Level of ischemia and brain functions in the Mongolian gerbil in vivo.
The Mongolian gerbil (Meriones unguiculatus) provides a very useful animal model to study the effects of ischemia on brain functions. In this model it is possible to induce two levels of ischemia in the same animal. Thus, monitoring the brain in vivo in real-time will provide meaningful information regarding the development of ischemic injury as well as the follow-up during the recirculation period. The aims of the study were as follows: (1) To elucidate the mechanism behind the development of ischemic depolarization under unilateral and bilateral carotid artery occlusion. (2) To exclude the possibility that removal of the dura mater will affect the results. (3) To correlate the kinetics of the recovery processes to the level of ischemia. We tested the correlation between energy depletion level (evaluated by intramitochondrial NADH redox state) and the development of ischemic depolarization (ID) and vasospasm (evaluated by extracellular K+, DC potential and 366 nm reflectance changes, respectively) under partial and complete ischemia (induced by unilateral or bilateral carotid artery occlusion) using the multiparametric monitoring system (MPA). In 12 out of 32 gerbils monitored by the MPA, the dura mater remained intact, while in the other 20, it was removed very gently before connecting the MPA to the brain. Two types of responses to unilateral carotid artery occlusion were recorded and the gerbils were divided into groups according to the development of the ID. In a third group of 5 gerbils we tested the effect of 1-5 min of bilateral occlusion on the various parameters monitored.(ABSTRACT TRUNCATED AT 250 WORDS)
Mayevsky
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Department of Life Sciences, Bar Ilan University, Ramat Gan, Israel.
D000818:Animals; D001921:Brain / Q000502:physiology / Q000503:physiopathology*; D002339:Carotid Arteries / Q000502:physiology; D004594:Electrophysiology / Q000295:instrumentation / Q000379:methods; D005849:Gerbillinae / Q000502:physiology*; D002546:Ischemic Attack, Transient / Q000503:physiopathology*; D009243:NAD / Q000378:metabolism; D010084:Oxidation-Reduction; D011188:Potassium / Q000378:metabolism
D009243:NAD; D011188:Potassium