The responses of cerebral precapillary vessels to changes in arterial blood pressure were studied in anesthetized cats equipped with cranial windows for the direct observation of the pial microcirculation of the parietal cortex. Vessel responses were found to be size dependent. Between mean arterial pressures of 110 and 160 mmHg autoregulatory adjustments in caliber, e.g., constriction when the pressure rose and dilation when the pressure decreased, occurred only in vessels larger than 200 micron in diameter. Small arterioles, less than 100 micron in diameter, dilated only at pressures equal to or less than 90 mmHg; below 70 mmHg their dilation exceeded that of the larger vessels. When pressure rose to 170- 200 mmHg, small vessels dilated while the larger vessels remained constricted. At very high pressures (greater than 200 mmHg) forced dilation was frequently irreversible and was accompanied by loss of responsiveness to hypocapnia. Measurement of the pressure differences across various segments of the cerebral vascular bed showed that the larger surface cerebral vessels, extending from the circle of Willis to pial arteries 200 micron in diameter, were primarily responsible for the adjustments in flow over most of the pressure range.

No abstract

Wei EP, Kontos HA, Said SI: Mechanism of action of vasoactive intestinal polypeptide on cerebral arteries. Amer J Physiol 239: H765-768, 1980 Wilson DA, O'Neill JT, Said SUMMARY The endothelium of mouse pial arterioles was injured in situ with a light/dye technique. The response of the arterioles to acetylcholine or to bradykinin was compared before and after the injury. All vessels failed to dilate after injury. In fact the predominant response now became constriction. The injured vessels were still capable of dilating to papaverine. Uninjured vessels continued to dilate to acetylcholine or bradykinin. The data show that relaxation of pial arterioles to acetylcholine or bradykinin is dependent on a normal endothelium. This is in keeping with demonstrations by others that an endothelial dependent relaxing factor or factors is(are) the mediator of the dilation to either acetylcholine or bradykinin. The present demonstration of such endothelial dependence is important because in contrast with the bulk of the literature it deals with in vivo, rather than in vitro data, and with microcirculation rather than large vessels. It is also important because it concerns brain circulation. The data suggests that endothelial injury, known to occur in a wide variety of pathologic states, could enhance vasospastic potential by eliminating dilating influences and/or converting them to constricting forces.

The mechanism of action of hypoxia on cerebral blood vessels and its role in the regulation of the cerebral circulation were investigated in anesthetized cats. Arterial hypoxia produced marked cerebral arteriolar vasodilation, which was partially reversed by perfusing the space under the cranial window with artificial cerebrospinal fluid (CSF) containing 6-94% oxygen. More marked increase in the local supply of oxygen, via perfusion of the space under the cranial window with fluorocarbon FC-80 equilibrated with 100% oxygen, completely eliminated the vasodilation induced by arterial hypoxia. Fluorocarbon equilibrated with 100% N2 had no effect on the vasodilation. The vasodilation associated with hypotension was completely reversed by perfusion with fluorocarbon equilibrated with 100% oxygen and was unaffected by perfusion with fluorocarbon or CSF equilibrated with gas not containing oxygen. The vasodilation associated with Metrazole-induced seizures was partially reversed by perfusion with fluorocarbon containing oxygen. The results show that hypoxia dilated cerebral blood vessels entirely via a local mechanism, that hypoxia is the dominant mechanism involved in the vasodilation associated with hypotension, and that it is, at least partially, responsible for the vasodilation associated with seizures.