Upregulation of vasoconstrictor receptors in cerebral arteries, including endothelin B (ETB) and 5-hydroxytryptamine 1B (5-HT(1B)) receptors, has been suggested to contribute to delayed cerebral ischemia, a feared complication after subarachnoid hemorrhage (SAH). This receptor upregulation has been shown to be mediated by intracellular signalling via the mitogen activated protein kinase kinase (MEK1/2)--extracellular regulated kinase 1/2 (ERK1/2) pathway. However, it is not known what event(s) that trigger MEK-ERK1/2 activation and vasoconstrictor receptor upregulation after SAH.We hypothesise that the drop in cerebral blood flow (CBF) and wall tension experienced by cerebral arteries in acute SAH is a key triggering event. We here investigate the importance of the duration of this acute CBF drop in a rat SAH model in which a fixed amount of blood is injected into the prechiasmatic cistern either at a high rate resulting in a short acute CBF drop or at a slower rate resulting in a prolonged acute CBF drop.
B M C Neuroscience, 2013, Vol 14
Journal Article; Research Support, Non-U.S. Gov't; Analysis of Variance; Animals; Antipyrine; Area Under Curve; Blood Pressure; Brain Ischemia; Butadienes; Carbon Isotopes; Cerebral Arteries; Cerebrovascular Circulation; Disease Models, Animal; Enzyme Inhibitors; Laser-Doppler Flowmetry; MAP Kinase Signaling System; Male; Motor Activity; Nervous System Diseases; Nitriles; Rats; Rats, Sprague-Dawley; Receptor, Endothelin B; Receptor, Serotonin, 5-HT1B; Signal Transduction; Subarachnoid Hemorrhage; Up-Regulation