Examination of the reactivity exhibited by the basilar artery of the brain in KrushinskyMolodkina rats before and after an induced epileptiform seizure accompanied by subarachnoid hemorrhages showed increased contractility of this artery in response to endothelin-1 and its reduced sensitivity to ATP 24 h after the seizure. Such changes in the reactivity of brain vessels may contribute to the development of vasospasm and secondary ischemia of the brain after an epileptic seizure.Key Words: epilepsy; subarachnoid hemorrhage; brain vessels; reactivity; endothelin During an epileptic seizure, especially if it is accompanied by generalized convulsions, the blood-brain barrier becomes more permeable and intracranial hemorrhages frequently occur. The resulting hematoma releases vasoactive factors that compromise brain hemodynamics and potentiate the vasospasm [6]. In addition, the reactivity of smooth-muscle cells in brain arteries is altered as a result of damage to neurons and changes in capillary filtration and in the composition of the cerebrospinal fluid. Since the nature of these changes has not been fully elucidated, we undertook the present study to evaluate the contraction and dilation of the basilar artery in response to vasoactive substances in rats that had sustained acute disturbances of cerebral circulation.
MATERIALS AND METHODSWistar rats and rats of the Krushinsky-Molodkina (KM) strain genetically predisposed to respond to strong acoustic stimulation by generalized convulsions [1,2] were used. Alternate exposure of KM rats, at 15-min intervals, to strong and weak acoustic stimuli according to a specially devised scheme resulted not only in convulsive seizures but also in subarachnoid hemorrhage (SAH) [1,2]. All tests in this study were performed with isolated basilar arteries from Wistar rats (group 1), intact KM rats (group 2), and KM rats that had developed, 24 h before the tests, an epileptiform seizure and an acute impairment of blood-brain barrier permeability accompanied by SAH (group 3).The rats of all three groups were killed under ether anesthesia 24 h after the audiogenic stress produced in group 3, and a basilar artery segment about 4 mm in length was dissected out above the junction of the vertebral arteries. The proximal end of the isolated segment was connected to a polyethylene cannula and then immediately placed in a thermostated flow-through (3 ml/min) chamber, where it was perfused at a constant rate of 1 ml/min by means of a Rabbit peristaltic pump. Both the perfusate and the solution fed to the chamber had the following composition (mM):