[Changes in the nitrite level of the blood in patients in the acute period of a subarachnoid hemorrhage of aneurysmatic etiology].

Subarachnoidal hemorrhage leads to impaired endothelium-dependent relaxation by inhibiting the synthesis of major vascular relaxation agent nitric oxide (NO). Nitrite, a closest product of the oxidation of NO, is responsible for the synthesis of the latter. The Griss reaction was used for daily measurement of blood nitrite levels in 32 patients with acute subarachnoidal hemorrhage of aneurysmal etiology. There were upward and downward changes in nitrite levels as compared to the levels of healthy individuals (0.26 +/- 0.06 mu/ml): the levels of nitrite were 1.5-3 times higher than the normal levels in the first 2 days after hemorrhage and its concentration was the minimum (less than 0.16 mu/ml) when there was the greatest likelihood of development of vascular spasm. There was an association of dynamic changes in nitrite levels with the course of the disease. If vascular spasm was absent, the concentration of nitrite returned to the normal range at week 2 of hemorrhage. When there was significant and permanent vascular spasm frequently leading to death, the levels of nitrite was constantly below the normal range.