Carbon monoxide: a novel pulmonary artery vasodilator in neonatal llamas of the Andean altiplano
Herrera, Emilio A., Reyes, Roberto V., Giussani, Dino A., Riquelme, Raquel A., Sanhueza, Emilia M., Ebensperger, German, Casnello, Paola, Mendez, Natalia, Ebensperger, Renato, Sepulveda-Kattan, Esteban, Pulgar, Victor M., Cabello, Gertrudis, Blanco, Carlos E., Hanson, Mark A., Parer, Julian T. and Llanos, Anibal J. (2008) Carbon monoxide: a novel pulmonary artery vasodilator in neonatal llamas of the Andean altiplano. Cardiovascular Research, 77, (1), 197-201. (doi:10.1093/cvr/cvm013).
Full text not available from this repository.
Aims: to study the nitric oxide (NO) and carbon monoxide roles in the regulation of the pulmonary circulation in lowland and highland newborn sheep and llamas.
Methods and results: we used neonatal sheep (Ovis aries) and llamas (Lama glama) whose gestation and delivery took place at low (580 m) or high (3600 m) altitude. In vivo, we measured the cardiopulmonary function basally and with a NO synthase (NOS) blockade and calculated the production of carbon monoxide by the lung. In vitro, we determined NOS and soluble guanylate cyclase (sGC) expression, NOS activity, and haemoxygenase (HO) expression in the lung. Pulmonary arterial pressure was elevated at high altitude in sheep but not in llamas. Sheep at high altitude relative to sea level had significantly greater total lung NOS activity and eNOS protein, but reduced sGC and HO expression and carbon monoxide production. In contrast, llamas showed no difference in NO function between altitudes, but a pronounced increase in pulmonary carbon monoxide production and HO expression at high altitude.
Conclusions: in the llama, enhanced pulmonary carbon monoxide, rather than NO, protects against pulmonary hypertension in the newborn period at high altitude. This shift in pulmonary dilator strategy from NO to carbon monoxide has not been previously described, and it may give insight into new treatments for excessive pulmonary vasoconstriction.
|Digital Object Identifier (DOI):||doi:10.1093/cvr/cvm013|
|Keywords:||hypoxia, anoxia, pulmonary circulation, endothelial function, nitric oxide, vasoconstriction, dilation|
|Subjects:||R Medicine > RB Pathology
Q Science > QP Physiology
|Divisions:||University Structure - Pre August 2011 > School of Medicine > Developmental Origins of Health and Disease
|Date Deposited:||19 Apr 2010 13:07|
|Last Modified:||27 Mar 2014 19:06|
|RDF:||RDF+N-Triples, RDF+N3, RDF+XML, Browse.|
Actions (login required)