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Morgan B.J.,John Rankin Laboratory of Pulmonary Medicine | Rio R.D.,Autonomous University of Chile
Respiratory Physiology and Neurobiology | Year: 2016

Chronic exposure to intermittent hypoxia (CIH) elicits plasticity of the carotid sinus and phrenic nerves via reactive oxygen species (ROS). To determine whether CIH-induced alterations in ventilation, metabolism, and heart rate are also dependent on ROS, we measured responses to acute hypoxia in conscious rats after 14 and 21 d of either CIH or normoxia (NORM), with or without concomitant administration of allopurinol (xanthine oxidase inhibitor), combined allopurinol plus losartan (angiotensin II type 1 receptor antagonist), or apocynin (NADPH oxidase inhibitor). Carotid body nitrotyrosine production was measured by immunohistochemistry. CIH produced an increase in the ventilatory response to acute hypoxia that was virtually eliminated by all three pharmacologic interventions. CIH caused a robust increase in carotid body nitrotyrosine production that was greatly attenuated by allopurinol plus losartan and by apocynin but unaffected by allopurinol. CIH caused a decrease in metabolic rate and a reduction in hypoxic bradycardia. Both of these effects were prevented by allopurinol, allopurinol plus losartan, and apocynin. © 2016 Elsevier B.V.

Bates M.L.,University of Wisconsin - Madison | Bates M.L.,John Rankin Laboratory of Pulmonary Medicine | Fulmer B.R.,John Rankin Laboratory of Pulmonary Medicine | Farrell E.T.,John Rankin Laboratory of Pulmonary Medicine | And 5 more authors.
Journal of Applied Physiology | Year: 2012

Hypoxia recruits intrapulmonary arteriovenous pathways in intact rats but not isolated rat lungs. J Appl Physiol 112: 1915-1920, 2012. First published March 15, 2012; doi:10.1152/japplphysiol.00985.2011.-Intrapulmonary arteriovenous anastomoses (IPAVS) directly connect the arterial and venous circulations in the lung, bypassing the capillary network. Here, we used solid, latex microspheres and isolated rat lung and intact, spontaneously breathing rat models to test the hypothesis that IPAVS are recruited by alveolar hypoxia. We found that hypoxia recruits IPAVS in the intact rat, but not the isolated lung. IPAVS are at least 70 μm in the rat and, interestingly, appear to be recruited when the mixed venous PO2 falls below 22 mmHg. These data provide evidence that large-diameter, direct arteriovenous connections exist in the lung and are recruitable by hypoxia in the intact animal. © 2012 the American Physiological Society.

Bates M.L.,John Rankin Laboratory of Pulmonary Medicine | Jacobson J.E.,Michigan State University | Eldridge M.W.,University of Wisconsin - Madison
Pediatrics | Year: 2014

Intrapulmonary arteriovenous anastomoses (IPAVs) are largediameter pathways that directly connect the arterial and venous networks, bypassing the pulmonary capillaries. Ubiquitously present in healthy humans, these pathways are recruited in experimental conditions by exercise, hypoxia, and catecholamines and have been previously shown to be closed by hyperoxia. Whether they play a role in pulmonary pathophysiology is unknown. Here, we describe IPAV recruitment associated with hypoxemia and riǵht-to-left shunt in a patient with status asthmaticus, treated with agonists of the β2-adrenergic pathway. Our observation of IPAVs in a pediatric patient, mechanically ventilated with 100% O2, suǵǵests that these pathways are recruited in clinically important circumstances and challenges the notion that IPAVs are always closed by alveolar hyperoxia. © 2014 by the American Academy of Pediatrics.

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