THE INTRINSIC REGULATION OF THE CIRCULATION IN THE PARIETAL CORTEX OF THE CAT

Abstract

A thermo-electric method previously used in similar studies in the medulla and hypothalamus was applied to the parietal regions of cats narcotized with pentobarbital or chlora-lose and immobilized with curara. Stimulation of cervical sympathetics caused vasoconstriction which was slow in onset, development, and recovery, and bilateral in distribution; threshold was lower than in hypothalamus, higher than in extracranial tissues; section of nerves caused vasodilatation in parietal region; vagodepressor and carotid sinus stimulation had only passive effects. Surface (pial) vessels of parietal region responded more rapidly, intensely, and reversibly than those of parietal cortex to sympathetic stimulation. Increased CO2 and decreased O2 content of blood caused dilatation of parietal vessels, decreased CO2 and increased O2 caused constriction; effects of changes in O2 were more marked here than in medulla or hypothalamus. Adrenalin had no direct effects; pituitrin was strongly vasodilator, acetylcholine and nitroglycerine less so, and histamine only slightly. Parietal circulation differs from that in hypothalamus and medulla in its greater subjection to vasoconstrictor nerve control and greater reactivity to changes in blood O2, as well as in responses to drugs. Intrinsic regulation of cerebral circulation is therefore more complicated than has been supposed.