Aim: Obesity has emerged as a critical risk factor for various cerebrovascular diseases. Studies have demonstrated the detrimental effects of obesity on vascular health, including endothelial dysfunction, inflammation, and oxidative stress, which may exacerbate vascular complications following hemorrhagic stroke. In this study, the effect of obesity on the severity of cerebral vasospasm after subarachnoid hemorrhage was investigated.
Material and methods: In this study, six experimental groups, each consisting of 10 rats, were defined (60 rats in total). Groups 1 and 2 comprised rats with normal body weight, Groups 3 and 4 comprised obese rats, and Groups 5 and 6 comprised rats that returned to normal body weight after being obese. Rats in Groups 2, 4, and 6, represented the study groups, and experimental SAH was induced in them. Groups 1, 3 and 5 were determined as the control group. Basilar artery lumen areas and wall thicknesses were measured and compared in all groups.
Results: The luminal area of the basilar artery was significantly reduced in Groups 2, 4, and 6, then in Groups 1, 3, and 5, respectively. This indicated the development of vasospasm. No significant differences were found in the basilar artery luminal areas and wall thicknesses between Groups 1, 3, and 5. However, there were significant differences between Groups 2, 4, and 6. The basilar artery luminal area was significantly smaller in Group 4 than in Groups 2 and 6. There was no significant difference in basilar artery luminal areas between Groups 2 and 6.
Conclusion: This study, conducted in rats, elucidated that the severity of vasospasm subsequent to subarachnoid hemorrhage escalated in the presence of obesity, and conversely, a return to normal body weight mitigated the severity of cerebral vasospasm. Prospective clinical investigations ought to scrutinize the correlation between obesity and vasospasm, emphasizing the necessity for vigilant monitoring of vasospasm post-SAH in obese patients.