Role of circulatory disturbances in the development of post-ischemic brain edema.
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.
Masaoka
H
H
Laboratory of Neuropathology and Neuroanatomical Sciences, National Institute of Neurological and Communicative Disorders and Stroke, Bethesda, MD 20892.
Klatzo
I
I
Tomida
S
S
Vass
K
K
Wagner
H G
HG
Nowak
T S
TS
D000818:Animals; D001929:Brain Edema / Q000209:etiology / Q000503:physiopathology*; D002545:Brain Ischemia / Q000150:complications / Q000503:physiopathology*; D002560:Cerebrovascular Circulation; D006940:Hyperemia / Q000150:complications / Q000503:physiopathology; D013997:Time Factors