%0 Journal Article
%T Hyperoxic Vasoconstriction of Human Pulmonary Arteries: A Novel Insight into Acute Ventricular Septal Defects
%A Priyadharshanan Ariyaratnam
%A Mahmoud Loubani
%A Robert Bennett
%A Steven Griffin
%A Mubarak A. Chaudhry
%A Michael E. Cowen
%A Levant Guvendik
%A Alexander R. J. Cale
%A Alyn H. Morice
%J ISRN Cardiology
%D 2013
%R 10.1155/2013/685735
%X Objectives. Acute rises in pulmonary artery pressures following postinfarction ventricular septal defects present a challenge. We hypothesised that the abnormally high oxygen content exposure to the pulmonary arteries may be a factor. We investigated the contractile responses of human pulmonary arteries to changes in oxygen tension. Methods. Isometric tension was measured in large and medium sized pulmonary artery rings obtained from lung resections for patients with bronchial carcinoma ( ). Fresh rings were mounted in organ baths bubbled under basal conditions with hyperoxic or normoxic gas mixes and the gas tensions varied during the experiment. We studied whether voltage-gated calcium channels and nitric oxide signalling had any role in responses to oxygen changes. Results. Hypoxia caused a net mean relaxation of 18.1% 15.5 ( ) from hyperoxia. Subsequent hyperoxia caused a contraction of 19.2% 13.5 ( ). Arteries maintained in normoxia responded to hyperoxia with a mean constriction of 14.8% 3.9 ( ). Nifedipine inhibited the vasoconstrictive response ( ) whilst L-NAME had no effect on any hypoxic vasodilatory response. Conclusions. We demonstrate that hyperoxia leads to vasoconstriction in human pulmonary arteries. The mechanism appears to be dependent on voltage-gated calcium channels. Hyperoxic vasoconstriction may contribute to acute rises in pulmonary artery pressures. 1. Introduction A postinfarction ventricular septal defect (VSD) is associated with acute rises in pulmonary artery pressures [1]. These acute rises in pulmonary artery pressure are, in turn, a significant predictor of mortality and morbidity and present a considerable challenge to the cardiac surgeon and the management of the patient in the acute intensive care setting [2]. The rise in pulmonary artery pressure may be because of failure of the right ventricle secondary to ischaemia or because of increased flow to the pulmonary artery stimulating a myogenic response. More interesting, however, is the possibility that the higher oxygen content through the pulmonary artery as a consequence of the left to right shunting of oxygenated blood may increase pulmonary artery tone especially in more subacute cases [3]. Despite lack of data on oxygen-dependent responses in isolated human pulmonary arteries, many potential mechanisms have been suggested in animal models. These range from calcium channel-dependent constrictive pathways to vasodilatory pathways involving Nitric Oxide (NO) release by the endothelium [4, 5]. Here we sought to evaluate the differential effect of hypoxia and
%U http://www.hindawi.com/journals/isrn.cardiology/2013/685735/