BRAIN DAMAGE IN RHESUS MONKEY RESULTING FROM PROFOUND ARTERIAL HYPOTENSION .I. ITS NATURE DISTRIBUTION AND GENERAL PHYSIOLOGICAL CORRELATES

Profound arterial hypotension was induced in 15 rhesus monkeys under pentobarbital anaesthesia, by a ganglion-blocking agent (Arfonad), head-up tilt and arterial bleeding. After respiratory arrest mechanical ventilation ensured normal arterial oxygenation. The following variables were recorded during and after the period of hypotension: arterial and venous sinus blood pressure, intracranial pressure, oxygen saturation or tension and Pco2 and pH of arterial and cerebral venous blood samples, arterial and cerebral venous glucose concentrations, respiratory rate, body temperature, electrocardiogram, electrocorticogram and somatosensory cortical evoked responses. The pial blood vessels were observed and photographed through a cranial window. The animals were divided neuropathologically into:. Group I (5 animals), normal brains. Group II (6 animals), ischaemic alterations in the arterial boundary zones of the cortices of cerebrum and cerebellum. In addition, lesions were seen in the basal ganglia (3 animals) and in the hippocampi (2 animals). Group III (4 animals), ischaemic alterations were diffuse in the cortex of cerebrum and cerebellum, and the hippocampi and variable in the basal ganglia. Brain damage occurred only when the cerebral perfusion pressure fell rapidly to below 25 mm Hg and was sustained at this level for at least 15 min. The time course of changes in the amplitude of the somatosensory cortical evoked response during hypotension clearly differentiated the 3 groups of animals. The survival time of the evoked response correlated inversely with the degree of brain damage; the duration of the period of reduced cerebral perfusion after the disappearance of the evoked response correlated directly with the degree of brain damage. The recovery of cerebral electrical activity and the return to consciousness was similar in animals of Groups I and II. Two animals in Group II showed motor disabilities. The animals in Group III failed to regain consciousness and showed a marked rise in intracranial pressure followed by a secondary loss of spontaneous respiration and cerebral electrical activity. At post mortem a downward herniation of the brain stem and inferior cerebellar vermis was seen. The lesions in the cerebral arterial boundary zones appear to result from a profound local reduction in cerebral blood flow which leads to a correspondingly localized metabolic disturbance, later recognisable as 'ischaemic cell change'. © 1969.