Pressor Effect of Increased Cerebrospinal Fluid Pressure and Vertebral Artery Occlusion With and Without Anesthesia

Abstract

The intracranial pressures of conscious, lightly anesthetized and fully anesthetized dogs were altered by means of previously implanted intraventricular cannulas, while systemic arterial pressures were simultaneously measured. One vertebral artery was occluded in all these experiments by the catheter used to record aortic pressure. Increased intracranial pressure, which probably acts by reducing cerebral blood flow, caused a rise in systemic arterial pressure whose magnitude depended on the presence and depth of anesthesia. When anesthesia was not used, but when the animals were resting quietly, a significant pressor response occurred within the physiological range of CSF pressure. The response was typically of slow onset, developing over a period of one half to two minutes. It was reproducible, but tended to diminish gradually in the course of several hours if the experiment was continued, although it could be restored if CSF pressure was further increased. The pulse rate tended to increase slightly, or remain the same, providing CSF pressure was not increased too greatly or too rapidly. Respiratory effects were variable, but most commonly a slightly increased rate and depth of respiration occurred at first, with a return towards normal as the systemic arterial pressure rose. Similar responses were seen during bilateral artery occlusion, by means of previously implanted inflatable cuffs, in dogs whose carotid sinuses had been excised. These effects were also slow in onset, and were accompanied by comparable respiratory changes. In anesthetized animals with intact carotid arteries, bilateral vertebral artery occlusion produced negligible pressor effects, but was found to augment the response to increased intracranial pressure. Observations in four dogs with chronic experimental renal hypertension did not reveal notable differences, except that these animals may be less sensitive than normal to increases in intracranial pressure. The results of these experiments are compatible with the hypothesis that basal systemic arterial pressure during sleep in some degree depends on the cerebrovascular resistance, although it will be important to determine the nature of the slow adaptation seen in these experiments. If this adaptation is brought about by compensatory cerebral vasodilation, this investigation is in accord with the concept of Dickinson and Thomson that some forms of chronic high blood pressure in man might be initiated by cerebral artery occlusion or narrowing of sufficient severity and extent to prevent adequate compensatory vasodilation.