| Project/Area Number |
01570503
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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 |
Circulatory organs internal medicine
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| Research Institution | Showa University |
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Principal Investigator |
KATAGIRI Takashi Showa Univ. Dept. of Medicine, Professor, 医学部, 教授 (90102293)
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| Co-Investigator(Kenkyū-buntansha) |
SUWA Yoshinobu Showa Univ. Dept. of Medicine, Assistant, 医学部, 助手
MUKAE Shuuji Showa Univ. Dept. of Medicine, Assistant, 医学部, 助手
YANAGISHITA Toshikuni Showa Univ. Dept. of Medicine, Assistant, 医学部, 助手 (70183671)
長谷川 茂夫 昭和大学, 医学部, 助手 (80211473)
下司 映一 昭和大学, 医学部, 助手 (50192050)
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| Project Period (FY) |
1989 – 1990
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| Project Status |
Completed (Fiscal Year 1990)
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| Budget Amount *help |
¥2,000,000 (Direct Cost: ¥2,000,000)
Fiscal Year 1990: ¥400,000 (Direct Cost: ¥400,000)
Fiscal Year 1989: ¥1,600,000 (Direct Cost: ¥1,600,000)
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| Keywords | acute myocardial ischemia / pump failure / non-ischemic myocardium / sarcoplasmic reticulum / mitochondria / electron microscopy / canine heart / catecholamine / 冠結紮 |
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| Research Abstract |
(Objects) We studied the mechanism of severe pump failure associated with acute myocardial infarction. We gave attention to the alteration of metabolism in non-infarcted myocardium. (Methods) Acute ischemic myocardium was produced by ligation of LCX in canine heart, and hemodynamics, myocardial blooD flow (MBF) and cardiac output (CO) were measured. Dogs were divided into two groups of which lift ventricular systolic pressure (LVSP) decreased less than 70% to prior value at 60 min after LCX ligation (pump failure : D group), and LVSP was kept higher than 70% as non-depressive group (ND group).And the effects of catecholamine (dobutamine : DOA and DOB) and phosphodiesterase inhibitor (AMN) on metabolic impairment in non-infarcted myocardium. DOA, DOB and AMN were dripped intravenously in some of D group for 30 min from 90 min after LCX ligation. Sarcolasmic reticulum (SR) and mitochondria (Mt) were extracted by centrifuge method from non-infarcted (NIZ) and infarcted heart muscle (IZ) a
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t 120 min after LCX ligation in both groups. Each myocardial cells were observed with electron microscopy. (Results) CO and MBF of NIZ were decreased significantly in D group. Ca-ATPase activity in SR from NIZ in D group was markedly reduced without degradation of SR protein and respiratory activity, activities of electron transport enzymes in Mt from NIZ were decreased too, compared with those of NIZ in ND group. For the purpose of improve the disturbed hemodynamics, DOA and DOB were administerd in some of D group. Recovery in respiratory activity and electron transport enzymes activities were found in Mt from NIZ, together with the improvement of hemodynamics, CO and MBF in NIZ. On the other hand in administration of AMN, mitochondrial function was restored without improvement of hemodynamics and MBF. In morphological analysis, Mt from NIZ in D group were slightly swollen and fused, but these changes were mild in DOA. DOB and AMN group. (Conclusion) These results suggest that occurrence of severe pump failure in acute myocardial infarction is due to the size of infarcted area in previous papers, metabolic impairment of SR and Mt in NIZ were demonstrated with reduction in MBF under severe pump failure which leads to malicious cycle in cardiogenic shocked heart. DOA and DOB showed the possibility to break the malicious cycle by improving coronary blood flow and AMN may be work n myocardium directly. Less
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