| Pulmonary hypertension syndrome (PHS) in broiler chickens poses a serious problem to the international poultry industry, and is an important cause of mortality that has been reported from many parts of the world. For broilers kept at altitudes of approximately 3000m, the onset of pulmonary hypertension, cardiac hypertrophy, heart failure, and oedema leading to PHS has been described. More recently similar symptoms and mortality rates were reported in broilers reared at lower altitudes of 1000 to 2000m and at altitudes down to sea level. A survey in the United States showed that PHS accounts for over 25% of annual broiler losses. An incidence of PHS of 5-10% was reported in China. A global incidence of 4-5% PHS has been reported and, at today's market prices, this mortality represents a cost to the industry of about one billion $US annually. It has been suggested that the fast-growing modern broiler is particularly susceptible to PHS, because rapid growth causes an increased demand for oxygen, which forces the heart to maintain an elevated cardiac output. The resulting increase in blood pressure within the pulmonary circulation can cause hypertrophy of the right ventricle and eventually congestive heart failure. This pathogenesis for PHS includes increased oxygen requirements by body tissues and low oxygen tensions in arterial blood. Further pathologic mechanism is not clear. The present study was conducted to further evaluate the pathogenesis of the acute and chronic forms of PHS, the muscularization in pulmonary arterioles and the changes of free radicals in broilers with PHS, and to obtain the methods preventing PHS.Test I , the changes of the muscularization and density in pulmonary arterioles in field cases of broilers with PHS induced by hypoxia. Twelve field cases with pulmonary hypertension syndrome in broilers due to hypoxia and twelve healthy birds from the same flock as control were randomly selected for histomorphological evaluation of pulmonary arterioles. The histopathological alterations of pulmonary arterioles in broilers with PHS and in controls were measured and analyzed. Refering to classified methods of pulmonary vascular muscularity for mammals, the classified methods of pulmonary vascular muscularity for birds were proposed. The arterioles with complete internal andexternal elastic lamina were identified as the muscular arterioles(MA); ones with partially internal elastic lamina in complete external elastic lamina were identified as the partially muscular arterioles(PMA); ones with a single elastic lamina were identified as the non-muscular arterioles(NMA). The result indicated that the ratio of vessel wall area to total vessel area (WA/TA) and the ratio of medial thickness in pulmonary arteries to blood vessel diameter were more significantly increased (P<0.01) in sick birds than in healthy birds and that the percentage of pulmonary vascular muscularity were also significantly increased (P<0.01) by measuring the percentage of thick-walled peripheral lung vessels at <200 U m and <60 y m . The density of pulmonary artery were significantly decreased (P<0.01). Histopathological observation showed the intimal cellular proliferation and medial hypertrophy.Test II, acute and chronic pulmonary hypertension induced by excess sodium. Tostudy the pathogenesis of pulmonary hypertension syndrome (PHS) in broilers, two hundred and forty 1-day-old Arbor Acres commercial broilers were divided randomly into control (C) and experimental (T\ and T2 ) groups that were treated with 0, 600 and 1200 mg-L-1 Na+ from NaCl (sodium chloride) in their drinking water respectively from 8 to 42 days of age. Experimental and control birds were selected for the dynamic evaluations of the signs and incidence of PHS, the ratio of right ventricle to total ventricle (RV/TV), packed cell volume (PCV), filtration index of red cell, blood volume and histopathological alteration of pulmonary arterioles in different groups respectively at 9,14,21,28, 35 and 42 day of age. The results indicated that the high sodium...
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