CAJ | 학술논문

目的：评价迷走神经?M受体通路在鞘内吗啡后处理减轻大鼠心肌缺血再灌注损伤中的作用。方法鞘内置管成功的健康成年雄性SD大鼠70只，体重250～350 g，采用随机数字表法分为7组（ n＝10）：假手术组（ Sham组）、心肌缺血再灌注组（ I∕R组）、鞘内注射吗啡后处理组（ MP组）、颈部双侧迷走神经离断组（ VT组）、VT＋MP 组、M受体拮抗剂阿托品＋MP 组（ ATP＋MP 组）和ATP组。采用结扎左冠状动脉缺血30 min恢复灌注的方法制备大鼠心肌缺血再灌注损伤模型。 MP组于再灌注即刻鞘内输注吗啡3μg∕kg 10μl，持续5 min；I∕R组输注生理盐水10μl，持续5 min；VT＋MP组于再灌注前10 min离断颈部双侧迷走神经；ATP＋MP 组于再灌注前10 min静脉输注阿托品0．1 mg∕kg 0．5 ml，持续5 min。于再灌注30 min内记录室性心律失常[室性早搏（ PVCs）及室速∕室颤（VT∕VF）]发生次数。于再灌注120 min时处死大鼠后取心肌组织，测定梗死区（IS）和缺血危险区（ AAR）体积，计算IS∕AAR比值。结果与Sham组比较，其余各组PVCs和VT∕VF发生次数增加， IS∕AAR比值升高（P＜0．05）；与I∕R组比较，MP 组PVCs和VT∕VF发生次数减少，IS∕AAR比值降低（P＜0．05）；与MP组比较，VT＋MP组和ATP＋MP组PVCs和VT∕VF发生次数增加，IS∕AAR比值升高（ P＜0．05）。结论迷走神经?M受体通路参与了鞘内吗啡后处理减轻大鼠心肌缺血再灌注损伤的过程。
목적：평개미주신경?M수체통로재초내마배후처리감경대서심기결혈재관주손상중적작용。방법초내치관성공적건강성년웅성SD대서70지，체중250～350 g，채용수궤수자표법분위7조（ n＝10）：가수술조（ Sham조）、심기결혈재관주조（ I∕R조）、초내주사마배후처리조（ MP조）、경부쌍측미주신경리단조（ VT조）、VT＋MP 조、M수체길항제아탁품＋MP 조（ ATP＋MP 조）화ATP조。채용결찰좌관상동맥결혈30 min회복관주적방법제비대서심기결혈재관주손상모형。 MP조우재관주즉각초내수주마배3μg∕kg 10μl，지속5 min；I∕R조수주생리염수10μl，지속5 min；VT＋MP조우재관주전10 min리단경부쌍측미주신경；ATP＋MP 조우재관주전10 min정맥수주아탁품0．1 mg∕kg 0．5 ml，지속5 min。우재관주30 min내기록실성심률실상[실성조박（ PVCs）급실속∕실전（VT∕VF）]발생차수。우재관주120 min시처사대서후취심기조직，측정경사구（IS）화결혈위험구（ AAR）체적，계산IS∕AAR비치。결과여Sham조비교，기여각조PVCs화VT∕VF발생차수증가， IS∕AAR비치승고（P＜0．05）；여I∕R조비교，MP 조PVCs화VT∕VF발생차수감소，IS∕AAR비치강저（P＜0．05）；여MP조비교，VT＋MP조화ATP＋MP조PVCs화VT∕VF발생차수증가，IS∕AAR비치승고（ P＜0．05）。결론미주신경?M수체통로삼여료초내마배후처리감경대서심기결혈재관주손상적과정。
Objective evaluate the role of vagus nerve?muscarinic cholinergic receptor ( M recep?tor) pathway in mitigation of myocardial ischemia?reperfusion (I∕R) injury by intrathecal morphine postcon?ditioning in rats. Methods Seventy adult male Sprague?Dawley rats in which intrathecal catheters were suc?cessfully placed without complications, weighing 250-350 g, were randomly assigned into 7 groups ( n=10 each) using a random number table:sham operation group (Sham group), I∕R group, intrathecal morphine postconditioning group ( MP group) , vagal transection ( VT) group, VT+ intrathecal morphine postcondi?tioning group (VT+MP group), atropine (ATP, M receptor antagonist) + morphine postconditioning group ( ATP+MP group) , and ATP group. Myocardial I∕R was produced by occlusion of the anterior descending branch of left coronary artery for 30 min followed by 2 h of reperfusion. Morphine ( 3μg∕kg, 10μl) was in?trathecally infused over 5 min starting from onset of reperfusion in MP group. Normal saline 10 μl was in?trathecally infused over 5 min starting from onset of reperfusion in NS group. The bilateral vagus nerves were transected at 10 min before reperfusion in VT+MP group. Atropine ( 0?1 mg∕kg, 0?5 ml) was intravenously infused over 5 min starting from 10 min before reperfusion in ATP+MP group. The occurrence of cardiac ar? rhythmia ( premature ventricular contractions ( PVCs) and ventricular tachycardia ( VT)∕ventricular fibrilla?tion ( VF) ) within the first 30 min of reperfusion was recorded. The rats were sacrificed at 120 min of reper?fusion, and myocardial specimens were obtained for determination of myocardial infarct size ( IS) as a per?centage of area at risk (AAR). IS∕AAR ratio was calculated. Results Compared with Sham group, the number of PVCs and VT∕VF and IS∕AAR ratio were significantly increased in the other groups. Compared with I∕R group, the number of PVCs and VT∕VF and IS∕AAR ratio were significantly decreased in MP group. Compared with MP group, the number of PVCs and VT∕VF and IS∕AAR ratio were significantly in?creased in VT+MP and ATP+MP groups. Conclusion Vagus nerve?M receptor pathway is involved in miti?gation of myocardial I∕R injury by intrathecal morphine postconditioning in rats.