ABSTRACT 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 thickwalled 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.

Broilers were divided at 42 to 44 d of age into a Control group (n=3O) and a Treatment group (n=3O). The mean pulmonary arterial pressure (mPAP) and electrocardiogram (ECG) leads II and aVF were measured 1, 2 and 4 h after an intravenous injection of 0.9% saline (Control group) or Nw-nitro-L-arginine methyl esther (L-NAME), an inhibitor of nitric oxide synthase and thus an inhibitor of endothelial nitric oxide (NO) production (Treatment group). At 1 and 2 h but not 4 h post-injection, L-NAME signlfican ti), inc r e ased the mPAP and the amplitudes of the EGG S-wave and RS-wave leads Ⅱ and aVr when compared with Control values. The correlation coefficients between the mPAP and the ECG S-wave and RS-wave amplitudes for lead rt within the Treatment group were-0.848 and-0.553 at 1 h and-0-798 and-0.512 at 2 h, respectively. The corresponding coefficients for lead aVF were-0.735,-0.596,-0-663 and 4).794, respectively. After suitable mPAP and EGG values hnd been recorded at each time intertmJ, sodium nitroprusslde (SNP), which acts as a short-lived NO donor molecule, was injected intravenously via a fight-cardiac catheter. Within 5 rain after the SNP injection, the mPAP and the ECG lead II S-wave and RS-wave amplitudes were transiently reduced to levels that, at 1 and 2 h after L-NAME injection, did not differ from Control values. Within I0 min after the SNP injection, all values returned to the levels previously induced by L-NAME. These results demonstrate that L-NAM~ increased the myocardial contractility and PAP, whereas SNP transiendy reversed the effects of L-NAME on myocardial contractility and PAP. It appears likely from these results that the pulmonary vascular endothelium releases NO that in turn reduces the pulmonary vascular resistance or attenuates myocardial contractility in broiler chickens.

Objective: The present study was conducted to examine the activity of protein kinase Cα (PKCα) in the pulmonary arterioles of broilers during the pathophysiological progression leading to pulmonary hypertension on one hand and the association between activation of PKCα and pulmonary vascular remodeling on the other hand. Method: One hundred and sixty Avian-2000 broilers were divided equally into control group and cold temperature group. All the birds were reared according to normal temperature schedule before day 14, and the lighting schedule provided 24h light per day. Thereafter, birds in cold temperature group were subjected to low temperature by lowering 1~2 °C per day to 14~12°C, and then remained constant until day 49, while birds in control group were still brooded at standard temperature. All the birds received pelleted diet throughout the study. Samples of heart, blood and lung were collected at day 24,32,39,45 of age, respectively. Right ventricle to total ventricle ratio (RV/TV) and packed cell volume (PCV) were measured. Vessel wall area to vessel total area ratio (WA/TA) and mean media thickness in pulmonary arterioles (mMTPA) was examined using computer-image analytic software. Expression of PKC in pulmonary muscular arterioles was investigated by immunohistochemistry technique, and quantified by measuring optical density (OD) using computer-image analytic software. Results: Incidence of pulmonary hypertension syndrome (PHS) amounted to 12.5% in birds exposed to cold, which was fairly high compared to 3.75% of the control group (P<0.05). PCV elevated after day 32 (P<0.05), and RV/TV ratio increased on day 45 (P<0.05). Both the WA/TA and mMTPA of birds subjected to cold were significantly elevated when compared with that of control group during every individual’s life span (P<0.05). The OD values showed an upward trend but did not significant increase before day 32 (P>0.05), however, one week later (at day 39 of age), there was a much larger rise in broilers kept under cold temperature and the difference between the two groups was very pronounced (P<0.05). There was still a trend on day 45 although the difference was less significant (P>0.05). The increased PKCα expression was positively correlated with the values of mMTPA and WA/TA. Conclusion: PKCα expression was up regulated to a certain extent during the pathophysiological progression leading to pulmonary hypertension, and activation of PKCα might be involved in the development of pulmonary vascular remodeling.

We investigated the effect of organic versus inorganic dietary selenium in laying hens on the productivity, selenium distribution in egg and selenium content in blood, liver and kidney. Sixty Leghorn laying hens were fed a basic diet containing 0.23 mg Se/kg DM (dry matter) for 2 weeks and then were allocated randomly into three groups. Thereafter, the hens were given the same basic diet without supplementation, or with 0.51 mg Se/kg DM as sodium selenite (SS) or Se-malt (SM). During the experiment, egg rate and dietary intake were recorded, blood was sampled on days 10 and 20, and six eggs were sampled on days 8, 16 and 24 from each treatment group for Se content determination. At the end of the experiment, 10 hens from each treatment were slaughtered, and liver and kidney were sampled for the determination of Se content. The result showed that with the increase of dietary Se level, the Se content in egg, blood, liver and kidney was elevated (Po0:05), but the hens’ productivity was not affected. SS increased liver Se content more than SM (Po0:05), while the Se content both in blood and kidney did not differ significantly between the SS and SM treatments. Se from SM and SS mainly deposited in the egg yolk. This suggests that the metabolic route of Se from SM is similar to that of Se from SS in laying hens.

Objective: Pulmonary vascular remodelling is one of the important pathological bases of broiler pulmonary hypertension syndrome (PHS). Nitric oxide (NO) has been found to inhibit proliferation and to induce apoptosis in pulmonary artery smooth muscle cells (SMC) in mammals with pulmonary hypertension. The present study was conducted to evaluate the effects of NO precursor L-arginine on pulmonary vascular remodelling in broilers with pulmonary hypertension induced by cold exposure and to examine whether NO-induced apoptosis in pulmonary arteriole SMC is involved in the regulatory mechanisms Methods: Two hundred and forty mixed-sex commercial broilers were equally assigned to three groups and reared in normal brooding temperatures before day 14. Starting on day 14 continuing until the end of the experiment, the control group was brooded in normal temperatures whereas the other two groups were subjected to low ambient temperatures with or without L-arginine added to the basal diets. Cumulative PHS mortality and body weight were recorded in each group. Right/total ventricle ratio (RV/TV), plasma NO concentration and pulmonary vascular morphological changes were analyzed. TdT-mediated dUTP-biotin nick-end labeling (TUNEL) assay was used to detect apoptosis in pulmonary arteriole SMC. Result: L-arginine, in group A, had no effect on body weights under cold temperature condition. Birds kept in group B had increased PHS mortality, RV/TV ratio, vessel wall area/vessel total area ratios (WA/TA) and mean media thickness in pulmonary arterioles (mMTPA) (P<0.05). Percentages of apoptotic SMC in pulmonary arterioles in group B were not altered by cold exposure (P>0.05). Supplemental dietary L-arginine in group A elevated plasma NO level (P<0.05), reduced PHS mortality (P<0.05), attenuated pulmonary vascular remodelling and increased the percentages of apoptotic SMC (P<0.05) when compared with the group B. Conclusion: Supplemental L-arginine partially inhibited pulmonary vascular remodelling that occurred secondary to increased pulmonary pressure; NO-induced apoptosis in arteriole SMC might contribute to its regulatory effect on pulmonary vascular structural changes. Keywords: L-arginine; Pulmonary vascular remodelling; Apoptosis; Broiler; Cold temperature