Histopathologic, biochemical and morphometric effects of melatonin on vasospasm in experimental subarachnoid hemorrhage

It has been previously demonstrated that activation of lipid peroxidation and increase in arachidonic acid metabolites which occur following a subarachnoid hemorrhage are indicators of neuronal injury that take place during late term vasospasm. The purpose of this experimental study is to investigate the histopathologic, biochemical and morphometric effects of melatonin on tonus of basillary artery and oxidative balances during subacute vasospasm following a subarachnoidal hemorrhage24 male wistar rats weighing between 300-350g were used in the study. Rats were divided randomly in to 4 groups. Rats in group I, II and III (except group IV) were operated under general anesthesia with sterile technique. A burr hole was made on the interparietal-occipital suture line and cysterna magna was exposed. 0,3ml of cerebrospinal fluid was drained and 0.2ml of otogenous blood obtained from tail artery was injected slowly into cysterna magna. Having sutured the surgical wound in group I (n=6, 10mg) and III (n=6, 5mg), the first dose of the melatonin was administrated intraperitoneally and then 2nd dose was administreted intraperitoneally at 24th hour after surgery. Rats in group II (n=6) and group IV (n=6) did not receive any treatment. Rats in group II (n=6) and group IV (n=6) did not receive any treatmentMorphometric evaluation of basillary artery was conducted and results were compared between groups using Kruskall-Wallis variance analysis. In group I which received 5mg melatonin and in group III which received 10mg melatonin, total area of basillary artery and area of vessel wall were found to be increased suggesting vasodilation (p<0.05). No significant changes were observed in levels of TAS, TOS and OSI in comparasion to control and subarachnoid hemorrhage groups (p>0.05In our study, regular therapeutic doses of melatonin were administered but the drug head no significant effect on total levels of antioxidants. As a result, melatonin causes a morphometric vasodilation on vasospasm of basillary artery after subarachnoid hemorrhage. It does not have a significant effect on the oxidative balance of brain tissue. This could have been caused by insufficient data on density and distribution of melatonin receptors in the paranchyma and vascular bed.Key words: Cerebral vasospasm, Subarachnoid hemorrhage, Oxidative metabolism, Morphometry, Histopathology