Sodium chloride-induced acute and chronic pulmonary hypertension syndrome in broiler chickens.

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.

Effect of vitamin C on pulmonary hypertension and muscularisation of pulmonary arterioles in broilers.

1. Three hundred and eighty 1-day-old Arbor Acres broilers were divided into control (A) and experimental (B, C, D, and E) groups. 2. After 14 d of age the experimental groups were subjected to a cool temperature challenge by lowering the temperature 1 to 2 degrees C per day down to 12 degrees C, and maintaining this temperature until 7 weeks of age. 3. At the same time, 1.5 mg/kg 3,3,5-triiodothyronine (T3) was added to the diet of groups D and E, and 500 mg/kg ascorbic acid (vitamin C) to the diet of groups C and E. 4. The incidence of pulmonary hypertension syndrome (PHS), body weight gain and feed intake were measured weekly. Lung and blood samples were collected weekly from 10 birds per group beginning on d 14, and the percentage of thick-walled peripheral lung vessels (% TWPV) and packed cell volume (PCV) were determined. 5. The lower ambient temperature and diets supplemented with T3 increased PHS incidence and % TWPV and decreased body weight gain. 6. There was an increase in PCV after 5 weeks of age under lower ambient temperature 3 and the PCV values 14 were also significantly increased by T3. 7. Vitamin C supplementation reduced PHS incidence and % TWPV but did not change packed cell volume, body, weight gain, feed intake, or feed conversion. 8. It is concluded that vitamin C reduced PHS and the associated muscularisation of pulmonary arterioles induced by exposing broilers to cool environmental temperatures and feeding them with T3.