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However, in the postischemic phase, NO (probably derived from neurons or macrophages) contributes to neuronal injury.
However, more recent data indicate that postischemic neuronal injury is a dynamic process during which neurons continue to die for a long period after the initiating ischemic insult (Fig. 11.22).240 This delayed neuronal death, which was first demonstrated in models of global cerebral ischemia, has been demon- strated during focal ischemia as well.
Recent data indicate that cerebral infarction undergoes gradual expansion and that a reduction in injury attributed to a particular therapeutic intervention is no longer apparent when the injury is evaluated after a long postischemic recovery period.240 Long-term (>1 month) evaluation of the efficacy of a particular intervention is therefore important.
These data indicate that neuronal injury continues well into the postischemic recov- ery period and that the neuroprotective benefit that is evi- dent shortly after ischemia may not persist for the long term.
Although barbiturates reduce only the component of the CMR associated with electrophysiologic work (approximately 60% of the CMRO2 in the awake state), hypothermia causes a reduction in both electrophysiologic energy consumption and energy utilization related to the maintenance of cellular integrity; mild hypothermia may preferentially suppress the latter.299 A substantial number of laboratory studies have demon- strated that mild degree of hypothermia (2蚓-4蚓) during an episode of ischemia can confer substantial protection as histologically measured.269,270 In addition, hypothermia initiated in the immediate postischemic period confers a protective benefit.300
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