Abstract:

Aims: We aimed to investigate the role of neuron damage in experimental animals following vasospasm, by increasing perfusion of neuronal tissue through vasodilation using the venom of PcTx1, and to determine its effectiveness in reducing neuron damage after vasospasm. Methods: Thirty adult male Wistar albino rats weighing between 300 and 400 grams were used and divided into three groups: the Sham group (Group 1, n=10), to which no application was made; the SAH (control) group (Group 2, n=10), in which a double SAH model was created and 1 cc of saline was administered intraperitoneally; and the SAH+PcTx1 group (Group 3, n=10), in which a double SAH model was created and 1 cc/kg of PcTx1 venom was administered intraperitoneally daily. Basilar artery diameter and immunochemical measurements were performed histopathologically, and neurohistopathological findings were scored semiquantitatively in terms of vascular changes, neuron degeneration, gliosis, and bleeding criteria using a scale of 0 (none), 1 (mild), 2 (moderate), or 3 (severe). eNOS immunopositivity was also evaluated. The detection of apoptosis in the brain was performed by evaluating the effector enzyme caspase-3 immunoreactivity of the exogenous apoptosis pathway. Results: The most severe vascular spasm and degeneration-necrosis of brain tissue gray matter neurons were seen in Group 2, whereas the vascular narrowing was less severe in Group 3. Brain parenchyma and neuron and neuroglial reactions were milder in Group 3. eNOS expression was detected at a higher level in Group 1, Group 2, and Group 3, respectively. For apoptosis and caspase-3 immunoreactivity of the exogenous apoptosis pathway, no immunopositive reactions were observed in Group 1. Conclusion: For the occurrence and formation mechanisms of vasospasm after subarachnoid hemorrhage, this pathological condition is thought to result from multifactorial and various biochemical reactions. In our study, it was found that psalmotoxin effectively prevented vasospasm and significantly reduced tissue damage after vasospasm.

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