The effects of peripheral leukocytes on the hippocampal neuronal changes in transient global ischemia and unilateral cerebral hemispheric infarction.
10.3346/jkms.1999.14.3.304
- Author:
Hyang Won LEE
1
;
Heasoo KOO
;
Kyung Gyu CHOI
;
Kee Duk PARK
;
Byung Chul LEE
Author Information
1. Department of Neurology, Ewha Womans University College of Medicine, Seoul, Korea. ihwoon@medikorea.net
- Publication Type:Original Article ; Research Support, Non-U.S. Gov't
- Keywords:
Leukocytes;
Delayed neuronal damage;
Hippocampus;
Ischemia;
Infarction
- MeSH:
Animal;
Cerebral Infarction/pathology*;
Female;
Gerbillinae;
Hippocampus/pathology*;
Leukocyte Count;
Leukocytes/physiology*;
Male;
Neurons/pathology*;
Reperfusion Injury
- From:Journal of Korean Medical Science
1999;14(3):304-314
- CountryRepublic of Korea
- Language:English
-
Abstract:
The participation of activated leukocytes and subsequent production of chemical mediators has been well accepted in the pathophysiology of hypoxic-ischemic injury. This study was performed to see the effects of leukocytes on hippocampal neuronal damage in transient global ischemia induced by 10-min occlusion of bilateral common carotid arteries (CCAs) with reperfusion for various times, and in complete unilateral ischemia induced by 24-hr ligation of left CCA. Leukopenia was induced by intraperitoneal injection of cyclophosphamide for 4 days. The results showed that hippocampal neuronal damages were worse at 6-hr reperfusion in leukopenic experimental group than in the control group. In comparison, 24-hr and 3-day reperfusion leukopenic groups showed less numbers of damaged neurons and milder changes. The 5-day reperfusion group showed inconsistent changes. Unilateral CCA occlusion showed extensive infarction in 83.3% of gerbils in the control group, compared to 25% of gerbils in the experimental group (p<0.05). These results strongly suggest that the number of peripheral leukocytes were closely related to the development of delayed neuronal damage of hippocampus in transient global ischemia and the incidence of infarction induced by 24-hr unilateral CCA ligation.
