| Objective: Morphine as classical opioid analgesics produces strong analgesic effects by stimulating the opioid receptors in the central nerve system. Central nervous system have many opioids. According to research, remote intrathecal morphine postconditioning(RMPC) can offer cardioprotection against ischemic reperfusion injury, but the mechanism of the protection is not very clear. Cardiovascular physiology activity mainly is regulated by the autonomic nervous system. Improving the vagus nerve excitability and activating muscarinic cholinergic receptor can reduce myocardial ischemia-reperfusion injury. The objective of our research was to evaluate the role of vagus nerve-muscarinic cholinergic receptor(M receptor) pathway in mitigation of myocardial ischemia-reperfusion injury by intrathecal morphine postconditioning in rats.Methods: seventy adult male Sprague-Dawley rats in which intrathecal catheters were successfully 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(ITMP group),vagal transection(VT) group, VT + intrathecal morphine postconditioning group(VT+ITMP group), atropine(ATP, M receptor antagonist) + morphine postconditioning group(ATP+ITMP 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(3 μg/kg,10 μl) was intrathecally infused over 5 min starting from onset of reperfusion in MP group. Normal saline 10 ul was intrathecally 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+ITMP group. Atropine(0.1 mg/kg,0.5ml) was intravenously infused over 5 min starting from 10 min before reperfusion in ATP+ITMP group. The occurrence of cardiac arrhythmia(premature ventricular contractions(PVCs) and ventricular tachycardia(VT) / ventricular fibrillation(VF)) within the first 30 min of reperfusion was recorded. The rats were sacrificed at 120 min of reperfusion, and myocardial specimens were obtained for determination of myocardial infarct size(IS) as a percentage of area at risk(AAR). IS/AAR radio was calculated.Results: Compared with Sham group, the number of PVCs and VT/VF and IS/AAR radio were significantly increased in the other groups. Compared with I/R group, the number of PVCs and VT/VF and IS/AAR radio were significantly decreased in ITMP group. Compared with ITMP group, the number of PVCs and VT/VF and IS/AAR radio were significantly increased in VT+ITMP and ATP+ITMP groups.Conclusions: Vagus nerve-M receptor pathway is involved in mitigation of myocardial I/R injury by intrathecal morphine postconditioning in rats. |
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