title: Increasing pulmonary artery pulsatile flow improves hypoxic pulmonary hypertension in piglets.
abstract: Pulmonary arterial hypertension (PAH) is a disease affecting distal pulmonary arteries (PA). These arteries are deformed, leading to right ventricular failure. Current treatments are limited. Physiologically, pulsatile blood flow is detrimental to the vasculature. In response to sustained pulsatile stress, vessels release nitric oxide (NO) to induce vasodilation for self-protection. Based on this observation, this study developed a protocol to assess whether an artificial pulmonary pulsatile blood flow could induce an NO-dependent decrease in pulmonary artery pressure. One group of piglets was exposed to chronic hypoxia for 3 weeks and compared to a control group of piglets. Once a week, the piglets underwent echocardiography to assess PAH severity. At the end of hypoxia exposure, the piglets were subjected to a pulsatile protocol using a pulsatile catheter. After being anesthetized and prepared for surgery, the jugular vein of the piglet was isolated and the catheter was introduced through the right atrium, the right ventricle and the pulmonary artery, under radioscopic control. Pulmonary artery pressure (PAP) was measured before (T0), immediately after (T1) and 30 min after (T2) the pulsatile protocol. It was demonstrated that this pulsatile protocol is a safe and efficient method of inducing a significant reduction in mean PAP via an NO-dependent mechanism. These data open up new avenues for the clinical management of PAH.
authors.affiliation: Department of Medicine, Pulmonary Hypertension Research Group (CRIUCPQ), Laval University.
authors.forename: Audrey
authors.initials: A
authors.lastname: Courboulin
authors.affiliation: Institut National de la Recherche Agronomique.
authors.forename: Chantal
authors.initials: C
authors.lastname: Kang
authors.affiliation: Université Diderot Paris, Sorbonne Paris Cité; Hôpital Lariboisière, Physiologie clinique Explorations Fonctionnelles; INSERM U 965.
authors.forename: Olivier
authors.initials: O
authors.lastname: Baillard
authors.affiliation: Department of Medicine, Pulmonary Hypertension Research Group (CRIUCPQ), Laval University.
authors.forename: Sebastien
authors.initials: S
authors.lastname: Bonnet
authors.affiliation: Service de Cardiologie, Centre Hospitalier Universitaire Tours; pierre.bo@wanadoo.fr.
authors.forename: Pierre
authors.initials: P
authors.lastname: Bonnet
mesh_terms: D000818:Animals; D006328:Cardiac Catheterization / Q000295:instrumentation / Q000379:methods*; D004195:Disease Models, Animal; D006439:Hemodynamics; D006976:Hypertension, Pulmonary / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology* / Q000628:therapy*; D000860:Hypoxia / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology* / Q000628:therapy*; D008168:Lung / Q000098:blood supply; D011651:Pulmonary Artery / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D011673:Pulsatile Flow; D013552:Swine; D014664:Vasodilation