂量肾上腺素产生的水平。
Although epinephrine increases cerebral blood flow (CBF) and left ventricular blood flow (LVBF) during cardiopulmonary resuscitation (CPR), the effects of high dosages on LVBF and CBF and cerebral O2 uptake have not been examined during prolonged CPR. We determined whether log increment dosages of epinephrine would enhance LVBF and CBF and cerebral O2 uptake in an infant swine CPR model. We compared these responses with epinephrine to those with the alpha-adrenergic agonist, phenylephrine. CPR was performed in five groups (n = 6) of pentobarbital-anesthetized piglets (3.5-5.6 kg) receiving a continuous epinephrine infusion (0, 1, 10, and 100-mu-g.kg-1.min-1) or phenylephrine infusion (40-mu-g.kg-1.min-1). Plasma epinephrine concentrations increased 10-100-fold in the control group during CPR and in a stepwise manner such that concentrations were increased by more than 10(4) in the 100-mu-g.kg-1.min-1 epinephrine group. In the control group with no epinephrine infusion, LVBF decreased to < 10 ml.min-1.100 g-1 by 5 min of CPR. With epinephrine in dosages of 10 and 100-mu-g.kg-1.min-1, LVBF at 5 min was 75 +/- 19 and 44 +/- 15 ml.min-1.100 g-1, respectively, which was significantly greater than values in the control group. With more prolonged CPR, LVBF remained significantly greater than that in the control group but only at 10-mu-g.kg-1.min-1 of epinephrine. Phenylephrine also increased LVBF for 10 min of CPR when compared with the control group. All dosages of epinephrine and phenylephrine maintained CBF close to prearrest values for 20 min of CPR. With prolonged CPR, 10 and 100-mu-g.kg.min-1 epinephrine resulted in significantly greater CBF than that in the control group. Incremental dosages of epinephrine did not statistically increase cerebral O2 uptake or lower the cerebral fractional O2 extraction when compared with the control group, despite the higher CBF that was generated. tn this immature animal CPR model, 10-mu-g.kg-1.min-1 epinephrine is an optimal dosage for maximizing both CBF and LVBF, a dosage that substantially exceeds the current recommended epinephrine dosage for human infant CPR. In addition, for short periods of CPR, 40-mu-g.kg-1.min-1 phenylephrine increases CBF and LVBF to levels similar to those generated by high dosages of epinephrine.