1989 Fiscal Year Final Research Report Summary
Research for elucidating the mechanism of ischemia-reperfusion injury at cardiopulumonary bypass, and taking countermeasures against it (1990)
| Project/Area Number |
63440052
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| Research Category |
Grant-in-Aid for General Scientific Research (A)
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| Allocation Type | Single-year Grants |
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| Research Field |
Thoracic surgery
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| Research Institution | Keio University |
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Principal Investigator |
INOUE Tadashi Keio University; Surgery; Professor, 医学部外科, 教授 (30050991)
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| Co-Investigator(Kenkyū-buntansha) |
ISEKI Harukazu Keio University; Surgery; Assistant, 医学部外科, 助手 (00212960)
SUZUKI Takaaki Keio University; Surgery; Assistant, 医学部外科, 助手 (10196834)
NAGUMO Masashi Keio University; Surgery; Assistant, 医学部外科, 助手 (70198365)
YOZU Ryohei Keio University; Surgery; Assistant, 医学部外科, 講師 (30129738)
SOMA Yasuhiro Keio University; Surgery; Lecturer, 医学部外科, 講師 (40051437)
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| Project Period (FY) |
1988 – 1989
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| Keywords | Ischemic myocardium / Reperfusion injury / Polymorphonuclear leukocytes / Free radical / Endothelial cell |
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| Research Abstract |
Recently the reperfusion injury, especially by oxygen-derived free radicals, has been noticed in cardiac surgery. But the mechanism has not been clarified. As one of sources of reperfusion injury, we noticed respiratory burst of polymorphonuclear leukocytes (PMNs), which produce a lot of free radicals. At first we looked over the change of chemiluminescence (ChL) activity in PMNs during cardiopulmonary bypass to investigate whether respiratory burst of PMNs would be apt to occur. The activity increased 1.82 times (p<.05) 30 min. after reperfusion. This result pointed out that the respiratory burst of PMNs would be liable to occur after reperfusion, namely it suggested that PMNs would take a part in reperfusion injury. Next we investigated whether leukocyte depletion of reperfuming blood would reduce the degree of reperfusion injury of not under the canine cross circulation method. The group reperfused with leukocyte depleted blood showed better recovery of left ventricle function, less peroxidation products, and less CPK-MB release. Pathologically, electron micrograph showed more extracellular edema, much platblete adhesion on the endothelium, much endothelial cell damage, and more mitochondrial damage in this group. In contrast to this group, in the group reperfused with whole blood less endothelial and mitochondrial damage. Further we tried to examine endothelial and mitochondrial damage in the group in administration of superoxide dismutase, as a free radical scavenger, during heart arrest. This group showed much the same endothelial and mitochondrial damage as the whole blood group. These results suggest that PMNs would take some parts in reperfusion injury, and free radical derived endothelial damage just after reperfusion would occur as the trigger of the foll owing PMNs derived reperfusion injury. After this, the endothelial change after reperfusion will be required on closer investigation.
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