Synthetic Analogs of 6-Bromohypaphorine, a Natural Agonist of Nicotinic Acetylcholine Receptors, Reduce Cardiac Reperfusion Injury in a Rat Model of Myocardial Ischemia

The data available to date indicate that the activation of nicotinic acetylcholine receptors (nAChR) of alpha 7 type can reduce heart damage resulting from ischemia and subsequent reperfusion. We have studied two new synthetic D-analogs of 6-bromohypaphorine, which are selective agonists of alpha 7 nAChR, in a rat model of myocardial ischemia. Acute myocardial infarction in animals was induced by occlusion of the left coronary artery with its subsequent reperfusion under mechanical lung ventilation. It was found that one of the analogs was more active, and treatment with it at the onset of reperfusion statistically reduced infarct size. This analog also prevented changes in the concentration of potassium and sodium ions in the blood, occurring during occlusion/reperfusion injury. The data obtained indicate that hypaphorine analogs are promising for the development of drugs that reduce the adverse effects of myocardial infarction.

Automated summary

The activation of alpha 7 nicotinic acetylcholine receptors has been found to reduce heart damage caused by ischemia and reperfusion. In a rat model of myocardial ischemia, two synthetic D-analogs of 6-bromohypaphorine, selective agonists of alpha 7 nAChR, were studied. It was discovered that one of the analogs was more effective in reducing infarct size and preventing changes in potassium and sodium ion concentrations in the blood. These findings suggest that hypaphorine analogs show promise for the development of drugs to mitigate the adverse effects of myocardial infarction.