Objective: To investigate the combined effect of cerebral ischemia and tissue plasminogen activator on cerebrovascular autoregulation and evaluate the probably mechanisms of ischaemia-reperfusion injury after thrombolysis. Methods: The middle cerebral artery occlusion model was used in male Wistar rats to induce 90 mins of focal cerebral ischemia. External and internal diameter of middle cerebral artery was measured in vitro using a pressure myograph system

and mechanical parameters and myogenic tone were calculated. Arteries were either nonischemic(control;n=6)

nonischemic and perfused with rtPA for 50~60 mins(rtPA;n=6)

ischemic(ISC;n=8)

or ischemic and perfused with rtPA for 50~60 mins (rtPA-ISC;n=8). The data were then compared among the groups. Results: Control arteries increased myogenic tone from 60 mmHg to 120 mmHg and responded myogenic reactivity

all other groups decreased tone at 120 mmHg and lost myogenic reactivity;Diameters of control arteries showed the leas(tP<0.05 vs all three others)

rtPA-ISC group showed the largest(P<0.05 vs all three others);Compared with control and rtPA arteries

ISC and rtPA-ISC arteries showed an increased strain(P<0.01 for all)

a decreased β values (P<0.01 for all)

and rightward shift of the stress-strain relationship. Conclusion: These results demonstrate that both ischemia and rtPA perfusion diminish myogenic reactivity of cerebral artery and that the combination may produce an additive effect;at same time

ischemia can alter mechanical properties of cerebral artery. These changes may contribute to cerebral ischemia-reperfusion injury during or after thrombolysis by altering upstream cerebrovascular resistance.