A new model of concussive brain injury in the cat produced by extradural fluid volume loading: II. Physiological and neuropathological observations

作者：RONALD L. HAYES, Daniel Stålhammar, John Theodore Povlishock, Arletha M. Allen, Brian J. Galinat, Donald P. Becker, Henry H. Stonnington · 发表于：Brain Injury · 年份：1987 · DOI：10.3109/02699058709034449 · 被引用次数：76 · 研究领域：Traumatic Brain Injury and Neurovascular Disturbances、Automotive and Human Injury Biomechanics、Trauma, Hemostasis, Coagulopathy, Resuscitation

This study examined physiological and histopathological changes in the cat produced by a new experimental fluid injury device. Spontaneously breathing (N = 14) and artificially ventilated (N = 45) cats were subjected to systemically varied magnitudes of fluid percussion brain injury. Within certain injury ranges, increasing magnitudes of fluid percussion injury produced increasing durations of apnea, as well as greater transient increases in mean arterial blood pressure, intracranial pressure and cerebral perfusion pressure. Acute increases in intracranial pressure may have been related to cerebral vasodilatation produced by the systemic hypertension following brain injury. Injuries associated with pressure transients greater than 10 atm ms produced concussive responses, including irreversible apnea in spontaneously breathing cats and temporary pupillary dilatation, increases in heart rate and mean arterial blood pressure in artificially ventilated cats. Injuries greater than 39 atm ms frequently produced histopathological and physiological indices of significant irreversible brain damage, including fixed and dilated pupils, systemic cardiovascular hypotension and deteriorating blood gases. Injury magnitudes less than 20 atm ms did not produce macroscopic evidence of histopathology, intermediate injury ranges produced increasing evidence of subarachnoid and petechial hemorrhage while injury levels greater than 40 atm ms frequently produced significant histopathology including...