Dynamics of Oxidative Stress Indices and Endogenous Factors of Vascular Regulation in Patients with Non-Traumatic Subarachnoid Hemorrhage Due to Rupture of Cerebral Aneurysms

INTRODUCTION The main reasons for the unsatisfactory outcome of surgical treatment of patients with non-traumatic subarachnoid hemorrhage (SAH) due to ruptured cerebral aneurysms are vascular spasm (VS) and delayed cerebral ischemia. Lysis of blood clots in the subarachnoid space leads to the release of a large number of various vasoactive factors that stimulate cytotoxic, inflammatory reactions and oxidative stress, which may be one of the reasons for the development of VS and secondary ischemic brain damage. THE AIM OF THE STUDY Study of the dynamics of oxidative stress indicators and factors of endogenous vascular regulation in patients with non-traumatic SAH due to ruptured cerebral aneurysms. MATERIAL AND METHODS A total of 80 patients in the acute period of SAH due to ruptured cerebral aneurysms were treated and examined. The average age of the patients was 51.7 years. The control group (norm) included 25 practically healthy people, whose average age was 32.7±8.6 years. The study used the blood serum and cerebrospinal fluid of the patients. The study points were 0, 1, 3, and 7 days after the patient’s admission to the hospital. The severity of oxidative stress was assessed by the level of malonic dialdehyde (MDA) and total antioxidant activity of blood serum (TAA); vasotonic function of vascular endothelium by the content of stable metabolites of nitric oxide (NOx) and the concentration of angiotensin-converting enzyme (ACE). Biochemical studies were carried out on the biochemical analyzer “Olympus AU 2700” (Beckman Coulter, USA). RESULTS It was revealed that patients with SAH already had pronounced oxidative stress upon admission to the hospital (increased MDA level, decreased TAA level), which led to an imbalance in the endogenous regulation of vascular tone (decreased NOx level, increased ACE concentration) and increased by the 7th day after admission to the hospital. High lactate dehydrogenase (LDH) activity was observed, the peak of which was on the 7th day of observation. Determination of LDH activity may be promising as a biomarker of ischemic brain injury and a prognostic indicator of the development of an unfavorable outcome. CONCLUSIONS The obtained data indicate the need for a comprehensive approach to the treatment of patients with subarachnoid hemorrhage. The most relevant therapeutic goal is the removal of blood from the subarachnoid space of the brain to prevent increased oxidative stress and angiospasm.