Disturbances of Protein and Polyamine Metabolism After Eversible Cerebral Ichemia

Abstract

The high sensitivity of the brain to ischemia is generally attributed to the misrelationship between the high metabolic demands and the low energy reserves of this organ. In fact, complete cessation of blood flow in the nonanesthetized normothermic brain leads to complete depletion of energy reserves and a cessation of all endergonic metabolic processes within less than 5 min (Lowry et al., 1964). However, experimental observations from our and other laboratories have clearly established that this process is not irreversible. Provided that a no-reflow can be prevented, reoxygenation of the brain will result in a reactivation of energy metabolism after complete cerebrocirculatory arrest of as long as 1 hr (Hossmann and Kleihues, 1973; Pluta, 1987). However, it has also been shown that the recovery of energy metabolism correlates closely with the restoration of the electrophysiological function of the brain (Schmidt-Kastner et al., 1986). Most ischemic experiments exceeding a duration of 5 to 10 min nevertheless result in more or less severe brain injury when the animals are allowed to survive for some time (Siesjö, 1988b). The foci of ischemic cell injury are accentuated in the so-called selectively vulnerable areas of the brain, i.e., the third layer of the cerebral cortex, hippocampal subfields CA1 and CA4, the dorsolateral aspect of the striate nucleus, and, under conditions of hyperglycemia, the pars reticulata of the substantia nigra (Pulsinelli et al., 1982; Kirino and Sano, 1984; M. L. Smith et al., 1988).