| Pulmonary hypertension (PH) and right ventricular hypertrophy had been commonly considered as key role in the mechanism of ascites in broilers. Though studies substantiated that the excess sodium could induce AS in broilers, it is unclear weather PH develops in the AS induced by excess sodium in broilers. So, in the present study, the layer and broilers were used to investigate the mechanism of PH in the development of ascites syndrome (AS) induced by excess sodium from drinking water in broilers. We examined the differences in hemodynamics, right cardiac function, pulmonary artery structure between layers and broilers during drinking water with excess sodium, and expression of oncogene c-myc mRNA of pulmonary artery in broiler chickens.1. The hemodynimics was determined dynamically by right ventricular catheters in layer and broiler chickens. The results shows: (1) The AS was induced successfully by excess sodium from drinking water in broiler chickens, the incidence of ascites in treated group (16.3%) was significantly higher than that of control(2.5%) (P<0.01). (2) From 15 to 50 days of age, the mean pulmonary artery pressure (mPAP) of broilers in treated group (2.91±0.29~3.62±0.39 kPa) were significantly higher than that of control group(2.18±0.40~2.41 ±0.39 kPa)(P<0.05). (3) The packed cell volume of birds were significantly elevated (P<0.05) by excess salt compared with that of control, and significantly correlated with mPAP (15~50 day, r=0.616, P<0.01). (4) The excess salt in drinking water could induce right ventricular hypertrophy, and significantly correlated with mPAP (22 day, r=0.532, P<0.05; 50 day, r=0.756, P<0.01). (5) Mean femoral artery pressure (mFAP) of the birds in the treated group also increased significantly (P<0.05), but the extent of mFAP increased (24.0%) was less than that of mPAP(54.0%).(6) The mPAP, mFAP, PCV and AHI of the treated group were not affected by excess salt in layers. These data indicate that the excess salt in the drinking water induce the pulmonary hypertension that play an important role in the pathogenesis of AS in broiler chickens.2. In this experiment, the right ventricular pressure (RVP), the maximum increasing rate of right ventricular (RV±dp/dtmax) were measured dynamically. The results showed: (1) The right ventricular systolic pressure of trial group were significantly higher than that of control group int the beginning(P<0.05), but the right ventricular diastolic pressure of experimental group were significantly higher than that of control group in the end (P<0.05). (2) The RV±dp/dtmax of the treated group was significantly higher than that of control group in the beginning(P<0.05), but significantly lower than that of control group in the end(P<0.05). The data suggest that in the development of AS, the right ventricle function showed functional compensation at first, and then, showed compensatory hypertrophy of right ventricle, in the end, showed decompensation and right heart failure.3. By using the microscopic image analysis program, the measurement of ratio of vessel wall area (WA) to vessel total area (TA) and mean medial thickness in pulmonary arterioles (mMTPA) were accomplished in different groups. The results showed that the ratio of WA/TA, the mMTPA , and the percentage of muscular artery (MA%) and partially muscularized artery (PMA%) of experimental groups were higher than that of control group at 36 , 43, 50 days of age. WA/TA, mMTPA, MA%, and PMA% were positively correlated with mPAP and AHI. The data indicate that pulmonary vascular structural remodeling (PVSR) was induced by excess salt and PVSR might be one of the factors in the formation of pulmonary hypertension.4. The expression of c-myc mRNA oncogene was observed by in situ hybridization and image analysis. The results showed that c-myc mRNA of pulmonary artery smooth muscular cells expression was increased significantly by excess salt from drinking water (treated group: 118.86±19.71-243.11 ± 38.04 vs control group: 79.04±21.68-89.8 ± 16.88). We suppose that the... |
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