Role of circulatory disturbances in the development of post-ischemic brain edema

• Published in: Neurochemical pathology Vol. 9; p. 21
• Main Authors: Masaoka, H, Klatzo, I, Tomida, S, Vass, K, Wagner, H G, Nowak, Jr, T S
• Format: Journal Article
• Language: English
• Published: United States 01.07.1988
• Subjects: Animals; Brain Edema - etiology; Brain Edema - physiopathology; Brain Ischemia - complications; Brain Ischemia - physiopathology; Cerebrovascular Circulation; Hyperemia - complications; Hyperemia - physiopathology; Time Factors
• ISSN: 0734-600X
• DOI: 10.1007/bf03160354

Two post-ischemic circulatory disturbances that play a significant role in pathophysiology of an ischemic lesion are: (1) reactive hyperemia or hyperperfusion and (2) hypoperfusion. The reactive hyperemia promptly follows release of major cerebral artery occlusion, and it is associated with the opening of the blood-brain barrier to serum proteins and ensuing edema. Prevention or reduction of reactive hyperemia results in significant amelioration of edema and the resulting ischemic brain tissue injury. The post-ischemic hypoperfusion, studied in gerbils, develops soon after recirculation and usually lasts up to 6 h. Its relationship to post-ischemic edema is evident in repeated ischemic insults. In these studies, three ischemic insults of 5 min duration when applied at 1 h intervals, i.e., during the period of hypoperfusion, resulted in a cumulative effect, post-ischemic edema and tissue injury becoming considerably more pronounced that those following a single 15 min ischemia. There was no cumulative effect when the ischemic insults were spaced 3 min or longer than 6 h apart. These observations indicate that repeated ischemic insults taking place during the phase of post-ischemic hypoperfusion may significantly increase the development of edema and brain tissue injury.