By J. Ristić (auth.), B. B. Mršulja, Lj. M. Rakić, I. Klatzo, Maria Spatz (eds.)

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B (In Press) . 8. H. and Kamijyo, Y. (1974): Cerebral infarction. Evolution of histopathological changes after occlusion of a middle cerebral artery in primates. J. Neuropath. Exp. Neurol. 33: 409-421. 9. S. and Jamaris, J. (1977): Ultrastructural investigations of regional ischemia in the rhesus monkey (Research in Progress, Unpublished Observations) . 10. A. and Kleihues, P (1973): Reversibility of ischemic brain damage. Arch. Neurol. 29: 375-384. 11. R. H. (1970): Transorbital approach to the middle cerebral artery of the squirrel monkey: A technique for experimental cerebral infarction applicable to ultrastructural studies.

Ole in the pathomechanism of ischemic injury; more pronounced cellular degeneration and neuropilic vacuolization was found in hypertensive as compared to normotensive postischemic gerbils (7). The behavior of biogenic amines in the postischemic period following l-h ischemia is somewhat peculiar. Norepinephrine (NE), dopamine (DA) and serotonin (5-nT) were slightly reduced during l-h ischemia, but following the recovery period, 5-HT content returned to the control values, DA was more reduced and NE concentration was enhanced over the control level (Fig.

PATHOCHEMISTRY OF THE POST·ISCHEMIC PERIOD 51 These data provide additional biochemical evidence supporting earlier findings on the existence of the maturation phenomenon following ischemic insult; the phenomenon was also confirmed 'by the histochemical studies in hippocampus (19). The main feature of this phenomenon is the fact that the rate of maturation of ischemic injury is directly related to the intensity of ischemic insult, a lesser intensity resulting in delayed lesion development. The importance of the maturation phenomenon is still intriguing.

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