Affiliation:
1. Laboratory of Experimental Brain Research, and Departments of Neurosurgery and Neurology, University of Lund, Lund, Sweden
Abstract
The influence of severe tissue lactic acidosis during incomplete brain ischemia (30 min) on cortex morphology was studied in fasted rats. Production of lactate in the ischemic tissue was varied by preischemic infusions (i.v.) of either a saline or a glucose solution. The brains were fixed by perfusion with glutaraldehyde at 0, 5, or 90 min of recirculation. In saline-infused animals (tissue lactate about 15 μmol g−1), changes observed at 0 and 5 min of recirculation were strikingly discrete: slight condensation of nuclear chromatin. mild to moderate mitochondrial swelling, and only slight astrocyte edema. These changes had virtually disappeared after 90 min recirculation and. at this time. only discrete ribosomal changes were observed. In contrast. glucose-infused rats (tissue lactate about 35 μmol g−1) showed severe changes: marked clumping of nuclear chromatin and cell sap in all cells was already evident at 0 and 5 min recirculation, while mitochondrial swelling was mild to moderate. Although tissue fixation was inadequate at 90 min. the ultrastructural appearance indicated extensive damage. It is concluded that excessive tissue lactic acidosis during brain ischemia exaggerates structural alterations and leads to irreversible cellular damage. A tentative explanation is offered for the paucity (<0.2%) of condensed neurons with grossly swollen mitochondria. previously considered a hallmark of ischemic cell injury.
Subject
Cardiology and Cardiovascular Medicine,Neurology (clinical),Neurology
Cited by
386 articles.
订阅此论文施引文献
订阅此论文施引文献,注册后可以免费订阅5篇论文的施引文献,订阅后可以查看论文全部施引文献