Hosomi Naohisa, Ohyama Hideo, Ichihara Shin-Ichiro, Takahashi Tsutomu, Naya Takayuki, Kohno Masakazu
Department of Cardiorenal and Cerebrovascular Medicine, Kagawa University School of Medicine, Japan.
J Stroke Cerebrovasc Dis. 2007 May-Jun;16(3):103-8. doi: 10.1016/j.jstrokecerebrovasdis.2006.12.001.
Postischemic delayed hypoperfusion (PDH) is based on the imbalance between local vasodilators and vasoconstrictors. We evaluated the time course of cerebral blood flow and cerebral specific gravity representing cerebral edema after transient forebrain ischemia induced by bilateral occlusion of the common carotid arteries in anesthetized gerbils to determine whether PDH is a significant factor in development of cerebral edema. PDH appeared 45 minutes after reperfusion followed by the increase of cerebral edema. Thereafter, the local cerebral blood flow recovered from PDH 24 hours after reperfusion in spite of the stable cerebral specific gravity. Furthermore, cerebral specific gravity established a linear correlation with the local cerebral blood flow 120 minutes after reperfusion in the 3 different durations of cerebral ischemia (30, 60, and 90 minutes). It is suggested that cerebral edema is not the cause in PDH development, but PDH may cause cerebral edema.
