Siesjö B K
Laboratory for Experimental Brain Research, University of Lund, Sweden.
Crit Care Med. 1988 Oct;16(10):954-63. doi: 10.1097/00003246-198810000-00006.
This article provides a brief review of recent developments regarding the pathophysiology of ischemic brain damage, and offers hypotheses explaining the pathogenesis of selective neuronal vulnerability and of tissue infarction, respectively. It is suggested that selective neuronal vulnerability, observed after brief periods of ischemia and after hypoglycemic coma, qualifies as an excitotoxic lesion, which causes postsynaptic damage to neurons innervated by excitatory amino acids by enhancing calcium influx. However, ischemic damage often involves glial and vascular cells as well, and causes infarction. It is hypothesized that this type of brain damage is related to acidosis and that enhanced acidosis is detrimental because it accelerates delocalization of protein-bound iron, with an ensuing free-radical damage to membrane lipids and proteins.
