On the control of microcirculation in the cerebral cortex during and following ischemia.
The aim of the present study was the elucidation of the functional behaviour of the pial arteries and their microvascular effectors which are responsible for the microcirculation in the cerebral cortex - large and small pial arteries (PA), sphincters at the offshoots at the pial arteries (SOPA), precortical arteries (PCA) and pial arterial microanastomoses (PAMA) - both under ischemic and postischemic conditions. During ischemia the majority of the studied microvessels underwent dilatation which under conditions of decreased intravascular pressure seems to be active and should be aimed at compensating for the defficiency of the blood supply to the cerebral tissue. Besides, a constriction of some microvessels, especially of SOPA and PCA, was also observed, the amount of such responses of SOPA being increased in the postischemic period. It might be conjectured that the vasoconstrictor responses may be responsible for the ischemic damage of some cortical areas, but it may be also directed to a redistribution of blood to compensate for ischemic changes in individual areas of the cerebral tissue. The active constriction of SOPA in the postischemic period might be also considered as a compensatory microvascular reaction which is directed to restrict the excessive blood supply to the brain tissue and to prevent edema development in it.
D000818:Animals; D002540:Cerebral Cortex / Q000098:blood supply*; D005260:Female; D002546:Ischemic Attack, Transient / Q000503:physiopathology*; D008297:Male; D008833:Microcirculation; D011817:Rabbits; D012039:Regional Blood Flow