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The effects of dehydroepiandrosterone sulfate (DHEAS) on mimetic aging action of cultured neurons were studied in two models: the cultured cerebral cortex neurons were exposed to the xanthine oxidase-hypoxanthine(XO-HPX) system; serum free culture of cerebral cortex neurons. The results indicated that when cultured neurons were incubated for 6 h with XO-HPX system or 24 h serum free cultures, LDH release and MDA content increased while the number of surviving neurons decreased. The activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) decreased and morphological injury developed. DHEAS (25, 50, 100 micrograms.L-1) concentration-dependently increased the number of surviving neurons and the activities of SOD and GSH-Px. It also inhibited the elevation of LDH and MDA induced by free radical and serum free cultures. The results suggest that DHEAS prevent the toxicity of free radical and serum free culture insults by suppressing the generation of lipid peroxide and increasing the activities of antioxidant enzymes.

Objective: To evaluate the effect of nimodipine and papaverine (Pap) on the spastic arteries with delayed cerebral vasospasm (DCVS) in dogs., Methods: A model of DCVS in dogs was induced by the cisterna magna injections of fresh autologous blood twice. The diameter of the basilar arteries with and without DCVS was measured with the aid of a JVC operative microes cope in vivo after nimodipine and Pap were directly placed around the arteries., Results: The dilation of the basilar arteries was obviously induced by application of nimodipine and Pap in the dogs without DCVS no dilation was induced by application of nimodipine and slight dilation by application of Pap but in those with DCVS., Conclusion: The cerebral blood flow is improved by the effect of nimodipine on non-spastic arteries. Pap has been found to reverse slightly the narrowing of the basilar arteries with DCVS and to dilate the arteries without DCVS, but the vasodilation effect is transient.

The clinical and pathological features of 20 cases of moyamoya disease complicated with primary intraventricular hemorrhage (PIVH) and verified by CT scanning, cerebral angiography and autopsy were reported. It seemed to the author that moyamoya disease appeared to be prone to cause PIVH, this hemorrhage being likely due to ischemic malacia in the ventricular wall. The tortuous, abnormal network vessels ruptured and bled as a result of infarction and damage of the walls of the miliary aneurysms. PIVH might be divided into two types: the panventricular hemorrhage and partial ventricular hemorrhage, according to the amount of blood that filled into the ventricles. 6 cases of the panventricular type were fatal. The symptoms were in conformity with the traditional concept of the most critical, intraventricular hemorrhage. The external ventricular drainage in combination with lumber puncture drainage would be the better way of treatment for these patients. 14 cases of the partial ventricular hemorrhage type showed the clinical features of acute subarachnoid hemorrhage (SAH). The treatment was similar to SAH too, and the prognosis was much better. It would be worth noting that moyamoya disease should be a factor not to be neglected in causing PIVH.