Pathogenesis And Control Of Pulmonary Hypertension Syndrome In Broilers

Broiler pulmonary hypertension syndrome (PHS), also known as ascites syndrome (AS), is a devastating metabolic disease that affects young, fast-growing commercial broilers, and has been reported from many parts of the world. Worldwide, approximately 4% of all broilers die from PHS, amounting to a loss estimated at $1 billion annually. Only in China, an average incidence of 4.5% was reported, which counts for a loss of about $468 million annually. The primary triggers for PHS under most conditions of commercial broilers growthout include fast growth and cool temperature. Both triggers increase the metabolic requirement for oxygen and thereby force the heart to increase its cardiac output. Pulmonary hypertension is initiated whenever the relatively inelastic pulmonary vasculatrue of susceptible broilers cannot accommodate the rapidly increasing cardiac output at a low pulmonary arterial pressure, or when inappropriate constriction of the pulmonary vasculature directly evaluate the pulmonary vascular resistance to pulmonary blood flow. After the onset of pulmonary hypertension, susceptible broilers proceed through a cascade of events to terminal PHS, including systemic hypoxemia, pulmonary vascular remodeling, right-sided congestive heart failure, increased intravascular pressure in the liver portal system and, ascites. However, the mechanisms for PHS are not well understood. The present study was conducted to evaluate changes of protein kinase Ca (PKCa), nitric oxide synthase (NOS) and apoptosis of smooth muscle cells in pulmonary arterioles during the pathological progression leading to pulmonary hypertension as for further investigation of the pathogenesis of PHS, and to assess different methods preventing PHS.Test 1 The association between activation of PKCa and pulmonary vascular remodeling. One hundred and sixty Avian-2000 commercial broilers were divided equally into a normal temperature control group (NT) and a low temperature group (LL). All thebirds were reared according to normal temperature schedule before day 14, and then, birds in the group LL were exposed to low temperatures by lowing 1-2 per day from 28 (day 14) down to 14-12(day 21), and remained constant until the end of the experiment, while the controls were still reared at normal temperatures. PHS incidence was recorded in each group. Ratios of right ventricle to total ventricle (RV/TV), packed cell volume (PCV) and hemoglobin (Hb) were measured on days 24, 32, 39 and 45, respectively. Vessel wall area to vessel total area (WA/TA), mean media thickness in pulmonary arterioles (mMTPA) were determined by computer-image analytic technique, and the expression of protein kinase Ca (PKCa) in pulmonary arterioles detected by imrnunohistochemical and computer-image analytic technique. PHS incidence amounted to 3.75% of the group NT and 12.5% of the group LT, respectively, and the difference was very pronounced (P < 0.05). Broilers exposed to the cold had elevated RV/TV ratio, PCV, Hb as well as PKCa expression. Cold exposure caused pulmonary vascular remodeling characterized by thickening of media layer and narrowing of the vessel lumen of arterioles. PKCa expression was positively correlated with both the mMTPA and WA/TA.Test 2. The effect of L-arginine on NOS activity. Two hundred and forty Avian-2000 commercial broilers were divided equally into a normal temperature control group (NT), a low temperature group (LT) and a low temperature with supplemental L-arginine group (LA). All birds were brooded at normal temperatures before day 14. Birds in the group LA and LT were subjected to cold temperatures by lowing 1-2 per day from 28 (day 14) down to 14-12 (day 21), and then remained constant until day 49; while birds in the group NT were still reared in normal temperatures. All the birds were fed pelleted diets whereas those kept in the group LA fed the same diets supplemented with 10g kg L-arginine from day 14 to 49. Birds died from PHS were recorded daily and accumulative PHS incidences calculated in the end of the experiment. Ratios of RV/TV, concentrat...