CAJ | 학술논문

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,5 min后行胸外按压,机械通气.按压1 min后随机分为4组(n=10):AG组(20 mg/kg)、L-NAME组(25 mg/kg)、肾上腺素(0.02 mg/kg)及对照组(生理盐水2 mL).按压5 min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4 h.分别于基础、胸外按压1 min、自主循环恢复后15,30,60,120 min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)nmaHg,P=0.001]且均高于对照组[(20±5)mmHg,P=0.000];AG组左室+dp/dtmax、-dp/dmax均值[(3201±604),(3480±490)mmHg/s/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/dmax、-dp/dtmax出现不同程度下降,但AG组与L-NAME组保持在基础水平,且AG组[(4783±912),(4409±827)mmHg/g]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.
목적 관찰일양화담재심폐복소중적변화규률,비교선택성유도형일양화담합매억제제안기고(AG)여비선택성일양화담합매억제제좌선초기정안산갑지(L-NAME)대토심장취정복소적영향.방법란주대학궤능실험실,40지가토건립심장취정모형,5 min후행흉외안압,궤계통기.안압1 min후수궤분위4조(n=10):AG조(20 mg/kg)、L-NAME조(25 mg/kg)、신상선소(0.02 mg/kg)급대조조(생리염수2 mL).안압5 min후급여전제전.지속감측혈류동역학지표급좌실내압변화지자주순배회복후4 h.분별우기출、흉외안압1 min、자주순배회복후15,30,60,120 min채혈검측혈일양화담함량.수거채용중복측량수거적방차분석.결과흉외안압기간,관맥관주압균치AG조(40±10)mmHg고우L-NAME조[(33±8)nmaHg,P=0.001]차균고우대조조[(20±5)mmHg,P=0.000];AG조좌실+dp/dtmax、-dp/dmax균치[(3201±604),(3480±490)mmHg/s/s]고우L-NAME조[(2417±348),(2303±352)mmHg/s,P=0.000].자주순배회복후,AG조평균동맥압균치(79±8)mmHg여L-NAME조[(70±7)mmHg,P=0.103]차이무통계학의의,단균고우대조조[(58±8)mmHg,P=0.000、0.015];대조조여신상선소조+dp/dmax、-dp/dtmax출현불동정도하강,단AG조여L-NAME조보지재기출수평,차AG조[(4783±912),(4409±827)mmHg/g]고우L-NAME조[(3554±847),(3398±764)mmHg/s,P=0.001、0.023].결론 AG、L-NAME능증가심폐복소기간관맥관주압,개선심장서축공능,방지복소후조기심공능장애적발생,차AG명현우우L-NAME.
Objective To observe the changes of nitric oxide (NO) levels in plasma during cardiopul-monary 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 ei-ther 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. Hernodynamics variables and cardiac functions were monitored with appropriate instrumentation. Arterial blood NO levels were examined at baseline, 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 + stan-dard deviation coronary perfusion pressure was higher in the AG group (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 ventricular + 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 b-NAME group (3554±847, 3398±764 mmHg/s; P = 0.001 and 0.023, respectively). Conclu-sions 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 signifi-canfly superior to L-NAME.