Abstract 142

We hypothesized that sodium channel inhibition before or at the end of ABI would attenuate changes in cerebral vascular tone and CSF cAMP. Three groups of piglets with closed cranial window were studied: group 1 asphyxia (n=5), group 2 pre-treatment with 50 mg/kg of sodium channel blocker HOE642 (n=6), group 3 treatment at the end of asphyxia (n=6). ABI was sustained 60 min by ventilating the piglets with 10% O2/CO2 with reventilation. Pial arteriolar diameters (PAD) and CSF cAMP were measured. Reactivity to topical isoproterenol (ISO) was evaluated after ABI/recovery. Groups did not differ as to BP, pH, pO2, and pCO2 at baseline, asphyxia and reventilation. Data were analyzed by ANOVA with repeated measures. The table shows relative changes in PAD and CSF cAMP over baseline. (*p<0.05). Changes between periods in PAD and CSF cAMP were attenuated in group 2 compared to group 1 (p<.05) with a significant relationship between CSF cAMP and PAD in both asphyxia and pretreated groups (p<0.01) (r value of control > pretreatment). We observed preservation of cerebral vascular tone and cAMP with sodium channel inhibition.

Table 1 No caption available.
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