Experimental study of the effects of diazepam on vasospasm in a subarachnoid rat model through pathological and biochemical analysis.

Subarachnoid hemorrhage (SAH), characterized by bleeding in the subarachnoid space, is associated with high morbidity and mortality, primarily due to cerebral vasospasm. Recent studies suggest oxidative stress and inflammation play crucial roles in vasospasm pathogenesis. This study investigates the effects of diazepam, a benzodiazepine with vasodilatory properties, in a rat SAH model. Three groups of female Sprague Dawley rats were analyzed: a control group, an SAH-induced group without treatment, and an SAH-induced group treated with 3 mg/kg of diazepam. Our findings revealed SAH significantly increased Total Oxidant Status (TOS), Oxidative Stress Index (OSI), and inflammatory markers (IL-1β, IL-6, TNF-α) in both tissue and serum samples. Diazepam treatment mitigated these effects, showing reduced TOS, OSI, and cytokine levels compared to the untreated SAH group. Additionally, diazepam helped maintain thiol-disulfide balance, with higher Total Thiol and Native Thiol levels, indicating a protective effect against oxidative damage. Histopathological examination revealed significant vasospasm and inflammatory infiltration in the SAH group, which was partially alleviated in the diazepam-treated group. Diazepam may serve as an adjunct therapy in SAH management by modulating oxidative stress and inflammation, potentially alleviating vasospasm and related ischemic injuries.