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1.
静脉注射纤维素粒子复制肉鸡肺动脉高压模型,观察肺小动脉中膜5-羟色胺(5-HT)表达和肺小动脉管壁病理形态学变化,探讨5-HT与肺血管重构的关系。80羽科宝肉鸡分为对照组(n=30)和试验组(n=50)。20日龄时,试验组每羽鸡静脉注射0.3 mL的纤维素悬液;对照组每羽鸡静脉注射等体积生理盐水。记录肺动脉高压综合征(PHS)发病率,并分别于21、28、35、42 d从各组随机抽样,测定右心室/全心室质量比(RV/TV)、红细胞压积(PCV)、血红蛋白(Hb)、肺小动脉管壁面积/管总面积(WA/TA)、平均中膜厚度(mMTPA)和肺厚壁末梢血管百分比(TWPV%);采用免疫组化方法标记5-HT,并用病理图像分析软件检测肺小动脉5-HT的量。结果表明:试验组肉鸡PHS发病率显著高于对照组(P<0.05);RV/TV值在35、42 d时显著升高(P<0.05);PCV在28、35 d时显著升高(P<0.05);Hb值在35 d时显著升高(P<0.05);血管mMTPA、WA/TA和TWPV%在35、42 d时均显著升高(P<0.05);肺小动脉5-HT含量升高,在各时间点均差异显著(P<0.05),且5-HT含量...  相似文献   

2.
低温致肉鸡腹水综合征及用L-精氨酸的预防   总被引:3,自引:1,他引:2  
40 0只 1日龄 AA肉鸡 ,14日龄时保优淘弱 ,随机分群 ,其中 10 0只为正常温度 (2 0℃ )对照组 ,15 0只为低温(11℃ )试验组 ,10 0只为低温 (11℃ )试验鸡日粮添加 1%L -精氨酸组 ,用单因子低温诱发肉鸡腹水综合征 ,于不同时间分别用红细胞压积、心脏指数、腹水和心电图的各导联波幅变化判定肉鸡腹水综合征。结果表明 :环境温度为 11℃时 ,低温试验组肉鸡复制出腹水综合征模型 ,腹水综合征发生率为 9.33%、心脏指数 (RV/ TV)为 15 .3%(>0 .2 5 )、红细胞压积 (PCV)为 2 1.33%(>36 %)、心电图 导联 S波振幅为 0 .39m V和净增重为 0 .0 9kg,均显著地高 (低 )于正常对照组 (3%、4%、10 %、0 .0 8m V、0 .5 2 kg) (P<0 .0 1)。日粮添加 1%L-精氨酸的低温试验肉鸡腹水综合征发生率为 3%、心脏指数为 9%、PCV为 12 %、心电图 导联 S波振幅为 0 .17m V、净增重为 0 .5 2 kg,与低温试验组比较 ,差异显著 (P<0 .0 1) ;与对照组比较 ,差异不显著 (P>0 .0 5 ) ,说明 L -精氨酸能够增加肉鸡体重、降低腹水综合征的发生。  相似文献   

3.
环境低温和T3对肉鸡内皮素、一氧化氮和肺动脉压的影响   总被引:4,自引:2,他引:2  
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。  相似文献   

4.
静脉注射纤维素微粒诱发肉鸡腹水综合征模型的建立   总被引:1,自引:0,他引:1  
通过翅静脉注射CM-32纤维素微粒,观察血清白蛋白(ALB)、总蛋白(TP)、血细胞压积(PCV)、血红蛋白(Hb)、腹水等方面的变化,探讨建立肉鸡腹水综合征(AS)模型的可行性。试验分为2组,试验组在20日龄时注射0.3 mL纤维素悬液,对照组注射等量生理盐水。饲养期间统计临床型AS的发病率,并分别于21、28、35、42日龄从各组随机抽样,测定右心/全心重量比值(RV/TV),检查ALB、TP、PCV、Hb、腹水液等。结果试验组AS发病率(12%)显著高于对照组(3.3%),RV/TV值显著增加。纤维素微粒阻塞在肺血管,引起明显的炎性细胞聚集和肉芽结缔组织增生。试验组血清ALB、TP在42日龄明显低于对照组,PCV在28、35日龄时显著高于对照组(P<0.05),Hb在35日龄时显著高于对照组(P<0.05),其腹水液为典型的漏出液,表明翅静脉注射CM-32纤维素微粒成功诱发了AS。  相似文献   

5.
5-羟色胺(5-HT)介导的肺血管重构是肉鸡肺动脉高压综合征(PHS)形成的重要病理机制,而5-羟色胺转载体抑制剂已被证明能够抑制肉鸡肺血管重构,降低PHS的发病率,但其机理尚不十分清楚.为了从肺组织胶原蛋白沉积的角度探讨5-羟色胺转载体抑制剂抑制肉鸡肺血管重构的机理.本试验采用翅静脉注射纤维素颗粒的模型诱发肉鸡PHS,分别给诱病肉鸡灌服两种5-羟色胺转载体抑制剂,即氟西汀(fluoxetine)和西酞普兰(citalopram).使用分光光度法测量肉鸡肺组织胶原蛋白含量,采用ELISA方法测量肺组织5-羟色胺浓度,观察各组肉鸡肺组织胶原蛋白含量和5-羟色胺浓度的差异.结果显示,发病组肉鸡肺组织5-羟色胺浓度和胶原蛋白含量高于正常对照组肉鸡,而氟西汀和西酞普兰均能降低PHS肉鸡肺组织胶原蛋白含量和5-羟色胺浓度,表明5-羟色胺转载体抑制剂能降低肺成纤维细胞合成胶原蛋白的能力,进而影响肺血管重构和PHS的发生.  相似文献   

6.
将380只AA商品肉鸡随机分为A组100只,B、C、D和E组各70只,14日龄前常规饲养。14日龄后,B、C、D和E组舍温按每日1~2℃由25℃、逐步降至12℃,同时日粮中按1.5mg/kg的剂量添加T3以诱发肺动脉高压综合征(PHS);C、D组在日粮中分别按500、100mg/kg的剂量添加维生素C和E;而E组同时添加维生素C和E,A组仍常规饲养,至试验结束。记录每周各组鸡群的PHS发病数、平均体质量和采食量,并每周每组取10只鸡采血和扑杀,测定其红细胞压积(PCV)、血浆、肺和肝组织的超氧化物歧化酶(SOD)及脂质过氧化物的降解产物丙二醛(MDA)浓度;取心脏测定其右心室和全心室质量比(RV/TV)。结果显示,环境低温和日粮添加T3极显著增加了肉鸡PHS的发病率(P<0.01)。C、E组的肉鸡PHS发病率以及血浆、肺和肝组织的MDA值均极显著降低(P<0.01),血浆、肺和肝组织的SOD值均极显著增加(P<0.01),但增重、饲料转换率、血液PCV值和心脏指数RV/TV值未发生改变;D组5周龄后的血浆MDA值则极显著降低(P<0.01)以及血浆、肺和肝组的SOD值极显著增加(P<0.01),而肺和肝组织的MDA值和肉鸡PHS发病率未发生改变。由此表明,日粮添加维生素C明显阻断了低温和T3条件下肉鸡体内脂质过氧化过程,有效清除了体内自由基,显著增强了体内抗氧化能力,成功防制了肉鸡PHS的发生;日粮中同时添加维生素C和E使低温加T3条件下的肉鸡体内抗氧化能力进一步加强;但维生素C或/和E未能改变在环境低温和日粮添加T3诱病条件下肉鸡的增重和饲料转换率,而日粮中单独添加维生素E则使低温加T3条件下的肉鸡体内抗氧化能力有一定的增强作用,但并未改变肉鸡PHS的发病率。  相似文献   

7.
本试验对引入青海高原西宁地区的35只西德长毛兔原种免及34只第一代仔免进行了标准肢导联、加压单极肢导联共6个导联的心电图描记。结果发现试验兔皆为窦性心律,种兔组和仔兔组的平均 R-R 间期分别为0.229±0.022和0.212±0.023秒,心率为262±25和283±31次/分,QRS 综合波平均心电轴分别为+32.2±18.8°和+55.5±26.4°。两组兔的 P 波和 T 波在Ⅰ、Ⅱ、Ⅲ和 aVF 导联皆呈正向,aVR 导联均为负向,在 aVL 导联上,P 和 T 波多数低平,不易辨别波向。试验兔Ⅰ、Ⅱ、aVF 导联的 QRS 综合波主棘波绝大多数为正向,呈 qR、R 或 Rs 型,aVR 导联多呈负向,呈 QS、rS 或 Qr 型,Ⅲ导联在种兔组以 RS 型为主,仔兔组以 Rs 型为主,aVL 导联在种兔组绝大多数呈 qR 型,而仔兔组 qR、R 与 Qr 型各约占一半。所测西德长毛免心电图的各项指标与平原上西德长毛兔和其它兔种大致相同,由此可以认为本次测定结果能够作为青海高原西宁地区西德长毛兔心电图的正常指标。  相似文献   

8.
对雷州山羊心电图测定与分析,了解雷州山羊心电图特征,并与人类心电图进行比较,以期为雷州山羊实验动物化提供心电图基本资料。用XDH-3型心电图仪测定安静及全清醒状态的雷州山羊13头,测定结果:①心电图均为窦性心律。②P波Ⅰ、Ⅱ、aVL导联直立,Ⅲ、aVF导联多为低平,aVR导联倒置,V1~V6导联直立。QRS波Ⅰ导联形态呈rsR型、qR型或qr型;Ⅱ导联呈rsR型、qR型或qr型;Ⅲ导联呈QS型或qr型;AVR导联呈QS型或RS型;AVL导联呈R型或QS型;AVF导联呈Qr型或qr型;V1~V6导联呈rs型或qR型。T波Ⅰ、Ⅱ导联直立;Ⅲ、aVR导联倒置;aVF导联负正双向或直立;V1~V6导联以负正双向为主,部分为直立尖锋或直立高尖锋。P波振幅变动范围为0.02~0.10 mV,在Ⅰ、Ⅱ、aVR、V5导联中最高。③P波时限变动范围为0.02~0.05 s;Q波时限介于0.01~0.03 s之间;Q波时限介于0.01~0.03 s之间;R波时限介于0.01~0.04 s之间;S波时限介于0.01~0.03 s之间;QRS综合波时限介于0.03~0.08 s之间;T波时限介于0.02~0.07 s之间;Q-T期间各导联时限介于0.28~0.36 s之间。④心电轴:无偏5例(占38.46%),右偏7例(占53.85%),左偏1例(占7.69%)。雷州山羊心率及心电图P波方向与人窦性P波方向基本一致,心电轴右偏,QRS波时限比人类短。  相似文献   

9.
对雷州山羊心电图测定与分析,了解雷州山羊心电图特征,并与人类心电图进行比较,以期为雷州山羊实验动物化提供心电图基本资料。用XDH-3型心电图仪测定安静及全清醒状态的雷州山羊13头,测定结果:①心电图均为窦性心律。②P波Ⅰ、Ⅱ、aVL导联直立,Ⅲ、aVF导联多为低平,aVR导联倒置,V1-V6导联直立。QRS波Ⅰ导联形态呈rsR型、qR型或qr型;Ⅱ导联呈rsR型、qR型或qr型;Ⅲ导联呈QS型或qr型;AVR导联呈QS型或RS型;AVL导联呈R型或QS型;AVF导联呈Qr型或qr型;V1-V6导联呈rs型或qR型。T波Ⅰ、Ⅱ导联直立;Ⅲ、aVR导联倒置;aVF导联负正双向或直立;V1-V6导联以负正双向为主,部分为直立尖锋或直立高尖锋。P波振幅变动范围为0.02-0.10 mV,在Ⅰ、Ⅱ、aVR、V5导联中最高。③P波时限变动范围为0.02-0.05 s;Q波时限介于0.01-0.03 s之间;Q波时限介于0.01-0.03 s之间;R波时限介于0.01-0.04 s之间;S波时限介于0.01-0.03 s之间;QRS综合波时限介于0.03-0.08 s之间;T波时限介于0.02-0.07 s之间;Q-T期间各导联时限介于0.28-0.36 s之间。④心电轴:无偏5例(占38.46%),右偏7例(占53.85%),左偏1例(占7.69%)。雷州山羊心率及心电图P波方向与人窦性P波方向基本一致,心电轴右偏,QRS波时限比人类短。  相似文献   

10.
本文采用标准肢导联、加压单极肢导联、胸部单极导联和 A—B 导联共11个导联对引入青海高原海拔3100米地区的新疆褐牛40头及其犊牛22头进行了心电图描记。结果发现试验褐牛皆为窦性心律,其中6例呈窦性心律不齐。成年组和犊牛组的 R—R 间期分别为0.984±0.189和0.850±0.120秒,QRS 综合波平均心电轴分别为+72.9±39.0°和+78.8±29.5°。V_2、V_3、V_4导联的 P 波和 T 波绝大多数呈贞向,QRS 综合波呈 qR 型,而 A—B 导联的 P 波和 T 波绝大多数呈正向,QRS 综合波呈 rS 型。在肢导联中,Ⅰ、Ⅱ、Ⅲ和 aVF 导联的 P波多数呈正向,aVR 导联的绝大多数呈负向,QRS 综合波波型多种多样。犊牛组与成年组心电图各波的波型和波向大致相同,但犊牛组各波和间期的时限略短。此外,在研究中还对褐牛的优选导联及放牧家畜心电图描记的有关问题做了初步探讨。  相似文献   

11.
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.  相似文献   

12.
观察自然腹水症肉鸡的红细胞压积(PCV)、右心/全心比(RV/TV)和A超的变化,同时用中西医结合的方法对肉鸡腹水症进行防治,结果表明,与对照组相比,腹水肉鸡PVC、RV/TV明显升高(P<0.01),腹水鸡A超检查出现特异增宽的水平波段.用中药和尿酶抑制剂(氢醌)结合的方法对肉鸡腹水症有明显预防和治疗作用.  相似文献   

13.
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.  相似文献   

14.
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.  相似文献   

15.
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.  相似文献   

16.
OBJECTIVE: The present study was conducted to examine the presence of protein kinase Calpha (PKCalpha) in the pulmonary arterioles of broilers during the development of pulmonary hypertension and pulmonary vascular remodelling. METHOD: One hundred and sixty day-old Avian-2000 broilers were divided equally into a control group and a cold temperature group. All the birds were reared in normal temperatures up to day 14, with the lighting schedule at 24 h per day. Thereafter, birds in the cold temperature group were subjected to low temperature by lowering 1-2 degrees C per day to 12-14 degrees C, and then kept constant until day 49, while birds in the control group were still brooded at normal temperatures. All the birds were fed a diet of pellets throughout the study. Samples of blood were taken from the wing vein, and of heart and lung collected after the birds were killed with an overdose of sodium pentobarbitial, at days 24, 32, 39 and 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 assessed by immunohistochemistry and quantified by measuring optical density (OD) using computer-image analytic software. RESULTS: The incidence of pulmonary hypertension syndrome (PHS) was 12.5% in birds exposed to cold, and 3.75% in the control group (P<0.05). PCV in the cold temperature group was 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 (P<0.05). The OD values were not significantly increased before day 32 (P>0.05), however, one week later (at day 39 of age), the difference between the two groups was significant (P<0.05). The increased PKCalpha expression was positively correlated with the values of mMTPA and WA/TA. CONCLUSION: PKCalpha expression was up-regulated during the development of pulmonary hypertension. The activation of PKCalpha might be involved in the development of pulmonary vascular remodelling.  相似文献   

17.
Increased metabolic rates, pulmonary hypertension and cardiac dysfunction are the most important features of the ascites syndrome in broiler chickens. However, the mechanism of cell injury causing the pathogenesis of the syndrome is not clearly understood. Our study aimed to examine the generation of hydroxyl radicals (OH*) in broiler chickens experiencing ascites. The hundred and fifty 1-d-old chickens were purchased from a local hatchery and reared in an open poultry house for 46 d. They were divided at random into three groups and ascites was induced in two groups by exposing them to low temperature or administration of triiodothyronine (T(3)). The third group served as control and was reared normally. Haematological, biochemical and pathological tests were used to determine the incidence of ascites: including total red blood cell (RBC), packed cell volume (PCV), release of alanine transaminase (ALT) and aspartate transaminase (AST) and ratio of right ventricular weight to total ventricular weight (RV/TV). A salicylate hydroxylation method was used to examine the generation of hydroxyl radicals (OH*) in treated groups. TWo hydroxylated salicylic acid metabolites, 2,3- and 2,5-dihydroxy benzoic acid (2,3- and 2,5-DHBA), were measured by HPLC to detect the generation of OH*. An ascites syndrome was observed in T(3) and low-temperature treated groups, as shown by necropsy changes and increases in f RBC, PCV, ALT, AST and the ratio of RV/TV. Concentrations of 2,3- and 2,5-DHBA were increased in groups experiencing ascites compared to control group. It is suggested that reactive oxygen species that is OH* ions, may be involved in the pathogenesis of the ascites syndrome in broiler chickens.  相似文献   

18.
试验测定了常温和低温下限饲肉鸡和非限饲肉鸡体内一氧化氮(NO)含量、红细胞比容(PCV)和心脏指数的变化,以探讨早期限饲降低肉鸡肺动脉高压综合征(PHS)发病率的机理。试验结果显示低温下肉鸡的PCV值、心脏指数和PHS的发病率显著升高,NO水平在低温早期显著降低,然而随着低温时间的延长,低温处理组肉鸡的血浆NO水平反而代偿性升高。早期限饲显著降低了肉鸡生长早期的红细胞压积值,并显著降低了42日龄心脏指数和PHS的发病率。限饲鸡在限饲期间血浆NO水平显著降低,但其他阶段与非限饲鸡差异不显著。这提示早期限饲能够缓解肉鸡肺动脉高压和右心肥大的产生,其机理可能与NO和PCV改变所致的血流动力学变化有关。  相似文献   

19.
20.

Objective

The purpose of the present study was to characterize the relationship between platelet-derived growth factor β receptor (PDGF-β receptor) expression and pulmonary vascular remodeling found in broilers subjected to cold temperature beginning at 14 days of age.

Method

One hundred and sixty-one-day-old mixed-sex Avian-2000 commercial broilers were randomly divided into a normal temperature group (control) and a cold temperature group (cold). All the birds were brooded in normal temperature up to day 14, with the lighting schedule at 24 h per day. Starting at day 14, birds in the cold group were moved to a pen in the cold house and subjected to low temperature, while birds in the control group were still brooded at normal temperature. On days 14, 23, 30, 37 and 44, the right/total ventricle weight ratio (RV/TV), packed cell volume (PCV), the vessel wall area to vessel total area ratio (WA/TA), mean media thickness in pulmonary arterioles (mMTPA) and the expression of PDGF-β receptor in pulmonary arterioles were measured, respectively. Cumulative pulmonary hypertension syndrome (PHS) morbidity was recorded in each group.

Results

Cool ambient temperature increased PHS morbidity of broilers. The values of WA/TA and mMTPA were also increased significantly compared with control group. PCV values in the cold temperature group were elevated from days 30 to 44, and RV/TV ratios were increased on days 37 and 44. Cold exposure enhanced PDGF-β receptor expression in pulmonary arterioles, and the PDGF-β receptor expression was significantly correlated with pulmonary vascular remodeling that was dedicated by increased WA/TA and mMTPA.

Conclusion

The results indicated that PDGF-β and its receptor were involved in the underlying mechanisms of pulmonary vascular remodeling in pulmonary hypertensive broilers.  相似文献   

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