Document Detail


Effects of hypercapnia with and without acidosis on hypoxic pulmonary vasoconstriction.
MedLine Citation:
PMID:  19717554     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Acute respiratory disorders and permissive hypercapnic strategy may lead to alveolar hypoxia and hypercapnic acidosis. However, the effects of hypercapnia with or without acidosis on hypoxic pulmonary vasoconstriction (HPV) and oxygen diffusion capacity of the lung are controversial. We investigated the effects of hypercapnic acidosis and hypercapnia with normal pH (pH corrected with sodium bicarbonate) on HPV, capillary permeability, gas exchange, and ventilation-perfusion matching in the isolated ventilated-perfused rabbit lung. No alteration in vascular tone was noted during normoxic hypercapnia with or without acidosis compared with normoxic normocapnia. Hypercapnia with normal pH resulted in a transient increase in HPV during the course of consecutive ventilation maneuvers, whereas hypercapnic acidosis increased HPV over time. Hypercapnic acidosis decreased exhaled NO during hypoxia more than hypercapnia with normal pH and normocapnia, whereas intravascular NO release was unchanged. However, inhibition of NO synthesis by nitro-L-arginine (L-NNA) resulted in a loss of the increased HPV caused by hypercapnic acidosis but not that caused by hypercapnia with normal pH. Furthermore, capillary permeability increased during hypoxic hypercapnia with normal pH but not hypoxic hypercapnic acidosis. This effect was NO-dependent because it disappeared during L-NNA administration. Ventilation-perfusion matching and arterial PO2 were improved according to the strength of HPV in hypercapnia compared with normocapnia during Tween nebulization-induced lung injury. In conclusion, the increased HPV during hypercapnic acidosis is beneficial to lung gas exchange by improving ventilation-perfusion matching and preserving the capillary barrier function. These effects seem to be linked to NO-mediated pathways.
Authors:
Farzaneh Ketabchi; Bakytbek Egemnazarov; Ralph T Schermuly; Hossein A Ghofrani; Werner Seeger; Friedrich Grimminger; Mostafa Shid-Moosavi; Gholam A Dehghani; Norbert Weissmann; Natascha Sommer
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Publication Detail:
Type:  In Vitro; Journal Article; Research Support, Non-U.S. Gov't     Date:  2009-08-28
Journal Detail:
Title:  American journal of physiology. Lung cellular and molecular physiology     Volume:  297     ISSN:  1522-1504     ISO Abbreviation:  Am. J. Physiol. Lung Cell Mol. Physiol.     Publication Date:  2009 Nov 
Date Detail:
Created Date:  2009-10-27     Completed Date:  2009-11-10     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  100901229     Medline TA:  Am J Physiol Lung Cell Mol Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  L977-83     Citation Subset:  IM    
Affiliation:
School of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran.
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MeSH Terms
Descriptor/Qualifier:
Acidosis, Respiratory / complications*,  physiopathology
Animals
Anoxia / complications*,  physiopathology*
Capillary Permeability / drug effects
Endothelium, Vascular / drug effects,  physiopathology
Hydrogen-Ion Concentration / drug effects
Hypercapnia / complications*,  physiopathology*
Lung / blood supply*,  drug effects,  physiopathology
Male
Metalloporphyrins / pharmacology
Nitric Oxide / metabolism
Nitroarginine / pharmacology
Partial Pressure
Pulmonary Ventilation / drug effects
Rabbits
Vasoconstriction / drug effects,  physiology*
Chemical
Reg. No./Substance:
0/Metalloporphyrins; 0/manganese(III)-tetrakis(4-benzoic acid)porphyrin; 10102-43-9/Nitric Oxide; 2149-70-4/Nitroarginine

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