1990 Fiscal Year Final Research Report Summary
Experimental Studies on the Occurrence of Cardiac Hypertrophy in Ischemic Heart and Its Possible Mechanisms
| Project/Area Number |
63480224
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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 |
Circulatory organs internal medicine
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| Research Institution | Toyama Medical and Pharmaceutical University |
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Principal Investigator |
SASAYAMA Shigetake Toyama Med. & Pharm. Univ. Professor, 医学部, 教授 (70109007)
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| Co-Investigator(Kenkyū-buntansha) |
MIWA Kunihisa Toyama Med. & Pharm. Univ. Assistant, 医学部, 助手 (70166221)
FUJITA Masatoshi Toyama Med. & Pharm. Univ. Hospital Assistant Professor, 附属病院, 講師 (50190046)
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| Project Period (FY) |
1988 – 1990
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| Keywords | Coronary occlusion / Myocardial hypertrophy / Myocardial cell / Ultrasonic dimension gauge / Adrenergic alpha1 receptor / Adrenergic beta receptor / Calcium channel drug binding receptor |
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| Research Abstract |
We evaluated whether repeated brief coronary occlusion induces myocardial hypertrophy in the region subjected to reversible ischemic insult. In 5 conscious dogs, a subendocardial segment length in the area perfused by the left circumflex coronary artery (LCCA) was measured along with left ventricular pressure. After complete recovery from surgery, 167 (mean) 2 min LCCA occlusions were repeated for 22 days. The resting end-diastolic segment length in the LCCA area was increased by 6.6% (p<0.05). On histologic examination, there was a disproportionate increase in myocardial cell size in the LCCA area compared with the area perfused by the left anterior descending coronary artery (LAD) (18.2 mu vs. 15.4 mu, p<0.05). In an additional similarly instrumented 5 dogs, myocardial cell size in the LCCA and LAD areas was comparable (14.2mu vs. 14.0mu, p=NS). We conclude that the repeated brief ischemic episodes induced regional myocardial hypertrophy confined to the ischemic area.
The maximal bind
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ing site density (Bmax) for [^3] prazosin binding was 13.0<plus-minus>6.5 (fmol/mg protein) (mean <plus-minus>SD) in the nonischemic area and 14.6<plus-minus>9.5 (fmol/mg protein) in the ischemic area. The dissociation constant (K_D) was 0.17<plus-minus>0.13 (nM) in the nonischemic area and 0.17<plus-minus>0.17 (nM) in the ischemic area. Both the parameters were not significantly different. The Bmax, 72.2<plus-minus>35.5 (fmol/mg protein) and the K_<D'> 1.00<plus-minus>0.25 (nM) for H dihydroalloprenolol binding, in the nonischemic area were not significantly different from those (Bmax : 76.8<plus-minus>25.8 (fmol/mg protein), K_<D:> 1.43<plus-minus>0.75 (nM) in the ischemic area, respectively. The Bmax, 250<plus-minus>126 (fmol/mg protein) and the K_<D'> 0.24<plus-minus>0.03 (nM) for [^3H] (+) PN200-100 binding in the nonischemic area were also insignificantly different from 175<plus-minus>19 (fmol/mg protein) and 0.03<plus-minus>0.14 (nM) in the ischemic area, respectively. These results suggest that the mechanism contributing to myocardial hypertrophy induced by repeated occlusion appears to involve no quantitative and qualitative changes of adrenergic alpha1 and beta, and also calcium channel drug binding receptors. Less
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