|
|
|
Journal of Korean Neurosurgical Society 1997;26(3): 335-346. |
| The Effect of Nimodipine and 21-aminosteroid(U74389G) on Cerebral Infarction and Cerebral Blood Flow during the Continuous and Repeated Interruptions of the Focal Cerebral Blood Flow in Cats. |
| Hyeon Seon Park, Jin Yang Joo, Sun Ho Kim, Kyu Chang Lee |
| Department of Neurosurgery, College of Medicine, Yonsei University, Seoul, Korea. |
|
|
|
|
|
| ABSTRACT |
|
Temporary interruption of cerebral blood flow is an effective maneuver to prevent and/or to control excessive bleeding during cerebrovascular procedures. Despite the benefits of temporary arterial occlusion, there is still a risk of ischemic neuronal damage associated with this procedure. It remains controversial whether it is safer to use brief periods of interrupted temporary occlusion separated by reperfusion periods or single continuous temporary occlusion. Two injury mechanisms, disturbed calcium homeostasis and lipid peroxidation, participate in the neuronal damage caused by temporary occlusion but their contributions to the two different types of temporary occlusion are presumed to be different in some degrees. The authors investigated the effect of nimodipine(calcium channel blocker) and U74389G(21-aminosteroid, lipid peroxidation inhibitor) on the focal cerebral blood flow and the size of cerebral infarction in two different types of temporary occlusion(a single, one hour continuous occlusion or three 20-minute repeated occlusions during a 40-minute interval) using the cat focal ischemic model. Results are as follows: 1) Intermittent, repeated occlusion caused lesser cerebral infarction than single continuous occlusion. 2) Postischemic hypoperfusion was more severe in intermittent repeated occlusion group but it was not statistically significant. 3) Nimodipine and U74389G reduced the size of cerebral infarction caused by two types of temporary occlusions significantly but there was no difference between two treatments. 4) U74389G ameliorated the postischemic hypoperfusion caused by both types of temporary occlusion but nimodipine did not. 5) Nimodipine protected caudato-putamen from the ischemic injury more effectively than U74389G. On the basis of the above findings, both types of injury mechanism(disturbed calcium homeostasis and lipid peroxidation) seemed to contribute to the two types of temporary occlusion(single continuous and intermittent repeated), in the similar extent. It is presumed that nimodipine has a preventive effect during the ischemic period and U74389G has a protective effect during reperfusion period. |
| Key Words:
Continuous and internittent occlusion; Focal cerebral blood flow; Postischemic hypoperfusion; Nimodipine; U74389G |
|
|
|
Full text via DOI 
Download Citation 
