EFFECT OF REMACEMIDE HYDROCHLORIDE ON SUBARACHNOID HEMORRHAGE-INDUCEDVASOSPASM IN RABBITS

The purpose of this study was to assess the role of an excitatory amin o acid (EAA) receptor antagonist (remacemide hydrochloride) in a rabbi t model of subarachnoid hemorrhage (SAH)-induced cerebral vasospasm, C erebral angiograms were performed on 22 rabbits pre-SAH and 72 h post- SAH: 6 rabbits received an injection of mock cerebrospinal fluid (1 ml /kg) into the cisterna magna (group I, the control group); 6 rabbits w ere subjected to SAH but received no treatment (group II); autologous blood (1 ml/kg) from the central ear artery was injected into the cist erna magna of these rabbits; 6 rabbits were subjected to SAH (1 ml/kg) and treated with intraperitoneal (IF) bolus injections of remacemide hydrochloride (15 mg/kg) every 12 h beginning 30 minutes after SAH (gr oup III); and 4 rabbits were not subjected to SAH but received IP bolu s injections of remacemide hydrochloride every 12 h (group IV), Digita l subtraction angiography was used to measure the diameter of the basi lar artery, At 72 h post-SAH, vasospasm was evident in all untreated r abbits, The diameter of the basilar artery was reduced significantly b elow pre-SAH levels by 35.3 +/- 5.8% (mean +/- standard error of the m ean), Treatment with remacemide hydrochloride significantly ameliorate d vasospasm (27.3 +/- 5.4%, p < 0.001), These findings suggest that in this model EAAs may cooperate in the genesis of SAH-induced cerebral vasospasm and that NMDA receptor antagonism with remacemide hydrochlor ide can partially prevent the SAH-induced vasospasm of a large cerebra l artery.