Pathophysiology of Brain Injury after Subarachnoid Haemorrhage and its Management Options

Aneurismal subarachnoid hemorrhage (SAK) is a cerebrovascular accident with high mortality. It carries both short and long term consequences. Mechanisms of neurologic damage after SAK include intracranial hypertension, early and delayed brain vasoconstriction, as well as inflammatory response are involved. Vasoconstriction is a crucial phenomenon in both early and delayed phases and nitric oxide (NO) plays the key role. Aim of the study was to test following hypotheses in animal model: 1. Subarachnoid hemorrhage causes decrease of brain perfusion by mechanism of intracranial hypertension and early vasoconstriction, 2. Both administration of vasodilator - NO donor, and elimination of intracranial hypertension can reverse the early hypoperfusion, 3. SAH leads to generation of free radicals, 4. Administration of antioxidant (melatonin) can attenuate the free radical damage. Methods: Adult male Wistar rats were used for the experiments. SAH was induced by injection of arterial blood into prechiasmatic cistern. Perfusion of brain cortex was measured by Laser Speckle Contrast Analysis (LASCA). In the first experiment, SAH was induced and sodium nitroprusside (SNP, 10 µg / 5 µl) was administered into the lateral ventricle in 2 phases according to the dynamics of perfusion changes: (1) all animals received..