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pubmed-article:10642383pubmed:abstractTextWe tested the hypothesis that regulation of the pulmonary circulation by endogenous endothelin (ET) during normoxia and hypoxia was altered in conscious dogs 1 mo after left lung autotransplantation (LLA). Sham-operated control and post-LLA dogs were chronically instrumented to measure the left pulmonary vascular pressure-flow (LP-Q) relationship. LP-Q plots were generated on separate days during normoxia and hypoxia (arterial PO(2) approximately 50 Torr) in the intact condition, after selective ET(A)-receptor inhibition (BQ-485), and after combined ET(A+B)-receptor inhibition (bosentan). Although LLA resulted in a chronic increase in pulmonary vascular resistance, the ET-receptor antagonists had no effect on the LP-Q relationship during normoxia in either group. The magnitude of hypoxic pulmonary vasoconstriction (HPV) was flow dependent in both groups, and the HPV response was potentiated post-LLA compared with control. ET(A)-receptor inhibition attenuated the HPV response to the same extent in both groups. ET(A+B)-receptor inhibition attenuated the HPV response to a greater extent than did ET(A)-receptor inhibition alone, and this effect was greater post-LLA compared with control. Plasma ET-1 concentration only increased during hypoxia in the LLA group. These results indicate that ET does not regulate the baseline LP-Q relationship in either group. Both ET(A)- and ET(B)-receptor activation mediate a component of HPV in conscious dogs, and the vasoconstrictor influence of ET(B)-receptor activation is enhanced post-LLA.lld:pubmed
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pubmed-article:10642383pubmed:dateRevised2007-11-14lld:pubmed
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pubmed-article:10642383pubmed:articleTitlePulmonary vasoregulation by endothelin in conscious dogs after left lung transplantation.lld:pubmed
pubmed-article:10642383pubmed:affiliationCenter for Anesthesiology Research, The Cleveland Clinic Foundation, Cleveland, Ohio 44195, USA.lld:pubmed
pubmed-article:10642383pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:10642383pubmed:publicationTypeResearch Support, U.S. Gov't, P.H.S.lld:pubmed
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