[Pathological and compensatory processes in the cerebral circulation during blood transfusion shock]. / Processus pathologique et compensatoire dans la circulation cérébrale lors du choc d'hémotransfusion.

In experiments on dogs the intravenous injection of heterogenous blood resulted in a decrease of total arterial pressure, weakening of the brain blood flow, fall of Po2 and pH in the brain cortex. A simultaneous constriction if inner carotid arteries is depending on direct action on the vascular wall of heterogenous proteins and on a release in it of physiologically active substances, such as serotonin. Fine pial arteries were dilated by the compensatory mechanism that was not associated with a decrease of intravascular and with direct action of hypoxia or acid metabolites on vascular walls. It was proposed that the trigger mechanism of this vasodilatation is hypoxic changes of metabolism in the nervous tissue.

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.