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Insulin administration protects neurologic function in cerebral ischemia in rats.

D RLeMay, LGehua, G BZelenock, L GD'Alecy

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Abstract

Hyperglycemia exacerbates neurologic damage in clinical and experimental central nervous system ischemia. The purpose of our study was to determine if insulin administration before significantly alters neurologic deficit and survival after ischemia using a newly developed rat cerebral ischemia model. One hour before the onset of ischemia, 40 200-300-g Sprague-Dawley rats received intraperitoneal injections of either 1 ml normal saline or 0.4, 0.5, or 0.6 units regular insulin in 1 ml normal saline. Rats were then intubated and ventilated with 1-1.5% halothane. The aortic arch was exposed, and snares were placed on the innominate, left carotid, and left subclavian arteries. A 20-minute occlusion was begun, and anesthesia was discontinued. Baseline plasma glucose concentration was similar (p = 0.48, Student's t test) in both groups, but it subsequently was significantly lower in the 0.4 unit insulin-treated group up to 4 hours after occlusion (p less than or equal to 0.0035, Student's t test). Neurologic de...

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Hyperglycemia exacerbates neurologic damage in clinical and experimental central nervous system ischemia. The purpose of our study was to determine if insulin administration before significantly alters neurologic deficit and survival after ischemia using a newly developed rat cerebral ischemia model. One hour before the onset of ischemia, 40 200-300-g Sprague-Dawley rats received intraperitoneal injections of either 1 ml normal saline or 0.4, 0.5, or 0.6 units regular insulin in 1 ml normal saline. Rats were then intubated and ventilated with 1-1.5% halothane. The aortic arch was exposed, and snares were placed on the innominate, left carotid, and left subclavian arteries. A 20-minute occlusion was begun, and anesthesia was discontinued. Baseline plasma glucose concentration was similar (p = 0.48, Student's t test) in both groups, but it subsequently was significantly lower in the 0.4 unit insulin-treated group up to 4 hours after occlusion (p less than or equal to 0.0035, Student's t test). Neurologic de...

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Available abstract

Hyperglycemia exacerbates neurologic damage in clinical and experimental central nervous system ischemia. The purpose of our study was to determine if insulin administration before significantly alters neurologic deficit and survival after ischemia using a newly developed rat cerebral ischemia model. One hour before the onset of ischemia, 40 200-300-g Sprague-Dawley rats received intraperitoneal injections of either 1 ml normal saline or 0.4, 0.5, or 0.6 units regular insulin in 1 ml normal saline. Rats were then intubated and ventilated with 1-1.5% halothane. The aortic arch was exposed, and snares were placed on the innominate, left carotid, and left subclavian arteries. A 20-minute occlusion was begun, and anesthesia was discontinued. Baseline plasma glucose concentration was similar (p = 0.48, Student's t test) in both groups, but it subsequently was significantly lower in the 0.4 unit insulin-treated group up to 4 hours after occlusion (p less than or equal to 0.0035, Student's t test). Neurologic de...

Key concepts: Medicine, Ischemia, Saline, Occlusion, Anesthesia, Insulin, Carotid arteries, Common carotid artery

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Insulin administration protects neurologic function in cerebral ischemia in rats. — Research Paper | ScholarLens