1991 Fiscal Year Final Research Report Summary
Myocardial beta-adrenoceptor Function after brain death
Project/Area Number |
02670606
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Research Category |
Grant-in-Aid for General Scientific Research (C)
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Allocation Type | Single-year Grants |
Research Field |
Thoracic surgery
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Research Institution | Osaka University |
Principal Investigator |
TANIGUCHI Kazuhiro Osaka University Medical School, Assistant Professor, 医学部, 助手 (90171842)
|
Co-Investigator(Kenkyū-buntansha) |
KANEKO Mitsunori Osaka University Medical School, Assistant Professor, 医学部, 助手 (70169580)
NAKATA Seizo Osaka University Medical School, Assistant Professor, 医学部, 助手 (50116068)
SHIRAKURA Ryota Osaka University Medical School, Assistant Professor, 医学部, 助教授 (00116047)
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Project Period (FY) |
1990 – 1991
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Keywords | beta-adrenergic Receptor / Brain Death / myocardial Injury / catecholamine |
Research Abstract |
Post-transplant cardiac dysfunction with poor response to catecholamine may partly relate to the exogenous catecholamine used for brain-dead (BD) donor maintenance. In this experimental study using canine BD model of intracranial hypertension, alterations in myocardial beta-adrenergic receptor (BAR) were investigated. To maintain the mean arterial pressure higher than 60 mmhg after BD massive crystalloid fluid infusion (Group I) or 0.4 - 1.3 ug/kg/min of epinephrine (EPI, Group II) were used. After 3 hour (I-3hr, II-3hr) or 6 hour (I-6hr, II-6hr) of DD, blood EPI level and myocardial BAR(^<125>I-iodocyanopindlol binding) were measured. group n EPI level BAR density BAR affinity. (ng/ml) (fmol/mq) (PM) control 4 0.12<plus-minus>0.05 68.9<plus-minus>6.6 17.9<plus-min I-3hr 4 0.09<plus-minus>0.04 64.7<plus-minus>5.8 18.4<plus-min I-6hr 4 N. D. 72.3<plus-minus>6.1 18.1<plus-minus II-3hr 4 4.93<plus-minus>0.67 59.2<plus-minus>5.9 19.0<plus-min II-6hr 4 7.04<plus-minus>0.83* 41.0<plus-minus>5.0# 18.6<plus-min (* : p<0.05 vs II-3h, # : P<0.05 vs others) The result suggests that myocardial BAR density may reduce after use of high dose catecholamine in brain-dead donor and this might be partly responsible for donor heart function in heart transplantation.
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