Mechanisms of selective head cooling for resuscitating damaged neurons during post-ischemic reperfusion

To evaluate the efficacy and the mechanism of application of selective head cooling on neuronal morphological damage during postischemic reperfusion in a rabbit model.

168 New Zealand rabbits were randomized into three groups. Group I [n = 24, (38 +/- 0.5) degrees C, non-ischemic control]; Group II [n = 72, (38 +/- 0.5) degrees C, normothermic reperfusion]; Group III [n = 72, (28 +/- 0.5) degrees C, selective head cooling, initiated at the beginning of reperfusion). Animals in three subgroups (n = 24, each) of Group II and Group III had reperfused lasting for 30, 180 and 360 min respectively. Using computerized image analysis technique on morphological changes of nucleus, the degree of neuronal damage in 12 regions were differentiated into type A (normal), type B (mild damaged), type C (severely damaged) and type D (necrotic). Fourteen biochemical parameters in brain tissues were measured.

As compared with Group I, the counts of type A neuron decreased progressively, and those of type B, C and D increased significantly in Group II during reperfusion (P < 0.01). In Group II, vasoactive intestinal peptide, b-endorphine, prostacyclin, T3 and Na+, K(+)-ATPase were correlated with the changes of type A; b-endorphine and thromboxane with type B; glucose and vasopressin with type C; Na+, K(+)-ATPase, glutamic acid, T3 and vasoactive intestinal peptide with type D (P < 0.05). As compared with Group II, the counts of type A increased, and those of type C and D significantly decreased in Group III (P < 0.01). In Group III, Ca2+, Mg(2+)-ATPase were correlated with the changes of type A, C and D (P < 0.01).

Selective head cooling for sex hours during postischemic reperfusion does improve neuronal morphological outcomes in terms of morphological changes.