Project/Area Number |
08670915
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Pediatrics
|
Research Institution | Tokyo WOMEN'S MEDICAL COLLEGE |
Principal Investigator |
KONDO Chisato Tokyo WOMEN'S MEDICAL COLLEGE, 医学部, 助手 (90192070)
|
Project Period (FY) |
1996 – 1997
|
Project Status |
Completed (Fiscal Year 1997)
|
Budget Amount *help |
¥2,200,000 (Direct Cost: ¥2,200,000)
Fiscal Year 1997: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 1996: ¥1,200,000 (Direct Cost: ¥1,200,000)
|
Keywords | pulmonary hypertension / nitric oxide / phosphodiesterase inhibitor |
Research Abstract |
This study was undertaken to evaluate the effect of phosphodiesterase inhibitor to potentiate vasodilatiory effect of inhaled nitric oxide on experimental pulmonary hypertension. Pulmonary hypertension of rats was induced by hypoxia (FiO2=0.11-0.18), and intravenous infusion of thromboxane B2 analog (U46619). Twenty ppm of nitric oxide effectively reduced mean pulmonary arterial pressure (mPAP) induced by hypoxia from 25+/-9 mmHg to 20+/-7 mmHg (p<0.01). However, after the addition of Aminphylline (0.4mg/kg/min) to inhaled nitric oxide, mean PAP did not furhter reduce (22+/-6 mmHg). Dipyridamole (0.14mg/kg/min) did not potentiate the effect of nitric oxide on hypoxia induced pulmonary hypertension (21+/-8mmHg with NO,vs.23+/-5mmHg with NO+dipyridamole, NS). Neither aminophylline nor dipyridamole did not potentiate the effct of NO on U46619-induced pulmonary hypertenison. These results suggest that aminophylline as well as dipyridamole are not potentiator of inhlaed nitric oxide to relief experimental pulmonary hypertension indudced by hypoxia or U46619.
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