1991 Fiscal Year Final Research Report Summary
Studies on the mechanism of myocardial reperfusion injury, especially role of interaction of endothelium
| Project/Area Number |
02670604
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Thoracic surgery
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| Research Institution | Mie University |
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Principal Investigator |
KUSAGAWA Minoru Mie University, . Faculty of Medicine, Department of Thorasic Surgery, Professor, 医学部, 教授 (10046336)
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| Co-Investigator(Kenkyū-buntansha) |
MUZUTANI Tetsuo Mie University., Faculty of Medicine, Department of Thoracic Surgery, Assistant, 医学部, 助手 (20115736)
SHIKANO Kazzuhisa Mie University., Faculty of Medicine, Department of Thoracic Surgery, Assistant, 医学部, 助手 (60206068)
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| Project Period (FY) |
1990 – 1991
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| Keywords | reperfusion injury / Injury of endothelium / Superoxide / EDRF / Endothelin^<-1> / ATP in myocyte / stunned myocardium / Ca^<++> influx |
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| Research Abstract |
Purpose of the research is to investigate a mechanism of post-ischemic myocardial reperfusion injury. We hypothesized two mechanisms that one is a deterioration of coronary endotherial cell function and smooth muscle function by ischemia and another one is a change of myocardial ATP and Ca content. In furmer, bradykinin-induced release of endothelium-derived relaxing factor (EDRF) and Endothlin^<-1> secretion was as a marker of endothelial functions in the experiment, endotherial cell from bovine artery in culture were grown on micro carrier beads and perfused to release EDRF. EDRF response was estimated by its ability to relax phenylephrine contracted ring of rat aorta. When cultured endothelial cells were re-oxygenated after exposure to anoxic condition for twenty minute (control group), EDRF releasing function was maintained in normal. The grop added activated neutrophils to endotherial cell during anoxia showed a significant depression of EDRF release but EDRF releasing function re
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covered by addition of SOD to anoxic endothelial cells. Endothelin^<-1> concentration in perfusate showed significant in the activated neutrophil group. It is concluded that activated neutrophils impaired EDRF releasing function of coronary artery endothelium resulting in post-ischemic no reflow phenomenon. Superoxide from neutrophils may contributed to impair microvascular reperfusion.
Myocardial ATP and Ca content in stunned myocardium was investigated by 31P-MRS and atomic obsorption spectro photometer in six hours stranged rat heart. After six hours in preservation, myocardial beta-ATP droped to less than 30% of normal, situation which led to significant increases in intracellular calcium levels and in particular contributions to calcium influx after reperfusion. Also cardiac function after reperfusion depressed influx after reperfusion. Also cardiac function after reperfusion depressed to the level of 50% of normal values. Administration of Ca-autagonist Nicardipine improved the cardiac function to 75% of normal and the valves of myocardial Ca content were singificantly lowered in geoup of hearts with Nicardipine. It is concluded that stunned myocardium may due to calcium influx rather than a low level of myocarial ATP content. Less
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