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SEARCH FOR potentiator of ingaled nitric oxide for experimental pulmonary hypertension

Research Project

Project/Area Number 08670915
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field Pediatrics
Research InstitutionTokyo 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)
Keywordspulmonary 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.

Report

(3 results)
  • 1997 Annual Research Report   Final Research Report Summary
  • 1996 Annual Research Report

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Published: 1996-04-01   Modified: 2016-04-21  

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