Oxidative stress is involved in the development of pulmonary hypertension syndrome (PHS) in broilers. l-Carnitine has an antiperoxidative effect and supplemental l-carnitine has been revealed to increase broiler heart weight. The present study was conducted to evaluate the effect of an addition of 100 mg/kg l-carnitine to the basal diets on PHS mortality in cold-exposed broilers. Two-hundred and forty mixed-sex broilers were equally assigned to three groups. The control group was reared in normal temperatures throughout the experiment. Starting on day 14 continuing until the end of the experiment, the other two groups were subjected to a step-down temperature programme (by lowering the temperature 1-2 degrees C per day down to 12-14 degrees C) with or without l-carnitine added to the basal diets. Cold exposure increased the right/total ventricle ratio (RV/TV) and plasma malondialdehyde (MDA), reduced superoxide dismutase (SOD) and led to pulmonary vascular remodelling in birds without feeding additional l-carnitine. Supplemental l-carnitine reduced plasma MDA, increased SOD, inhibited remodelling and postponed the occurrence of PHS for 1 week in cold-exposed broilers; nevertheless, it did not significantly influence the cumulative PHS mortality (p > 0.05). On days 24 and 32, birds fed supplemental l-carnitine had lower RV/TV and higher total ventricle/body weight (p < 0.05) but unchanged right ventricle/body weight ratios (p > 0.05) compared to their cold-exposed counterparts, indicating an increase in left ventricle weight. However, from day 39 on, their RV/TV ratios were suddenly increased (p < 0.05). It was suggested that the l-carnitine-induced increase in left heart weight might partially account for the postponed occurrence of pulmonary hypertension in the early stage by elevating cardiac output, which might, in turn, lead to the resulting increase in pulmonary pressure. In view of its complex effects on cardiopulmonary haemodynamics, l-carnitine supplementation may be impractical for reducing PHS.

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.