CAJ | 학술논문

目的：验证短期颈动脉压力感受器电刺激(Carotid baroreceptors stimulation，CBS）是否通过激活迷走神经的胆碱能抗炎通路减轻犬心肌缺血再灌注损伤。方法36只成年杂种犬随机分为三组(n=12)：缺血再灌注组(I/R组)、颈动脉压力感受器刺激组(CBS组)和迷走神经干切除术(Vagotomy)组(VAG组)。各个组别的实验犬分别结扎左冠脉前降支1 h和再灌注6 h完成心肌缺血再灌注损伤模型。CBS组在心肌缺血前2 h对右侧颈动脉窦开始进行高频电刺激，直到实验结束，刺激参数：频率50 Hz，脉宽0.5 ms，刺激强度随血压进行调整，以保持血压较刺激前下降10%。VAG组在颈动脉窦刺激前实施双侧颈迷走神经干切除术。于缺血前、缺血15 min、30 min、60 min和再灌注0.5 h、2 h、6 h时记录心率(HR)和平均动脉压(MAP)。各组随机抽取6只犬于再灌注6 h后分别经颈内静脉采血，采用ELISA法检测血清TNF-α、IL-1β、IL-6浓度。采血后，迅速取出缺血区心肌组织，检测髓过氧化物酶(MPO)活性观察中性粒细胞浸润情况。各组剩余6只犬于再灌注6 h后采用依文斯兰—氯化三苯基氮唑(TTC)双染色法检测心肌缺血和心肌梗死面积。结果与I/R组比较，CBS组心肌梗死面积，MPO活性，血清TNF-α、IL-1β、IL-6含量降低(P<0.05)；与I/R组比较，VAG组心肌梗死面积，MPO活性，血清TNF-α、IL-1β、IL-6含量差异无统计学意义(P>0.05)。结论短期颈动脉压力感受器电刺激可减轻犬心肌缺血再灌注损伤，抑制中心粒细胞向缺血组织浸润以及抑制全身炎症反应，其机制与短期颈动脉压力感受器电刺激激活迷走神经的胆碱能抗炎通路有关。
목적：험증단기경동맥압력감수기전자격(Carotid baroreceptors stimulation，CBS）시부통과격활미주신경적담감능항염통로감경견심기결혈재관주손상。방법36지성년잡충견수궤분위삼조(n=12)：결혈재관주조(I/R조)、경동맥압력감수기자격조(CBS조)화미주신경간절제술(Vagotomy)조(VAG조)。각개조별적실험견분별결찰좌관맥전강지1 h화재관주6 h완성심기결혈재관주손상모형。CBS조재심기결혈전2 h대우측경동맥두개시진행고빈전자격，직도실험결속，자격삼수：빈솔50 Hz，맥관0.5 ms，자격강도수혈압진행조정，이보지혈압교자격전하강10%。VAG조재경동맥두자격전실시쌍측경미주신경간절제술。우결혈전、결혈15 min、30 min、60 min화재관주0.5 h、2 h、6 h시기록심솔(HR)화평균동맥압(MAP)。각조수궤추취6지견우재관주6 h후분별경경내정맥채혈，채용ELISA법검측혈청TNF-α、IL-1β、IL-6농도。채혈후，신속취출결혈구심기조직，검측수과양화물매(MPO)활성관찰중성립세포침윤정황。각조잉여6지견우재관주6 h후채용의문사란—록화삼분기담서(TTC)쌍염색법검측심기결혈화심기경사면적。결과여I/R조비교，CBS조심기경사면적，MPO활성，혈청TNF-α、IL-1β、IL-6함량강저(P<0.05)；여I/R조비교，VAG조심기경사면적，MPO활성，혈청TNF-α、IL-1β、IL-6함량차이무통계학의의(P>0.05)。결론단기경동맥압력감수기전자격가감경견심기결혈재관주손상，억제중심립세포향결혈조직침윤이급억제전신염증반응，기궤제여단기경동맥압력감수기전자격격활미주신경적담감능항염통로유관。
Objective To test whether carotid baroreceptors stimulation could reduce acute myocardial isch-emia reperfusion injury (IRI) through the cholinergic anti-inflammatory pathway. Methods Thirty-six dogs were ran-domly allocated into three groups, each with 12 dogs:ischemia reperfusion group (I/R group), carotid baroreceptors stimulation group (CBS group) and vagotomy group (VAG group). Dogs were subjected to 1 h coronary artery occlu-sion followed by 6 h reperfusion alone (I/R group). Dogs in CBS group were treated with carotid baroreceptors stimu-lation 2 h before ischemia myocardial (with frequency of 50 Hz, pulse width of 0.5 ms, and intensity adjusted with blood pressure to keep the blood pressure 10%lower than before stimulation). Dogs in VAG group were treated with va-gotomy and carotid baroreceptors stimulation. Heart rate (HR), mean arterial pressure (MAP) were recorded before isch-emia, 15 min, 30 min, 60 min after ischemia, 0.5 h, 2 h, 6 h after reperfusion. Six dogs were selected in each group and collected for venous blood 6 h after reperfusion. Serum levels of inflammatory cytokines (TNF-α, IL-1β, IL-6) during re-perfusion were assayed, and the neutrophil infiltration (MPO activity) was quantified. The ischemia myocardial and infarct size were detected in the remaining 6 dogs in each group. Results Compared with I/R group, infarct size, MPO activity, serum levels of TNF-α, IL1-βand IL-6 in CBS group at 6 h after reperfusion were significantly lower (P<0.05). However, there was no statistically significant difference between VAG group and I/R group. Conclusion Carotid baroreceptors stimulation attenuates myocardial ischemia reperfusion injury. The underlying mechanism may be asso-ciated with activating the cholinergic anti-inflammatory pathway.