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心脏复苏后进行性心肌功能障碍。

Progressive myocardial dysfunction after cardiac resuscitation.

作者信息

Tang W, Weil M H, Sun S, Gazmuri R J, Bisera J

机构信息

Institute of Critical Care Medicine, University of Health Sciences, Chicago Medical School, IL 60064.

出版信息

Crit Care Med. 1993 Jul;21(7):1046-50. doi: 10.1097/00003246-199307000-00022.

Abstract

OBJECTIVE

To investigate left ventricular function by the Langendorff method after successful cardiac resuscitation in rats.

DESIGN

Prospective, randomized, controlled animal study.

SETTING

University research laboratory.

SUBJECTS

Adult, male Sprague-Dawley rats.

INTERVENTIONS

Myocardial function was investigated in three subsets of isolated, perfused rat hearts that were harvested either before inducing ventricular fibrillation (controls) or at defined intervals after successful resuscitation from ventricular fibrillation. Ventricular fibrillation was induced with an electrode catheter advanced into the right ventricle of 15 mature, mechanically ventilated Sprague-Dawley rats. After an interval of 4 mins of untreated ventricular fibrillation and an additional 5 mins of precordial compression, spontaneous circulation was restored by a direct current, transthoracic countershock. The heart of each animal was then harvested at either 2 or 20 mins after successful cardiac resuscitation. The same model was utilized for harvesting the controls. Animals were randomized to each of the three subsets immediately before induction of cardiac arrest.

MEASUREMENTS AND MAIN RESULTS

There was a progressive decrease in myocardial contractility of the isolated, perfused hearts. Mean left ventricular systolic pressure was 128 +/- 8 mm Hg in control animals. In hearts harvested at 2 mins after successful resuscitation, the maximal generated pressure was reduced to 106 +/- 9 mm Hg. When harvested at 20 mins after successful resuscitation, it was reduced to 81 +/- 11 mm Hg. There were corresponding decreases in the mean maximal rate of left ventricular pressure increase (dP/dtmax) from 2880 +/- 110 to 2470 +/- 120 mm Hg/sec at 2 mins and to 1810 +/- 135 mm Hg/sec at 20 mins. These decreases in contractility were associated with striking decreases in myocardial relaxation and compliance.

CONCLUSION

These studies, therefore, document progressive systolic and diastolic myocardial dysfunction immediately after successful cardiac resuscitation with restoration of spontaneous circulation.

摘要

目的

通过Langendorff方法研究大鼠心脏复苏成功后的左心室功能。

设计

前瞻性、随机、对照动物研究。

设置

大学研究实验室。

对象

成年雄性Sprague-Dawley大鼠。

干预措施

在三组分离的灌注大鼠心脏中研究心肌功能,这些心脏要么在诱发心室颤动前采集(对照组),要么在心室颤动成功复苏后的特定时间间隔采集。用一根电极导管插入15只成熟的、机械通气的Sprague-Dawley大鼠的右心室诱发心室颤动。在未经治疗的心室颤动持续4分钟和额外进行5分钟胸外按压后,通过直流电经胸除颤恢复自主循环。然后在心脏复苏成功后2分钟或20分钟采集每只动物的心脏。对照组采用相同模型采集心脏。在诱发心脏骤停前,将动物随机分为三个亚组。

测量指标和主要结果

分离的灌注心脏的心肌收缩力逐渐下降。对照组动物的平均左心室收缩压为128±8mmHg。在复苏成功后2分钟采集的心脏中,最大产生压力降至106±9mmHg。在复苏成功后20分钟采集时,降至81±11mmHg。左心室压力最大上升速率(dP/dtmax)的平均值相应下降,从2880±110降至复苏后2分钟时的2470±120mmHg/秒,以及复苏后20分钟时的1810±135mmHg/秒。这些收缩力的下降与心肌舒张和顺应性的显著下降相关。

结论

因此,这些研究证明了在成功进行心脏复苏并恢复自主循环后,立即出现进行性的收缩期和舒张期心肌功能障碍。

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