Pathophysiologic effects of nitric oxide (NO) and endothelin-1 in the gerbil model of gobal ischemia - a survey

These studies were performed in an attempt to clarify some of the pathophys iologic mechanisms which occur during and after global ischemia. Both nitri c oxide and endothelin were demonstrated in gerbils to participate in respo nses to ischemia. It was shown that endogenous nitric oxide influences earl y postischemic reperfusion, systemic blood pressure and postischemic dopami ne metabolism. Furthermore, the results indicated that nitric oxide played a role in dopamine release and that preischemic intracerebral nitric oxide formation significantly decreased ischemic dopamine release. In addition, i schemic release of endothelin-l was detected; participation of nitric oxide in this release was observed. Further indication of functional interaction s between nitric oxide and endothelin-l in postischemic reperfusion were in dicated by observations that endothelin-l antagonists inhibited early hypop erfusion caused by Nitro-L-arginin and late hypoperfusion caused by endogen ous endothelin-l. Nitric oxide was shown to decrease edema formation during the early postischemic period but contribute to edema formation during the late postischemic period. The findings indicate the importance of nitric o xide in stroke and ischemia.