1998 Fiscal Year Final Research Report Summary
Investigation of pathogenesis in retinal circulatory disturbances with the analysis of lenkocyte clynamics.
| Project/Area Number |
09671792
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Ophthalmology
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| Research Institution | KYOTO UNIVERSITY |
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Principal Investigator |
KIRYU Junichi Kyoto university , Graduate school of medicine, assistant proffessor, 医学研究科, 助手 (80281096)
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| Co-Investigator(Kenkyū-buntansha) |
HONDA Yoshihito Kyoto university , Graduate school of medicine, proffessor, 医学研究科, 教授 (90026930)
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| Project Period (FY) |
1997 – 1998
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| Keywords | lenkocytes / retina / endothelium / adhesion molecules |
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| Research Abstract |
After retinal ischemia reperfusion, leukocytes began to roll along the venous walls 4 hours after reperfusion. The flux of rolling leukocytes substantially increased and reached a peak (10240 cells/mm) 12 hours after reperfusion. The flux decreased notably to approximately one six the maximum level 48 hours after reperfusion. Few rolling leukocytes could be observed 96 hours after reperfusion. The difference in kind and density of adhesion molecules involved during ischemia reperfusion injury at each time point may account for this finding. The velocity of rolling leukocytes 12 hours after reperfusion was significantly lower than that recorded before or after then. The reduction could be due to the difference in kind and density of adhesion molecules at each time point, not to reduction of velocity of blood flow. Vasoconstriction occurred immediately after reperfusion and peaked 4 hours after reperfusion (66.8% in arteries, 90.1% in veins) Afterward, significant vasodilation occurred i
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n arteries and veins. In arteries, vasodilation peaked 1 2 to 24 hours after reperfusion (1 23-1 29%) and subsided 96 hours after reperfusion. Venous vasodilation peaked 24 hours after reperfusion and subsided 48 hours. The number of accumulated leukocytes began to increase 4 hours after reperfusion. The number increased with time and peaked at 931*187 cells/mm 24 hours after reperfusion. It is shown that mRNA expression of ICAM-l is upregulated after transient cerebral ischemia and peaks 12 hours after reperfusion. Our results in the retina are consistent with this observation.
In diabetic rats, the velocity of leukocytes in the retinal microcirculation was 1.38*0.31 mm/sec, and 1.27*0.20 mm/se in control rats. There was no significant difference between these two groups and no plugging or rolling leukocytes were observed. In contrast, the number of leukocytes entrapped in the retinal microcirculation was significantly higher in diabetic rats than in control rats. Thus, leukocytes of the diabetic rats were suggested to have increased adhesiveness and reduced deformability. It is possible that the velocity of leukocytes in retinal microcirculation is preserved in diabetic rats in spite of these changes of leukocyte properties, because leukocytes may circulate avoiding the injured pathway. Less
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