A Study of Equine Pulmonary Blood Vessel Function In Vitro

This study characterised the responses of isolated equine pulmonary artery vessels to hypoxia and a range of agonists, and compared responses of isolated bovine pulmonary vessels. In vivo studies have demonstrated an inability of the equine pulmonary vascular system to ensure that blood is directed to well-ventilated regions of the lung in lateral or dorsal recumbency. This phenomenon is accentuated when accompanied by general anaesthesia: the resulting hypoxaemia contributes to the morbidity and mortality associated with this procedure. Proper function is further hampered by the lack of a strong hypoxic vasocontrictor (HPV) response redirecting blood away from poorly ventilated lung regions. Both the HPV response and vasoactive agent-induced vasoconstriction have direct medial smooth muscle and endothelial cell components which were examined in this study. A simple and reproducible method of isolating and culturing vascular endothelial cells was developed and used to measure the release of vasoactive substances during normoxia and hypoxia. The rate of release of endothelin from cultured equine pulmonary artery endothelial cells was similar to that from bovine pulmonary artery and equine aorta cells; 4 h hypoxia had no effect on the rates of release from any of these cell types. Hypoxia stimulated prostacyclin release from bovine but not equine pulmonary endothelial cells. Isolated equine pulmonary artery had similar sensitivities to phenylephrine and 5-hydroxytryptamine, yet contracted with approximately 50% of the force when compared to bovine vessels. The contractile response to endothelin appeared to be mediated via the ETa receptor in equine pulmonary artery. The response of both equine and bovine pulmonary vessels to hypoxia was similar, although bovine vessels contracted more strongly than equine vessels in both absolute and relative terms. In conclusion, equine and bovine pulmonary vessels responded to vasoactive agents and hypoxia, but equine vessels of equivalent diameter contract less strongly. These differences do not appear to be caused by altered endothelial cell function. Instead they may reflect the presence of less smooth muscle within the medial layer and an intrinsically weaker response of equine pulmonary smooth muscle to hypoxia