Decreased vasoconstrictor responses in remote cerebral arteries after focal brain ischemia and reperfusion in the rat, in vitro

The effects of brain ischemia and reperfusion on smooth muscle function in remote cerebral and peripheral arteries are hardly known. Maximum vasoconstrictions (Emax) caused by 120 mmol/l KCl and 5-HT in endothelium-denuded ring preparations were measured in ischemic and control cerebral arteries of rats after a 1-h right middle cerebral artery occlusion followed by 0-min (I/NR) or 2-3-min (I/SR) reperfusion, and in peripheral arteries after I/SR. Surprisingly, vasoconstrictions to 5-HT and 120 mmol/l K+ were attenuated in remote brain vessels after I/SR, i.e. in the contralateral middle cerebral artery and the basilar artery, while I/NR depressed Emax of 5-HT and high KCl only in the ischemic middle cerebral artery. Pretreatment with N-(2-mercaptopropionyl) glycine (MPG, 100 mg/kg i.p.), a free radical scavenger, fully prevented the impairment of vasomotor function in the middle cerebral artery on both sides after I/SR. Moreover, vasomotor functions were normal in the coronary, renal and pulmonary arteries after I/SR. In conclusion, focal cerebral ischemia and reperfusion impaired vasoconstrictor responses in remote brain arteries of rats by a mechanism involving free radicals. The lack of similar effects in peripheral vessels indicates poor defence of brain arteries against remote injury caused by reactive oxygen species-dependent mechanisms.