心钠素在肉鸡腹水综合征发生发展中的作用

大群艾维菌商品代肉鸡从1日龄起用高能日粮常规饲养，以获得自然腹水综合征（ascites syndrome，AS）病例。应用放射免疫分析方法，分别测定了2～6周龄正常组、轻度腹水组、重度腹水组内鸡血浆和5周龄时心、肝、肺、肾等组织心钠素（atrial natriuretic polypeptide,ANP）的含量；用右心导管法测定了平均肺动脉压（mPAP），并用常规方法测定了腹水心脏指数（AHI），同时还对血浆ANP的含量与AHI、mPAP的相关性进行了分析。结果发现，随着日龄的增长，ANP的含量增加，AHI、mPAP也随着发生明显的变化；随腹水程度的加深，mPAP、AHI以及肉鸡血浆、组织ANP的含量均显著（P〈0．05）或极显著（P〈0．01）升高，组织中ANP的含量明显比血浆中的高；另外还发现，不同腹水程度肉鸡血浆ANP含量与5～6周龄时的mPAP、4～5周龄时的AHI相关性显著（P〈0．05）。结果表明，ANP参与了肉鸡AS的发生和发展过程并与肉鸡发生AS的程度有密切关系。     

一氧化氮供体硝普钠降低肉鸡肺动脉压试验研究

AA肉鸡100羽，随机等分为对照组、试验组、试验组肉鸡自8日龄起给予含0．2％的钠离子的饮水以诱发肉鸡肺动脉高压综合征，按常规方法饲养。并通过右心导管法观察血管内注入硝普纳（Sodium Nitroprusside,SNP)前后两组肉鸡肺动脉平均压（Mean pulmonary arterial pressure,mPAP)变化，与此同时，还观察一氧化氮（Nitric Oxide,NO)与肉鸡肺动脉压间的关系。结果发现试验组肉鸡mPAP高于对照组（P＜0．01），注入SNP后试验组和对照组肉鸡血浆NO水平都显著升高（P＜0．01），而mPAP都显著降低（P＜0．01），试验组肉鸡mPAP降压幅度大于对照组（P＜0．05）。表明SNP可通过释放NO降低肉鸡mPAP。     

A超对肉鸡腹水征的诊断

本研究探讨了用A超诊断肉鸡腹水征的方法，比较了正常与腹水鸡的红细胞压积，右心／全心的比值。结果发现与正常肉鸡相比，腹水鸡红细胞压积增高，右心；全心比值升高，液性平段增宽，A超对腹水的检出率与实际腹水的发生完全相符。提示A超可用于肉鸡腹水征的诊断。     

内皮素-1对肉鸡腹水综合征发生发展的影响

利用放射免疫分析方法，分别测定了35日龄正常组、轻度腹水组、重度腹水组肉鸡血浆内皮素-1（ET-1）、心钠素（ANP）的含量以及心、肝、肺、肾等组织ET-1的含量，并测定了腹水心脏指数（AHI）、平均右心室压（mRVP）和平均肺动脉压（mPAP）；同时还用硝酸还原酶法测定了血清中一氧化氮（NO）的水平。结果发现，随腹水程度的加深，mRVP、mPAP、AHI极显著（P〈0．01）升高，肉鸡血浆ET-1、ANP和组织中ET-1的含量以及血清NO浓度也显著（P〈0．05）或极显著（P〈0．01）升高，且重度腹水组高于轻度腹水组；另外还发现，血浆ET-1、ANP与mPAP、AHI以及心脏ET-1含量之间相关性显著（P〈0．05），而血清NO含量与上述指标之间无明显的相关性（P〉0．05）。结果表明ET-1、ANP、NO均参与了肉鸡AS的发生和发展过程并在其中起着重要作用，其中ET-1、ANP与肉鸡发生腹水的程度有密切的关系。     

L-精氨酸(L-Arg)和NaHCO3降低肉鸡腹水综合征病死率的田间试验

1800只3周龄肉仔鸡随机分成3组，每组600人，其中第I组为正常对照组，饲喂基础日粮；第Ⅱ组为NaHCO3试验组，饲喂基础日粮加0．3％NaHCO3；第Ⅲ组为L－Arg试验组，饲喂基础日粮加1％L－Arg。在常规条件下饲养8周，对自然死亡的肉仔鸡进行病理剖检，凡腹腔有大量腹水，PCV和HAI显著升高的，判定为死于肉鸡腹水综合征。结果对照组腹水综合征病死率为3．17％，显著地高于NaHCO3组的1．33％和L－Arg组的1．17％（P＜0．05）；NaHCO3组病死率略高于L－Arg组，但差异不显著（P＞0．05）。试验表明：在生产实际中，日粮中添加1％的L－Arg或0．3％的NaHCO3均可很好地预防因腹水综合征引起的死亡；在日粮精氨酸含量为1．35％和1．18％的基础上额外添加1％的L－Arg是有益的。     

肺动脉高压综合征发病过程中肉鸡血清和肺脏iNOS和cNOS活性变化

常规饲养条件喂养的大群AA肉鸡，按临床症状分为肺动脉高压组（M组），肺动脉高压腹水组（S组）和正常对照组（C组）。分别测定21、28、35和42日龄S组、M组和C组肉鸡的腹水心脏指数（AHI）、全心与体重比（WH／BW）、平均肺动脉高压（mPAP）、血清一氧化氮（NO）水平、肺脏和血清cNOS和iNOS活性。试验结果表明：（1）S组和M组全心与体重比值（TV／BW）以及S组血清NO水平均从28日龄起显著或极显著高于C组（P〈O．01或P〈0．05）；（2）S组肺组织cNOS水平显著或极显著低于C组（P〈0．01或P〈0．05）；（3）S组肺组织iNOS在21、35和42日龄显著或极显著高于C组（P〈0．01或P〈0．05）；（4）S组从28日龄起血清中cNOS和iNOS与C组差异显著或极显著（P〈0．01或P〈0．05）；（5）正常对照组肉鸡血清中iNOS活性在21、35和42日龄均显著或极显著低于血清中cNOS活性（P〈0．01或P〈0．05）。此研究结果提示cNOS和iNOS活性的变化与PHS发病机理有着密切的关系，并在其中发挥着重要的作用。     

环境低温和T3对肉鸡内皮素、一氧化氮和肺动脉压的影响

20 0只 AA肉鸡随机等分为对照组 (C)和试验组 (T) ,C组和 14日龄前 T组鸡按常规饲养。 T组自 14日龄起舍温从 2 5℃起每天降 1～ 2℃逐渐降至 12℃ ,同时在日粮中按 1.5 m g/ kg的剂量添加三碘甲腺原氨酸 (T3 )以诱发肺动脉高压综合征 (PHS)。分别于 2 1、2 8、35、42、49日龄测定 2组肉鸡平均肺动脉压 (m PAP)、红细胞压积 (PCV)、右心全心比 (RV/ TV)、血浆内皮素 (ET- 1)及一氧化氮 (NO)水平 ,同时记录 PHS发病率。结果显示 ,试验组肉鸡 m PAP升高 ,PHS发病率增加 ;PCV、RV/ TV及血浆 ET- 1水平与对照组相比都显著升高 (P<0 .0 1) ;m PAP变化与血浆 ET- 1含量变化之间存在显著正相关 ,2组间血浆 NO水平无显著差异 (P>0 .0 5 ) ,但都出现随日龄增加血浆 NO水平升高的现象。     

静脉注射L-氨基胍对肉鸡肺动脉压及其相关指标的影响

按常规饲养条件饲养AA雄性肉鸡120羽，30日龄时随机分为试验组（T组）和对照组（C组）。T组肉鸡静脉注射L-AG（40mg／kg），C组肉鸡静脉注射生理盐水。分别在注射L-AG和生理盐水1、2、4h后测定平均肺动脉压（mPAP）、诱导型一氧化氮合酶（iNOS）活性、原生型一氧化氮舍酶（cNOS）活性、一氧化氮（NO）含量、红细胞压积（PCV）、电解质浓度、pH、超氧化物歧化酶（SOD）活性、过氧化氢酶（CAT）活性和丙二醛（MDA）含量。结果显示：（1）试验组mPAP、NO含量和iNOS活性均显著或极显著低于对照组（P〈0．05或P〈0．01）；（2）PCV和Ca^2＋在给药后2h和4h与对照组差异显著（P〈0．05）；（3）K^＋浓度在给药1h和2h后显著或极显著低于时照组（P〈0．05或P〈0．01）。结果表明，L-AG通过抑制iNOS活性，引起肉鸡肺动脉压的升高，从而推测iNOS具有调节肉鸡体内mPAP的作用并与肉鸡肺动脉高压综合征发生有着密切的联系。     

高盐负荷诱发肉鸡肺动脉高压-腹水综合征

为探讨肺动脉高压在高盐负荷所致肉鸡腹水综合征发生发展的作用。将160只AA商品代肉仔鸡常规饲养至7日龄,随机分成对照组和试验组(饮水中添加0.30%氯化钠),分别于处理后1、2、3、4、5、6周,每组随机抽取8只鸡,利用右心导管法测定平均肺动脉压(mPAP),用温氏法检测红细胞压积(PCV),同时测定腹水心脏指数(AHI),统计腹水发生率。结果表明:(1)高盐负荷诱发肉鸡肺动脉高压,高盐处理1周试验组肉鸡肺动脉压升高为2.91±0.29kPa,显著高于对照组2.18±0.40kPa(P<0.05);并在整个处理期间持续升高,均显著(P<0.05)或极显著(P<0.01)地高于对照组;(2)高盐负荷诱发肉鸡AS,整个试验期间试验组的累计腹水发生率(16.3%)极显著高于对照组(2.5%)(P<0.01);(3)自分组后1周试验组的红细胞压积显著(P<0.05)或极显著(P<0.01)高于对照组,且与mPAP极显著相关(15～50日龄,r=0.612,P<0.01);(4)高盐负荷诱发肉鸡右心肥大,处理后2周试验组的AHI显著增高(P<0.05),与mPAP显著相关;并在整个处理期间相关程度逐渐密切(22日龄,r=0.532,P<0.05;50日龄,r=0.756,P<0.01)。这些结果说明肺动脉高压是高盐负荷所致肉鸡AS的中心环节,并且与右心肥大密切相关。     

硝苯地平对肉鸡肺动脉压和腹水综合征的影响

肉鸡的腹水综合征（AS）是普遍发生于商品代肉仔鸡群的一种疾病。其特征是右心肥大、肝脏肿大及明显的腹腔积水。Andrew等（1989）和Juian等（1993）根据肉鸡腹水综合征发病的病理变化和长期研究结果，提出肉鸡肺动脉高压假说即发病因子→缺氧→肺动脉高压→右心肥大→右心室衰竭→肝脏瘀血→腹水和死亡。其中肺动脉高压和右心肥大成为发病的关键环节。     

Effect of L-NAME on pulmonary arterial pressure,plasma nitric oxide and pulmonary hypertension syndrome morbidity in broilers

1. Experiments were conducted to evaluate the effect of a synthetic inhibitor of nitric oxide (NO) synthase (L-NAME) on pulmonary arterial pressure (PAP) and pulmonary hypertension syndrome (PHS) morbidity in broilers. 2. In Experiment 1, broilers were infused intravenously with L-NAME, and the mean pulmonary arterial pressure (mean PAP) and plasma NO were measured at 0, 1, 2 and 4 h after the start of infusion. The mean PAP increased and plasma NO was reduced at 1 to 2 h in broilers treated with L-NAME. 3. In Experiment 2, 180 Arbor Acres broilers were evenly divided into three groups: a control group (group C), and two groups exposed to low environmental temperatures and fed a 3, 3, 5-triiodothyronine (T3) supplemented diet alone (group A) or also including 100 ppm L-NAME (group B). 4. The PHS morbidity of group A was higher than for group C but lower than for group B. Plasma endothelin-1 was higher in broilers in groups A and B than in group C. Plasma NO was not significantly lower in broilers of group B when compared with those in group A. 5. The right/total ventricular weight ratio (RV/TV) and mean PAP were higher in groups A and B than in group C, and the RV/TV ratio increased one week earlier in group B than in group A. 6. These results suggest that L-NAME increases broiler PAP by inhibiting the endogenous synthesis of NO, leading to pulmonary hypertension, right ventricular hypertrophy and the increased morbidity of PHS in broilers.     

The effects of dietary flax oil and antioxidants on ascites and pulmonary hypertension in broilers using a low temperature model

1. Three experiments were conducted using a low temperature model to induce pulmonary hypertension (PH) and ascites in broiler chickens. Diets containing 25 g or 50 g flax oil/kg food and control diets with an equivalent amount of animal/vegetable (A/V) blend oil, with and without supplemental antioxidants (vitamin C and vitamin E) were used. The amount of PH was assessed by the ratio of right ventricle weight to total ventricle weight (RV/TV ratio). Birds were considered to suffer from pulmonary hypertension syndrome (PHS) if the RV/TV ratio was greater than 0.299. 2. In experiment 1, the test diets contained 50 g oil/kg food and were given during the grower period only. Birds fed on the flax oil diet tended to have a lower incidence of PHS, ascites and lower RV/TV ratios than birds fed on the control diet. However, when the flax oil diet was supplemented with antioxidants, the incidence of ascites, PHS, haematocrit and whole blood and plasma viscosity increased compared with birds fed on the flax oil diet without antioxidants. These effects were not seen in experiment 2, when the test diets containing 30 g oil/kg food (25 g flax oil plus 5 g A/V blend oil/kg food compared to 30 g A/V blend oil/kg food) were given during the grower period. However, in experiment 3, when the test diets containing 30 g oil/kg food were given from day 1 to week 8, birds fed on the control diet supplemented with antioxidants had a higher incidence of PHS than those fed on the control diet alone. 3. In all 3 experiments, there was no significant effect of dietary fat source or supplemental antioxidants on total food intake or food conversion. 4. We conclude that diets containing 50 g flax oil/kg food tend to reduce the incidence of PHS and ascites in broilers using a low temperature model but the results were not statistically significant. In some cases, supplementing diets with a combination of vitamin E and vitamin C increased the incidence of ascites and PHS.     

Effects of early feed restriction and cold temperature on lipid peroxidation, pulmonary vascular remodelling and ascites morbidity in broilers under normal and cold temperature

Two experiments were conducted to evaluate the effects of early feed restriction on lipid peroxidation, pulmonary vascular remodelling and ascites incidence in broilers under normal and low ambient temperature. In experiment 1, the restricted birds were fed 8h per day either from 7 to 14 d or from 7 to 21 d, while the controlled birds were fed ad libitum. In experiment 2, the restricted birds were fed 80 or 60% of the previous 24-h feed consumption of full-fed controls for 7 d from 7 to 14 d. On d 14, half of the birds in each treatment both in experiment 1 and experiment 2 were exposed to low ambient temperature to induce ascites. Body weight and feed conversion ratio were measured weekly. The incidences of ascites and other disease were recorded to determine ascites morbidity and total mortality. Blood samples were taken on d 14, 21, 28, 35 and 42 to measure the plasma malondialdehyde (MDA), superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px). On d 42, samples were taken to determine the right/total ventricular weight ratio (RV/TV), vessel wall area/vessel total area ratio (WA/TA) and mean media thickness in pulmonary arterioles (mMTPA). Low-temperature treatment increased plasma MDA concentration. When broilers were exposed to a cool environment for 3 weeks, plasma SOD and GSH-Px activity were decreased compared with normal-temperature chicks. RV/TV, WA/TA and mMTPA on d 42 were increased in birds exposed to cold, consistent with the increased pulmonary hypertension and ascites morbidity. Early feed restriction markedly decreased plasma MDA concentration. The plasma SOD and GSH-Px activity of feed-restricted birds were markedly higher than those fed ad libitum on d 35 and d 42. All early feed restriction treatments reduced ascites morbidity and total mortality. On d 42, the RV/TV, WA/TA and mMTPA of feed-restricted broilers were lower than that of the ad libitum-fed broilers. The results suggested that early feed restriction alleviated the lipid peroxidation, promoted the activity of enzymatic antioxidant and inhibited pulmonary vascular remodelling. These changes might be associated with reduced ascites incidence.     

l-Arginine inhibiting pulmonary vascular remodelling is associated with promotion of apoptosis in pulmonary arterioles smooth muscle cells in broilers

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.     

The effect of dietary l-carnitine supplementation on pulmonary hypertension syndrome mortality in broilers exposed to low temperatures

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.     

L-arginine prevents reduced expression of endothelial nitric oxide synthase (NOS) in pulmonary arterioles of broilers exposed to cool temperatures

This study investigated nitric oxide synthase (NOS) expression in the endothelium of pulmonary arterioles of broilers during the development of pulmonary hypertension syndrome (PHS). PHS was triggered by exposing broilers to sub-thermoneutral (cool) temperatures and an additional 1.0% L-arginine was added to the basal diet to evaluate the effects of supplemental L-arginine on nitric oxide (NO) production, endothelial NOS expression, and the incidence of PHS. Cumulative mortality from PHS, right/total ventricle weight ratios (RV/TV), and body weights were recorded. Plasma NO concentration and NOS expression in the endothelium of pulmonary arterioles with an outer diameter ranging from 100 to 200 microm were determined. Birds exposed to cool temperatures had increased pulmonary hypertension and PHS mortality and diminished endothelial NOS expression. Supplemental dietary L-arginine reduced PHS mortality and elicited higher NOS expression within the pulmonary endothelium coincident with elevated NO production. The results demonstrated that broilers developing PHS exhibited diminished NOS expression in the endothelium of their pulmonary arterioles. Supplemental L-arginine prevented the reduced expression of NOS in the pulmonary endothelium, which might contribute to the increased production of NO by the pulmonary vasculature.     

Broiler pulmonary hypertension syndrome. I. Increased right ventricular mass in broilers experimentally infected with Aegyptianella pullorum

Infection with the obligatory intra-erythrocytic anaplasma-like rickettsia Aegyptianella pullorum in 4-week-old broilers at a moderate altitude of 1,200 m produced a significant increase in the mean relative right ventricular (RV) mass (RV: TV) from 0.23 in the controls to 0.31 in the infected group. This was accompanied by an increase in the number of birds suffering from severe RV hypertrophy from 14.3% in the controls to 50% in the infected group. Pulmonary hypertension and subsequent RV hypertrophy could have been caused by the severe anaemia experienced in the course of the infection or by metabolic or biochemical action of A. pullorum. As the agent does not occur on commercial broiler farms, it cannot play a practical role in the broiler ascites syndrome.     

L-Arginine inhibiting pulmonary vascular remodelling is associated with promotion of apoptosis in pulmonary arterioles smooth muscle cells in broilers

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.     

Changes in pulmonary arteriole protein kinase calpha expression associated with supplemental L-arginine in broilers during cool temperature exposure

The present study was conducted to examine the effect of supplemental L-arginine on pulmonary arteriole protein kinase Calpha (PKCalpha) expression in broilers exposed to cool temperature, to investigate further the molecular mechanisms of supplemental L-arginine on modulating pulmonary vascular functions in hypertensive broilers. Broilers were subjected to sub-thermoneutral (cool) temperature to induce pulmonary hypertension syndrome (PHS), and an additional 10 g/kg L-arginine was added to the basal diet to evaluate the effects of supplemental L-arginine on PHS mortality, plasma nitric oxide (NO) production and pulmonary arterioles PKCalpha expression. Supplemental L-arginine reduced PHS mortality but did not affect right/total ventricle (RV/TV) ratios in clinically healthy birds. Birds fed additional L-arginine had increased plasma NO and decreased PKCalpha protein expression in pulmonary arterioles; NO production was negatively correlated with PKCalpha expression. These results demonstrated that supplemental L-arginine diminished PKCalpha expression in birds exposed to cool temperature. It is suggested that NO-induced loss of PKCalpha expression might be partially responsible for its effects on dilating pulmonary vasculature and inhibiting pulmonary vascular remodelling in vivo.     

Reduced PKCalpha expression in pulmonary arterioles of broiler chickens is associated with early feed restriction

OBJECTIVE: The present study was conducted to investigate the effect of early feed restriction on protein kinase Calpha (PKCalpha) expression in pulmonary arterioles, which has been revealed to promote pulmonary vascular remodeling in pulmonary hypertensive broilers. METHODS: A total of 270day-old mixed sex commercial broilers were randomly distributed to a normal temperature control group (NT), a low temperature control group (LT) and a low temperature plus feed restriction group (LR). The PHS incidence, the right/total ventricular weight ratio (RV/TV), the vessel wall area/vessel total area ratio (WA/TA), the mean media thickness in pulmonary arterioles (mMTPA) and the expression of PKCalpha in the pulmonary arterioles were measured weekly. RESULTS: Low temperature treatment significantly increased the PHS mortality. The RV/TV, WA/TA and mMTPA values of group LT were significantly elevated compared with those of group NT on d 35 and 42. The LT chickens had increased PKCalpha expression compared with their NT counterparts on d 28 and afterwards. Feed restriction reduced the PHS mortality, RV/TV, WA/TA and mMTPA in cold-exposed broilers. The LR chickens had much lower PKCalpha expression in pulmonary arterioles than the LT chickens. CONCLUSION: Early time feed restriction inhibited pulmonary vascular remodeling in broilers, which might be partly attributed to reduced PKCalpha expression in pulmonary arterioles.