Waltz, Arthur G.

An infrared microscope was used for the remote detection of the surface temperature of the cerebral cortex of experimental cats. With this instrument a qualitative assessment of the circulation of the cerebral cortex can be made without interference with the integrity of the brain or vascular tissues or the reactivity of blood vessels. Although the instrument is sensitive enough to detect minor changes of cortical blood flow, its use appears limited to the detection of rapid or transient changes of cerebral circulation and is not suitable for long-term measurements of surface temperature of the brain.

The right seventh cranial nerve (n. VII) was exposed intracranially via a suboccipital approach in each of eight cats. Measurements of cerebral blood flow (CBF) were made from superficial cortex, sulcal cortex, basal cortex, the basal ganglia, and the centrum semiovale of each cerebral hemisphere of each cat by autoradiography using 14 Cantipyrine. In six cats, measurements of CBF were made during electric stimulation of n. VII; in two of these, the nerve was sectioned before stimulation. In the remaining two cats, measurements were made after exposure but without stimulation of n. VII; in these cats, there were no side-to-side differences of CBF. In each of the four cats with n. VII intact, CBF values were lower on the stimulated side. In each of the two cats with n. VII sectioned, CBF values were higher on the stimulated side. Thus, stimulation of n. VII causes regional increases of CBF only when centripetal effects of stimulation are prevented. Cerebral vasodilatation has been observed by others during stimulation of a sectioned or an intact n. VII. When an intact nerve is stimulated, vasodilatation apparently is unable to compensate for decreases of CBF mediated centripetally through brain stem structures and extracranial or basal cerebral vessels; moreover, such vasodilatation may be due in part to regulatory responses of vessels to decreases of perfusion pressure.

In cats in which one middle cerebral artery was occluded, cortical blood flow (CBF) was measured and the superficial cortical microvasculature was observed bilaterally before and after the intravenous injection of a vasoactive drug. Aminophylline produced decreased CBF in the nonischemic cerebral hemispheres of five of seven animals and arterial constriction in three. Ergotamine tartrate produced arterial constriction in the nonischemic hemispheres of four animals and decreased CBF in three. Neither drug consistently produced increased CBF in ischemic cerebral tissue. Acetazolamide caused vasodilatation in the nonischemic hemispheres of seven animals and increased CBF in five. Increased CBF was not due entirely to changes of Pa CO 2 . CBF also increased in ischemic hemispheres of four of the seven animals given acetazolamide.

To assess the effects of Pa CO CO 2 on cerebral ischemia and reactive hyperemia, the right middle cerebral artery was occluded in 18 cats. Four to six hours later, Pa CO 2 was adjusted by mechanical ventilation, with or without CO 2 , to less than 20 torr in four cats, 31 to 38 torr in six, and 46 to 68 torr in eight. Regional cerebral blood flow (CBF) then was measured at multiple sites in each hemisphere by autoradiography. In regions of brain tissue outside the distribution of the occluded middle cerebral artery, log 10 CBF correlated positively with Pa CO CO 2 . In ischemic regions, CBF was higher in normocapnic cats. Reactive hyperemia occurred in two cats of the hypocapnic group, in four cats of the normocapnic group, but in only one hypercapnic cat (Pa CO CO 2 = 46 torr). Hyperemia also was found outside potentially ischemic regions in five cats. Multiple hyperemic foci developed in six cats. Neither hypocapnia nor hypercapnia was associated with a smaller size or higher CBF of regions of cerebral ischemia produced by occlusion of a middle cerebral artery, although hypercapnia inhibited the development of hyperemia.

The right middle cerebral artery (MCA) was occluded in cats; after subsequent craniectomy cortical blood flow (CBF) was measured bilaterally with 85 Kr, and photographs of the superficial microvasculature were made. Ventilation was controlled, and Pa CO CO2 was altered by changing the concentration of CO 2 in the inspired air. In nonischemic cortex CBF varied as an exponential function of Pa CO CO2 , and the caliber of superficial arterial vessels (50 to 200µ in diameter) increased with increasing Pa CO CO2 . In ischemic cortex, changes of Pa CO CO2 produced no change of CBF in six of ten animals studied within one day of occlusion; in four of these six, there was no change in the caliber of arterial vessels. In the four other animals of this group, there was a paradoxical response (an increase of Pa CO CO2 produced a decrease of CBF of ischemic cortex), and in two of these four animals, there also was a paradoxical response of the caliber of arterial vessels. In eight animals allowed to survive 5 to 12 days after MCA occlusion, the arterial vessels of ischemic cortex regained some reactivity: a normal response of CBF to changes of Pa CO CO2 was found in four, and appropriate changes of vessel caliber were found in all eight. The ischemia-induced impairment of the reactivity of cortical vessels to changes of Pa CO CO2 casts doubt on the usefulness of CO 2 inhalation for the treatment of strokes of humans.