4.2 Article

Characteristics of the in vitro hypoxic pulmonary vasoconstrictor response in isolated equine and bovine pulmonary arterial rings

Journal

VETERINARY ANAESTHESIA AND ANALGESIA
Volume 31, Issue 4, Pages 239-249

Publisher

BLACKWELL PUBLISHING LTD
DOI: 10.1111/j.1467-2995.2004.00176.x

Keywords

equine; hypoxic pulmonary vasoconstriction; pulmonary artery

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Objective Hypoxaemia accompanies dorsal recumbency in the horse and frequently complicates general anaesthesia. The physiology associated with this phenomenon is poorly understood. One possible cause of poor tolerance to dorsal recumbency is an absent or reduced response to hypoxic pulmonary vasoconstriction (HPV). This study compared the HPV response in isolated pulmonary artery vessels from equivalent regions of equine and bovine lung. Animals Equine and bovine, in vitro study. Materials and methods Equine and bovine pulmonary arteries were removed from the lungs of euthanased horses and cattle. Measurements of isometric tension were made on isolated rings of pulmonary vessels at 3 7 degreesC in a Krebs' saline solution. Hypoxia was induced by bubbling with a nominally 0% O-2 gas mixture. Results A significant HPV response was observed above a baseline tension induced by phenylephrine (PE; 0.3 mum) or 5-hydroxytryptamine (5-HT; 0.1 mum). The HPV response in equine pulmonary vessels was approximately 33% less than the response observed in equivalent bovine vessels (equine 196 +/- 20%, versus bovine 290 +/- 32%; p < 0.05). Removal of the enclothelium (by rubbing the luminal surface) significantly reduced but did not abolish the HPV response. Incubation with the nitric oxide (NO) synthase inhibitor N-nitro-L-arginine methyl ester (L-NAME; 100 mum), or COX-1/ COX-2 inhibitor indomethacin (10 mum) markedly attenuated the HPV response in equine vessels. Conclusions These results suggest that a significant HPV response exists in isolated equine pulmonary vessels; a component of this response requires a functional endothelium. Inhibition of cyclooxygenase and NO synthase attenuated the response, suggesting the involvement of a COX product and/ or NO in mediating this effect either directly or indirectly. Alternatively, a non-COX related action of the nonsteroidal anti-inflammatory drug, indomethacin, may be involved.

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