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  • Title: Sodium chloride-induced acute and chronic pulmonary hypertension syndrome in broiler chickens.
    Author: Xiang RP, Sun WD, Zhang KC, Li JC, Wang JY, Wang XL.
    Journal: Poult Sci; 2004 May; 83(5):732-6. PubMed ID: 15141829.
    Abstract:
    Two hundred forty 1-d-old Arbor Acres commercial broiler chicks were divided into control and experimental (T1 and T2) groups that, between 8 and 42 d of age, were provided drinking water containing 0, 600, or 1,200 mg/L sodium from sodium chloride, respectively. The pulmonary hypertension syndrome (PHS) incidence and the right to total ventricle weight ratio (RV/ TV) were calculated weekly, and blood samples and lung tissues were collected weekly from 10 birds per group to evaluate the structural and hemodynamic characteristics of pulmonary vessels. Saline drinking water significantly increased the incidence of PHS and RV/TV ratios. In the T2 group the PHS mortality exhibited 2 peaks, including an acute peak from 14 to 21 d of age and a chronic peak from 35 to 42 d of age. During the acute peak of PHS mortality the blood volume (BV), filtration index (FI), and packed cell volume (PCV) increased in groups T1 and T2 when compared with the control group. During the acute peak there were no differences among groups in the ratio of wall to total area (WA/TA), medial thickness of pulmonary arteriole walls (mMTPA), the percentage of thick-walled peripheral lung vessels (%TWPV), the percentage of muscular arterioles (%MA), or the percentage of nonmuscular arterioles (%NMA) in pulmonary arterioles. During the chronic peak of PHS mortality, group T2 exhibited the highest values for %TWPV, %MA, WA/TA, and mMTPA and the lowest values for %NMA when compared with the T1 and control groups. Also during the chronic peak the groups did not differ in BV or FI, whereas PCV remained elevated above control values in groups T1 and T2. These observations indicate that hemodynamic changes related to viscous resistance to blood flow (BV, FI, PCV) predominated throughout the acute peak of PHS mortality, whereas, during the chronic stages of PHS mortality, increased vascular resistance to blood flow also was imposed by remodeling of the pulmonary vasculature.
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