Aim:The role of endothelin-1 (ET-1) secreted by vascular endothelial cells, which is an effective vasoconstrictor agent, in neurological damage due to severe head trauma is being investigated. It is thought that it will increase cerebral ischemia and hypoxia, especially due to its effects on blood vessels, and thus may increase secondary damage in traumatic CNS injuries by changing cerebral energy metabolism.Herein, we examined the role of ET-1, and how ET-1 was affected by blood sugar changes after severe head trauma.Material and Methods:Traumatic diffuse brain injury-induced rats were followed for 7 days. Blood glucose, blood gas, and haematocrit levels were examined in blood samples taken before the trauma, and at 2nd, 6th, 12th, 24th, 48th hours, and 7 days after the trauma.The mortality rate was approximately 42% and the fracture rate was 14%.Animals that died and had skull fractures were excluded from the study.Results:In the first group, post-traumatic plasma ET-1 levels of rats with head trauma (n=36) were significantly higher than baseline values (p<0.05). In rats in the second group (n=36), ET-1 levels measured in the 7-day follow-up after trauma were significantly higher when compared to baseline values (p<0.05). However, when ET-1 values in the first group were compared, the increase in ET-1 in the 2nd group was statistically significantly lower than in the 1st group (p<0.05).Conclusion:Keeping blood glycose levels within normal limits with insulin after severe head trauma significantly prevented the increase in ET-1. Thus, it can be said that secondary injury to cerebral blood flow can be prevented by reducing the occurrence of vasospasm that starts in the early post-traumatic period or by stimulating the release of nitric oxide. We believe that further studies on the role of ET-1 and insulin in the formation of secondary injuries after severe head trauma would be beneficial.