Acute and Chronic Pulmonary Hypertension Syndrome in Broiler Chickens

摘要

Two hundred and forty broiler chicks were divided randomly into control (C) and experimental (T_1 and T_2) groups that, between 8 and 42 days of age, were provided drinking water containing 0, 600 and 1200 mg·L~(-1) Na~+ from NaCl (sodium chloride), respectively. The incidences of PHS and the right to total ventricle weight ratio (RV/TV) were calculated weekly, and blood samples and lung tissues were collected weekly from ten randomly selected non-ascitic broilers per group. The saline drinking water significantly increased the incidence of PHS, RV/TV ratios, packed cell volume, blood filtration index reflecting erythrocyte deformability, and blood volume. During the chronic peak of PHS mortality (days 35 to 42), the non-ascitic broilers consuming saline drinking water had pulmonary arterioles that exhibited increases (P < 0.01) in the ratio of wall to total area (WA/TA), medial thickness of pulmonary arteriole walls (mMTPA), percentage of thick-walled peripheral lung vessels (%TWPV), and percentage of muscular arterioles (%MA), and decreases (P < 0.01) in the percentage of non-muscular arterioles (%NMA). Prior to 28 days of age, the blood filtration index and blood volume were consistently elevated (P < 0.01), however there were no (P > 0.05) saline-induced alterations in %TWPV, %MA, WA/TA, mMTPA or %NMA. Therefore when PHS is induced by excess sodium in the drinking water, both the acute and chronic phases of PHS mortality are characterized by increases in blood volume and blood viscosity, whereas only the chronic phase is characterized by remodeling of the pulmonary vasculature as revealed by proliferation, medial hypertrophy, and increased muscularity of the pulmonary arterioles. The acute changes presumably challenge the pulmonary vasculature to accommodate a higher flow of blood that offers a greater internal resistance to flow, whereas the chronic changes evidently serve to elevate the resistance to flow imposed by remodeling of the pulmonary vasculature.