CAJ | 학술논문

目的:研究KATP通道激活在高碳酸酸化预处理对兔心肌细胞保护效应中的作用.方法:将32只新西兰白兔(雌雄不限)随机分成缺血再灌注组(IR组)、高碳酸酸化预处理组(H组)、假手术组(P组)和优降糖+高碳酸酸化预处理组(H+G组),每组各8只.在IR组和P组,呼吸频率设置为35次/min,潮气量为15 mL/kg,控制呼气末二氧化碳分压[p(CO_2)]在40～50 mm Hg(1 mm Hg=0.133 kPa),持续30 min.在H组呼吸频率为25次/ min,潮气量为10 mL/kg,呼气末p(CO_2)的目标值为75～85 mm Hg, 维持在目标值5 min后, 恢复正常通气, 使呼气末p(CO_2)恢复到40～50 mm Hg.H+G组在进行低频率、低潮气量造成CO2蓄积前10 min静脉注射溶解优降糖的溶质0.3 mg/kg.除P组外,各组动物接受冠状动脉左前分支30 min阻断和3 h再灌注.然后称体质量,测量并计算出心肌缺血面积、梗死面积和心肌梗死面积与心肌缺血面积之比.结果:H组心肌梗死面积占缺血面积的百分比低于IR组和H+G组(P < 0.05或P < 0.01),H+G组与IR组相比差异无统计学意义(P > 0.05).结论:高碳酸酸化预处理可保护心肌免受缺血再灌注的损伤,KATP通道介导了高碳酸酸化预处理的心肌保护通路.
목적:연구KATP통도격활재고탄산산화예처리대토심기세포보호효응중적작용.방법:장32지신서란백토(자웅불한)수궤분성결혈재관주조(IR조)、고탄산산화예처리조(H조)、가수술조(P조)화우강당+고탄산산화예처리조(H+G조),매조각8지.재IR조화P조,호흡빈솔설치위35차/min,조기량위15 mL/kg,공제호기말이양화탄분압[p(CO_2)]재40～50 mm Hg(1 mm Hg=0.133 kPa),지속30 min.재H조호흡빈솔위25차/ min,조기량위10 mL/kg,호기말p(CO_2)적목표치위75～85 mm Hg, 유지재목표치5 min후, 회복정상통기, 사호기말p(CO_2)회복도40～50 mm Hg.H+G조재진행저빈솔、저조기량조성CO2축적전10 min정맥주사용해우강당적용질0.3 mg/kg.제P조외,각조동물접수관상동맥좌전분지30 min조단화3 h재관주.연후칭체질량,측량병계산출심기결혈면적、경사면적화심기경사면적여심기결혈면적지비.결과:H조심기경사면적점결혈면적적백분비저우IR조화H+G조(P < 0.05혹P < 0.01),H+G조여IR조상비차이무통계학의의(P > 0.05).결론:고탄산산화예처리가보호심기면수결혈재관주적손상,KATP통도개도료고탄산산화예처리적심기보호통로.
Objective: To investigate the function of the ATP-sensitive K+(KATP) channel activation on the protective effect of hypercarbonic acidosis preconditioning on rabbit myocardial cells. Methods: Thirty-two rabbits were randomly divided into 4 groups (n = 8 for each group): pseudo-operation group (group P), ischemia and reperfusion group(group IR), hypercarbonic acidosis group(group H) and hypercarbonic acidosis+ glybenzcyclamide group (group H+G). Animals were ventilated normally in group IR and group P, tidal volume 15 mL/kg, breathing rate 35 bpm .The PETCO_2 was maintained at the level of 40-50 mm Hg for 30 minutes. Animals received low-frequency, low volume ventilation in group H group H+G, tidal volume 10 ml/kg, breathing rate 25 bpm to achieve hypercarbonic acidosis. The target value of PETCO_2 was 75-85 mm Hg. This value was maintained for 5 minutes. The animals then were ventilated normally to make the PETCO_2 return to 40-50 mm Hg. Animals were injected with 0.3 mg/kg glybenzcyclamide 10min before achieving hypercarbonic acidosis with hypoventilation in group H+G. Animals received ligation of left anterior branch artery for 30 minutes and reperfusion for 180 minutes in each group except P group. The myocardial ischemia area, the myocardial infarction area and their ratios were calculated by the ismaeil methods. Results: The ratio of the myocardial infarction area to the myocardial ischemia was significantly less in group H than those of group IR and group H+G (P < 0.01). The value of the ratio was similar between group H+G and group IR(P > 0.05). Conclusion: Hypercarbonic acidosis preconditioning can protect the cardiomyocytes by activating the KATP channel.