Does nitric oxide synthase inhibition reduce caudate injury following transient focal ischemia in cats?
Inhibition of nitric oxide synthase decreases caudate injury volume from transient focal cerebral ischemia in cats. The beneficial effect is reversed by L-arginine and is not caused by favorable redistribution of blood flow during ischemia and reperfusion. Because L-NAME was efficacious when administered at reperfusion, nitric oxide generated during reperfusion appears to contribute to caudate injury.
Deviations in the pedobarographic data are reflected in the power generation of the ankle joint and can be of help in decision making of treatment in spastic hemiplegic CP. We speculate that efforts to normalize the heel segment pattern may result in decreased power generation differences.