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Ischaemic cerebral injury
follows a well documented sequence of events, including three phases: depolarization,
biochemical cascade and reperfusion injury. The importance of the failure of
neurotransmitter transport as a common pathway in the pathogenesis of ischaemic cerebral
injury has been attested. This substantial step has increased our understanding of the
pathogenesis of ischaemic neuronal injury and at the same time has opened up new
therapeutic prospects for improving brain protection. One such strategy is to use
appropriate pharmacological agents (Baumgartner et al. 1997, Lipton and Rosenberg
1994). Previous studies also suggest that the reperfusion phase is of paramount importance
with regard to the pathogenesis of ischaemic brain injury. Leukocyte infiltration can be
detected following ischaemic insult to the brain, so that the blood vessels will be filled
with leukocytes (primarily neutrophils) and oedema will develop. The adhesion of
leukocytes to the wall of blood vessels and their infiltration into the ischaemic brain
tissue can activate an inflammatory reaction driven by cytokines, which exacerbates the
degree of tissue injury on account of interference with normal microvascular perfusion and
the release of cytotoxic enzymes. (Feuerstein et al. 1998, Feuerstein et al.
1998). As you see ischaemic brain injury involves three sequential phases:
depolarization, biochemical cascade and reperfusion injury. |
