1992 Fiscal Year Final Research Report Summary
PREVENTION OF ISCHEMIA-REPERFUSION INJURY AND ESTABLISHMENT OF THE METHODS FOR CARDIAC PRESERVATION AND REPERFUSION
| Project/Area Number |
03454334
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Thoracic surgery
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| Research Institution | KYUSHU UNIVERSITY |
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Principal Investigator |
KOHNO Hiroyuki KYUSHU UNIV., MEDICINE,ASSISTANT PROF., 医学部, 助手 (80178227)
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| Co-Investigator(Kenkyū-buntansha) |
MASUDA Munetaka KYUSHU UNIV., MEDICINE, ASSISTANT PROF., 医学部, 助手 (10190365)
TOMINAGA Ryuji KYUSHU UNIV., MEDICINE, LECTURER, 医学部, 講師 (70136464)
KAWACHI Yoshito KYUSHU UNIV., MEDICINE, LECTURER, 医学部, 講師 (80117093)
YASUI Hisataka KYUSHU UNIV., MEDICINE, ASSOCIATE PROF., 医学部, 助教授 (20089923)
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| Project Period (FY) |
1991 – 1992
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| Keywords | MYOCADIAL PROTECTION / CARDIOPLEGIA / ISCHEMIA / REPERFUSION INJURY / ACE INHIBITOR / CAPTOPRIL / ISOLATED CARDIAC MYOCYTE / INTRACELLULAR CALCIUM CONCENTRATION |
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| Research Abstract |
1. To prevent intracellular calcium overload, we investigated the hyperpolarizing cardioplegia which we had made in 1991. The hyperpolirizing cardioplegia consists of low potassium and contains adenosine and pinacidil (potassium channel opener). As it keeps cell membrane hyperpolirizing, we assume that L-type calcium channels on cardiac myocyte is kept close and that intracellular calcium overload was prevented. We compared the protective effect of the hyperpolarizing cardioplegia with that of ordinary high potassium cardioplegia in isolated rat heart model. The protective effect of hyperpolarizing cardioplegia was similar to that of the high potassium cardioplegia.
2. We investigated the effects of cardioplegia containing angiotensin converting enzyme (ACE) inhibitor on ischemia/reperfusion in rat hearts. The cardioplegia contaning 2.5mmole/L captopril showed good myocardial protection during reperfusion but not during ischemia. Another ACE inhibitor, Enalapril and Lisinopril showed no effect during neither ischemia nor reperfusion. Because only captopril has a sulfhydryl, we considered myocardial protective effect of captopril might be due to free radical scavenging rather than ACE inhibition.
3. We planed to measure intracellular calcium concentration and intracellular pH during ischemia and reperfusion in isolated cardiac myocytes. We succeeded to get enough myocytes from ventricular muscle of rat for experiments to measure both intracellular calcium concentration and pH by loading of Fura-2 and BCECF. Because we have not yet succeeded to keep isolated myocyte in ischemia, we cannot report fully about this experiment.
4. Now, we are making a new experimental model in which we measure intracellular calcium concentration and pH in isolated rat of rabbit heart at global ischemia. When we establish this model, it might be one of the best model to examine calcium homeostasis during ischemia and reperfusion.
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