氨基胍与左旋硝基精氨酸甲酯在兔心脏骤停复苏中的比较

Comparison of the effects of aminoguanidine and NG-nitro-L-arginine methyl ester on resuscitation from cardiac arrest in rabbits

目的观察一氧化氮在心肺复苏中的变化规律，比较选择性诱导型一氧化氮合酶抑制剂氨基胍（AG）与非选择性一氧化氮合酶抑制剂左旋硝基精氨酸甲酯（L-NAME）对兔心脏骤停复苏的影响。方法兰州大学机能实验室，40只家兔建立心脏骤停模型，5min后行胸外按压，机械通气。按压1min后随机分为4组（n=10）：AG组（20mg／kg）、L-NAME组（25mg／kg）、肾上腺素（0．02mg／kg）及对照组（生理盐水2mL）。按压5min后给与电除颤。持续监测血流动力学指标及左室内压变化至自主循环恢复后4h。分别于基础、胸外按压1min、自主循环恢复后15，30，60，120min采血检测血一氧化氮含量。数据采用重复测量数据的方差分析。结果胸外按压期间，冠脉灌注压均值AG组（40±10）mmHg高于L-NAME组[（33±8）mmHg，P=0．001]且均高于对照组[（20±5）mmHg，P=0．000]；AG组左室＋dp／dtmax、-dP／dtmax，均值[（3201±604），（3480±490）mmHg／s]高于L-NAME组[（2417±348），（2303±352）mmHg／s，P=0．000]。自主循环恢复后，AG组平均动脉压均值（79±8）mmHg与L-NAME组[（70±7）mmHg，P=0．103]差异无统计学意义，但均高于对照组[（58±8）mmHg，P=0．000、0．015]；对照组与肾上腺素组＋dP／dfmax、-dp／dtmax出现不同程度下降，但AG组与LNAME组保持在基础水平，且AG组[（4783±912），（4409±827）mmHg／s]高于L-NAME组[（3554±847），（3398±764）mmHg／s，P=0．001、0．023]。结论AG、L-NAME能增加心肺复苏期间冠脉灌注压，改善心脏舒缩功能，防止复苏后早期心功能障碍的发生，且AG明显优于L-NAME。

Objective To observe the changes of nitric oxide （NO） levels in plasma during cardiopulmonary resuscitation （CPR） and to compare the effects of aminoguanidine （AG） and NG-nitro-L-arginine methyl ester （L-NAME） on CPR. Method This was a prospective, randomized animal study performed at the Function Laboratory of Lanzhou University. Cardiac arrest was electrically induced and was left untreated for 5 min. After performing chest compression for 1 min, 40 domestic rabbits were divided into four groups （ n = 10） to receive either 20 mg/kg AG, 25 mg/kg L-NAME, 0.02 mg/kg epinephrine or 2 ml saline placebo before defibrillation. Successfully resuscitated rabbits were observed for a further 4 h. Hemodynamics variables and cardiac functions were monitored with appropriate instrumentation. Arterial blood NO levels were examined at basehne, at the end of 1 min chest compression and at 15, 30, 60 and 120 min after survival. Repeated measures analysis of variance was used to determine statistical significance between groups. Results During chest compression, the mean ± standard deviation coronary perfusion pressure was higher in the AG gToup （40 ±10 mmHg） than in the L-NAME group （34±8 mmHg; P = 0.001） and was higher in both groups with the control group （20--.5 mmHg; both P = 0.000）. Left ventrieular ＋ dp/dtmax and - dp/dtmax were higher in the AG group than in the L-NAME group. In the surviving rabbits, the left ventricular ＋ dp/dtmax and - dp/dtmax, were higher in the AG and L-NAME groups than in the epinephrine and control groups and were higher in the AG group （4783± 912, 4409 ± 827 mmHg/s） than in the L-NAME group （3554 ± 847, 3398± 764 mmHg/s; P = 0.001 and 0.023, respectively）. Conclusions Both AG and L-NAME increased the coronary perfusion pressure, and improved left ventricular systolic and diastolic function during CPR and prevented post-resuscitation myocardial dysfunction. However, AG was significandy superior to L-NAME.