CAJ | 학술논문

通过氨基甲酸乙酯麻醉大鼠观察股神经电刺激对缺血-再灌注心肌的影响,旨在证实外周神经刺激对心肌有无保护效应,并明确其可能的作用机制.心肌缺血区和梗塞区分别用伊文思蓝和氯化硝基四氮唑蓝染色确定,心肌梗塞范围定义为心肌梗塞区重量占心肌缺血区重量的百分比.所得结果如下:(1)在心肌缺血30 min和再灌注120 min过程中,梗塞心肌占缺血心肌的(54.96+0.82)%.(2)高频电刺激(10 V,100 Hz,ims)股神经5 min可使心肌梗塞范围减少到(36.94+1.34)%(P＜0.01),表明高频电刺激股神经对缺血-再灌注心肌有保护作用.然而,低频电刺激(10 V,10 Hz,1 ms)股神经对缺血-再灌注心肌梗塞范围无影响.(3)预先应用非选择性阿片肽受体阻断剂纳洛酮(5mg/kg,i.v.)或非选择性KATP通道阻断剂格列苯脲(5 mg/kg,i.v.)均能完全取消高频电刺激股神经对缺血-再灌注心肌的保护作用.以上结果提示,高频外周神经刺激可以减小缺血-再灌注心肌的梗塞范围,其可能的作用机制是:高频电刺激股神经时中枢神经系统内释放的内源性阿片肽和由此激活的心肌KATP通道的开放介导了这种保护作用.
통과안기갑산을지마취대서관찰고신경전자격대결혈-재관주심기적영향,지재증실외주신경자격대심기유무보호효응,병명학기가능적작용궤제.심기결혈구화경새구분별용이문사람화록화초기사담서람염색학정,심기경새범위정의위심기경새구중량점심기결혈구중량적백분비.소득결과여하:(1)재심기결혈30 min화재관주120 min과정중,경새심기점결혈심기적(54.96+0.82)%.(2)고빈전자격(10 V,100 Hz,ims)고신경5 min가사심기경새범위감소도(36.94+1.34)%(P＜0.01),표명고빈전자격고신경대결혈-재관주심기유보호작용.연이,저빈전자격(10 V,10 Hz,1 ms)고신경대결혈-재관주심기경새범위무영향.(3)예선응용비선택성아편태수체조단제납락동(5mg/kg,i.v.)혹비선택성KATP통도조단제격렬분뇨(5 mg/kg,i.v.)균능완전취소고빈전자격고신경대결혈-재관주심기적보호작용.이상결과제시,고빈외주신경자격가이감소결혈-재관주심기적경새범위,기가능적작용궤제시:고빈전자격고신경시중추신경계통내석방적내원성아편태화유차격활적심기KATP통도적개방개도료저충보호작용.
The effects of femoral nerve electrostimulation (FNES) on ischemia-reperfused myocardium were examined in the urethaneanesthetized rats to determine whether FNES may provide cardioprotection and to observe the possible mechanism. The area at risk (AR) and infarct area (IA) were determined using Evans blue and nitro-blue tetrazolium staining, respectively. Infarct size (IS) was defined as 100 × IA/AR (%). The results are as follows: (1) During 30 min myocardial ischemia and subsequent 120 min reperfusion,the myocardial infarct size occupied (54.96±0.82)% of the area at risk. (2) FNES of high frequency (10 V, 100 Hz, 1 ms) significantly reduced myocardial infarct size to (36.94± 1.34)% (P＜0.01), indicating the cardioprotective effect FNES of high frequency on myocardial ischemia-reperfusion, while FNES of low frequency (10 V, 10 Hz, 1 ms) had no effect on myocardial infarct size. (3) Pretreatment with either naloxone (5 mg/kg, i.v), a nonselective opioid receptor antagonist, or glibenclamide (5 mg/kg, i.v), a KATP channel antagonist,completely abolished the cardioprotection of FNES (100 Hz) from myocardial ischemia-reperfusion. It is suggested that FNES of high frequency can protect myocardium from ischemia-reperfusion injury. The possible mechanism is that FNES of high frequency may induce the release of opioids from the central nervous system, and the activation of opioid receptors in the heart results in an opening of myocardial KATP channels which can protect myocardium.