Microvascular endothelial function and leukocyte adhesion mechanisms during inhalational anesthesia
| Project/Area Number |
07671686
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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 |
Anesthesiology/Resuscitation studies
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| Research Institution | Keio University |
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Principal Investigator |
MORISAKI Hiroshi Keio University, School of Medicine, Assistant Professor, 医学部, 専任講師 (60182226)
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| Co-Investigator(Kenkyū-buntansha) |
SUEMATSU Makoto Keio University, School of Medicine, Associate Professor, 医学部, 助教授 (00206385)
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| Project Period (FY) |
1995 – 1996
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| Project Status |
Completed (Fiscal Year 1996)
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| Budget Amount *help |
¥2,400,000 (Direct Cost: ¥2,400,000)
Fiscal Year 1996: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 1995: ¥1,500,000 (Direct Cost: ¥1,500,000)
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| Keywords | adhesion molecule / endothelium / sevoflurane / halothane / leukocyte / microcirculation / 吸入麻酔 / 好中球 |
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| Research Abstract |
While altering circulatory hemodynamics has been considered a major consequence of inhalational anesthesia, its primary events at a microvascular level remain to be clarified. The present study tested whether halothane or sevoflurane anesthesia evoked leukocyte adhesion through endothelial cell-dependent mechanisms. Rats were anesthetized with halothane or sevoflurane in 100% O_2 and lungs were mechanically ventilated. Leukocyte behavior in mesenteric venules was recorded through intravital video microscopy under monitoring microvascular hemodynamics. To examine the mechanisms for leukocyte rolling and adhesion, these studies were repeated after pretreatment with a monoclonal antibody against P-selectin (MAb PB1.3) or against intracellular adhesion molecule-1 (ICAM-1 ; MAb 1A29). Under baseline anesthetic conditions (1 minimum alveolar concentration ; MAC), venular wall shear rates in the sevoflurane-treated rats were about 2-fold higher than those with halothane. At 2MAC,halothane cau
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sed a marked arteriolar construction and decreasing shear rates concurrent with an elevation of venular leukocyte density. Sevoflurane induced leukocyte rolling and adhesion, which were attenuated by PB1.3 as well as 1A29, without alterations in the wall shear rates. On the other hand, halothane-induced leukocyte adhesion was not prevented by PB1.3 but by 1A29. In conclusion, halothane or sevoflurane anesthesia induces venular leukocyte rolling and adhesion, which may increase the risk of leukocyte-dependent tissue injury. In addition, P-selectin upregulation in venular endothelium plays a crucial role in the leukocyte adhesoion during sevoflurane anesthesia, shear-dependent adhesion mechanisms involving ICAM-1 is likely to be ascribable to the halothane-induced adhesion. The observation demonstrating the inhibitory effect of sodium nitroprusside on the anesthesia-induced adhesion suggests that supplement of exogenous NO serves as a therapeutic strategy to reduce a risk of leukocyte-dependent tissue injury. Compared with previous studies regarding immune system and anesthesia, our study is characterized by in vivo analysis of leukocyte dynamics. Less
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Report
(3 results)
Research Products
(5 results)
