Blood recirculation and pharmacological responsiveness of the cerebral vasculature following prolonged ischemia of cat brain.

Normothermic adult cats were submitted to 30 min complete cerebral ischemia by arterial inflow occlusion, and the brains subsequently recirculated with blood for 4 hours. Cortical blood flow was recorded with a heated thermocouple, cortical oxygen pressure with a multiwire oxygen electrode, and the pial arterial tone by photomicroscopy using an implanted glass window. In addition, blood pressure, blood flow through the innominate artery and the electrocorticogram were continuously monitored. During ischemia cortical oxygen pressure fell from 44 ± 5.8 to 0 torr (means ± S.E.), cortical heat conductance decreased from 15.1 ± 0.8 to 10.2 ± 0.5 X 10-4 cal X cm-1 X sec-1 X °C-1, and the pial arteries constricted to less than 50° of their initial diameter. Recirculation of the ischemic brain initiated reactive hyperemia (heat conductance 23.6 ± 3.6 X 10-4 cal X cm-1 X sec-1 X °C-l) which lasted for about 45 min. and which was accompanied by an increase in arterial Po2 to 74 ± 14 torr, and a dilatation of the pial arteries byabout 50°. Hyperemia was followed by postischemic hypoperfusion during which cortical Po2 returned to, or slightly below, normal (34 ± 4 torr), cortical heat conductance decreased to 13.9 ± 0.4 X 10-4 cal X cm-1 X sec-1 X °C-1 and pial arteries constricted by about 10°. The pharmacological responsiveness of the pial vasculature was tested before ischemia and during postischemic hypoperfusion by intra-arterial administration of alpha- and beta-adrenergic stimulating and blocking agents, the antiserotoninergic agent metergolin, and papaverine. The autonomic drugs and metergolin induced only minor changes in cortical blood flow or oxygenation but there was distinct vasodilatation and an increase in blood flow with papaverin both before and after ischemia. It is concluded that treatment of postischemic hypoperfusion is more efficient with drugs which cause direct relaxation of the vascular smooth muscle than with those which act on the autonomic receptor sites.