低温诱发肉鸡腹水综合征过程中肺动脉平滑肌细胞增殖的变化

本试验旨在研究低温诱发肉鸡腹水综合征(AS)过程中平滑肌细胞增殖在肺血管重塑过程中的动态变化,初步探讨肺血管重塑的机制。160只15日龄雄性AA商品代肉鸡随机分为对照组(22℃±1.5℃)和低温组(11℃±2℃)。试验持续至50日龄,期间每周每组随机取6只,取肺组织做石蜡切片,Weigert-间苯二酚复红染色,观察并测定血管重塑情况;采用免疫组织化学方法检测肺动脉增殖细胞核抗原(PCNA)蛋白表达,并对其半定量化,分析平滑肌细胞增殖情况。50日龄时统计整个饲养过程中AS发生率。结果显示:(1)低温组肉鸡AS发生率(18.75%)极显著高于对照组(1.25%)(P<0.01);(2)低温组肉鸡直径20-50μm和50-150μm肺动脉结构从36日龄开始较对照组发生了明显的重塑(P<0.01或P<0.05);(3)低温组肉鸡直径20-50μm和50-150μm的肺动脉平滑肌细胞增殖指数分别从22日龄和36日龄开始极显著高于对照组(P<0.01)。结果表明:低温诱发肉鸡AS过程中肺动脉结构发生了明显的重塑,肺动脉平滑肌细胞发生了明显的增殖,并且平滑肌细胞增殖促进了肺血管重塑,在肉鸡AS发生发展过程中起着重要的作用。     

低温诱发肉鸡肺血管重塑过程中肺动脉平滑肌细胞c-Myc蛋白表达的变化

试验旨在研究环境低温诱发肉鸡肺血管重塑过程中肺小动脉血管平滑肌细胞c-Myc蛋白的表达变化,初步探讨肉鸡肺血管重塑的发生机制.120只雄性AA商品代肉鸡15日龄时随机分为对照组((22±1.5)℃)条件下饲养)和低温组((11±2)℃条件下饲养).15～50日龄,每周每组随机取6只,取肺组织做石蜡切片,Weigert-间苯二酚复红染色,观察并测定m管重塑情况;采用免疫组织化学方法榆测肺动脉血管平滑肌细胞c-Myc蛋白表达,并对其进行半定量化.结果显示:(1)低温组肉鸡肺小动脉结构从36日龄开始较对照组发生了明显的重塑(P<0.01或P<0.05);(2)低温组肉鸡肺小动脉血管平滑肌细胞c-Myc蛋白表达从29日龄开始较对照组明显增加(P<0.01).结果表明:低温叫显诱发了肉鸡肺小动脉平滑肌细胞c-Myc蛋白的表达,且参与了肉鸡肺血管重塑的发生发展.     

环境低温对肉鸡肺小动脉壁c-mycmRNA表达的影响

对环境低温诱发肉鸡肺动脉高压综合征(Pulmonary hypertension syndrome,PHS)过程中肺小动脉壁c-mycmRNA的表达变化进行了研究,从而初步确定原癌基因c-myc在环境低温诱发肉鸡PHS过程中的参与作用,为肉鸡PHS发生机制的研究提供基础。120只雄性AA商品代肉鸡15日龄时随机分为对照组((22±1.5)℃)和低温组((11±2)℃)。15～50日龄,每周每组随机取6只,肺组织做石蜡切片,应用原位杂交染色法进行c-myc mRNA杂交,并结合图像分析法,测定环境低温诱发肉鸡PHS过程中肺小动脉壁原癌基因c-myc mRNA的表达情况。结果显示,低温组肉鸡PHS发生率(15.00%)极显著高于对照组(1.67%)(P<0.01);低温组肉鸡肺小动脉壁c-mycmRNA的表达从22日龄开始较对照组明显增加(P<0.05),从29～50日龄较对照组极显著升高(P<0.01)。结果表明,环境低温明显诱发了肉鸡肺小动脉壁c-myc mRNA的表达,且c-myc mRNA的表达参与了环境低温诱发的肉鸡PHS的发生发展。     

c-Jun在肉鸡腹水综合征过程中肺动脉壁的表达变化及维拉帕米的干预研究

本试验研究低温诱发肉鸡腹水综合征过程中肺动脉壁c-Jun的表达,及阻断钙信号对肺动脉壁c-Jun表达的影响和对肉鸡腹水综合征发生的干预情况,为肉鸡腹水综合征发生机制的研究提供基础。240只15日龄AA肉鸡分为对照组、低温组和维拉帕米组,15~50日龄每组随机取6只测定右心肥大指数,取肺组织做石蜡组织切片进行c-Jun免疫组化染色分析。结果显示,29~50日龄低温组肉鸡右心肥大指数较对照组和维拉帕米组明显升高(P0.05),低温组肉鸡20~50μm、50~100μm和100~200μm肺小动脉c-Jun阳性指数分别从22、29日龄和29日龄开始到50日龄极显著高于对照组和维拉帕米组(P0.01)。研究结果认为,低温诱发肉鸡腹水综合征过程中不同直径大小肺小动脉壁cJun表达明显增强,阻断钙信号可明显抑制肺小动脉壁c-Jun的表达和肉鸡腹水综合征的发生。     

BQ123抑制低温诱发肺动脉高压肉鸡的肺小动脉肌型化

本试验用高选择性内皮素A受体拮抗剂BQ123处理低温肉鸡的方法,通过动态观察肺动脉压及肌型、部分肌型及非肌型肺小动脉数量的变化,探讨内源性内皮素在肺血管重塑中的作用。结果显示:30日龄时,低温组平均肺动脉压极显著高于常温组、低BQ123组及高BQ123组(P<0.01);低温组肌型及部分肌型肺小动脉的占位比均极显著高于常温组、低BQ123组及高BQ123组(P<0.01);低温组非肌型肺小动脉占位比极显著低于常温组、低BQ123组和高BQ123组(P<0.01),高BQ123组显著高于低BQ123组(P<0.05)。结果表明,BQ123可明显抑制低温肉鸡肺动脉高压和非肌型肺小动脉的肌型化的发生发展,因此认为内源性ET在低温诱发肺动脉高压肉鸡肺血管重塑的发生发展过程中起重要作用。     

BQ123对低温诱发的肉鸡肺血管重塑的影响

动态观察了肺小动脉中膜平滑肌的增殖及管腔面积的改变,探讨内皮素受体拮抗剂BQ123 对低温诱发的肉鸡肺血管重塑的影响。200只16日龄AA肉鸡随机均分为4组: 常温(20 ℃)对照组、低温(7~9 ℃)组、低温低剂量BQ123组和低温高剂量BQ123组。23日龄、30日龄时测定肺动脉压,并取肺组织做石蜡切片, 以Weigert间苯二酚复红染色,形态学计算机图象分析法测定肺细小动脉外径和内径、管总面积和管腔面积,计算中膜厚度占外径百分值(%)mMTPA及管壁面积/管总面积WA/TA(%)。结果显示:(1)BQ123 抑制低温肉鸡平均肺动脉压的升高,23日龄时低温高剂量BQ123组显著低于低温组(P<0 05),30 日龄时低温低剂量BQ123 组和低温高剂量BQ123组均极显著低于低温组(P<0 01);(2)BQ123 抑制低温肉鸡肺小动脉WA/TA(%)的升高,30~50μm的肺小动脉,低温组极显著高于低温低剂量BQ123 组及低温高剂量BQ123 组(P<0 01),其它分级的肺小动脉组间差异性与此类似;(3) BQ123抑制低温肉鸡肺小动脉的mMTPA的升高,30~50μm的肺小动脉,23日龄时低温组极显著高于低温低剂量BQ123 组和低温高剂量BQ123 组(P< 0 01), 30 日龄时低温组显著高于低温低剂量BQ123组(P<0 05)、极显著高于低温高剂量BQ123组(P<0 01),30μm以下的肺小动脉组间差异性与此类似,50~120μm     

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。     

维拉帕米对肉鸡肺动脉高压发生过程中肺动脉平滑肌细胞c-Fos表达的影响

研究低温诱发肉鸡肺动脉高压过程中肺动脉平滑肌细胞c-Fos的表达情况,及钙拮抗剂维拉帕米对c-Fos表达和肺动脉压的影响,从而探讨肉鸡肺动脉高压的发生机制。180只AA肉鸡14日龄随机分为对照组、低温处理组和维拉帕米组,14~49日龄,每组每周随机取6只测定肺动脉压,取肺组织固定做石蜡组织切片进行c-Fos免疫组织化学染色分析。结果显示,低温处理1周后肉鸡肺动脉压明显升高(P0.05),20~50μm肺动脉平滑肌细胞c-Fos表达在处理后1周开始明显升高,50~100μm肺动脉c-Fos表达在处理后2周开始明显升高(P0.05),而维拉帕米组肉鸡肺动脉压和c-Fos的表达在相应的时间内较低温组明显降低(P0.05)。结果表明肺动脉平滑肌细胞c-Fos在低温诱发的肉鸡肺动脉压升高的过程中表达增强,阻断钙通道可抑制肉鸡肺动脉平滑肌细胞c-Fos的过高表达和肺动脉压升高。     

环境低温和T3致肉鸡腹水、肺动脉高压和肺微细动脉肌型化

21 0羽 AA商品肉鸡随机分为 A、B、C 3个组 ,常规饲养。 1 4日龄后 A组鸡正常对照 ,而 B、C组鸡舍温按每日1～ 2℃由 2 5℃逐步降至 1 2℃ ,同时 C组在日粮中按 1 .5 mg/ kg的剂量添加甲状腺素 T3以诱发肉鸡腹水综合征 ( as-cites syndrom e,AS)。结果表明 :低温和 T3能显著增加 AS发病率、红细胞压积 ( PCV)值、右心室与全心室重量比( RV/ TV)、平均肺动脉压 ( m PAP)和厚壁末梢血管百分率 ( TWPV % ) ( P<0 .0 1 )。从而揭示了环境低温和 T3诱发的AS患鸡已发生了肺动脉高压和肺微细血管肌型化     

红三叶异黄酮对肉鸡肺血管重构和平滑肌细胞凋亡的影响

为观察在低温环境下红三叶异黄酮对肉鸡肺血管重构和平滑肌细胞凋亡的影响,选取270只10日龄肉鸡,随机分为常温对照组(Ⅰ)、低温组(Ⅱ)和低温黄酮组(Ⅲ),每组6个重复,每个重复15只,Ⅰ组和Ⅱ组饲喂基础饲粮,Ⅲ组饲喂添加红三叶异黄酮20mg/kg的试验饲粮,分别于14,21,28,35,42日龄从各组随机抽取6只肉鸡,观察各组肉鸡肺血管病理形态学变化,检测Caspase-3和Bcl-2蛋白表达情况。结果表明,Ⅱ组肉鸡肺小动脉结构在28,35,42日龄比Ⅰ组肺小动脉管壁有不同程度增厚、管腔变窄,发生了明显的重构现象(P0.05或0.01)。Ⅲ组与Ⅱ组相比,在28,35,42日龄肺血管重构现象减轻(P0.05或0.01),肉鸡肺动脉高压综合征(PHS)发病率降低,血管平滑肌细胞Caspase-3蛋白阳性率增高,Bcl-2蛋白表达下降;表明红三叶异黄酮能有效减轻肉鸡肺血管重构,其机制可能与调节平滑肌细胞凋亡有关。     

Characteristics of the in vitro hypoxic pulmonary vasoconstrictor response in isolated equine and bovine pulmonary arterial rings

OBJECTIVE: Hypoxaemia accompanies dorsal recumbency in the horse and frequently complicates general anaesthesia. The physiology associated with this phenomenon is poorly understood. One possible cause of poor tolerance to dorsal recumbency is an absent or reduced response to hypoxic pulmonary vasoconstriction (HPV). This study compared the HPV response in isolated pulmonary artery vessels from equivalent regions of equine and bovine lung. ANIMALS: Equine and bovine, in vitro study. MATERIALS AND METHODS: Equine and bovine pulmonary arteries were removed from the lungs of euthanased horses and cattle. Measurements of isometric tension were made on isolated rings of pulmonary vessels at 37 degrees C in a Krebs' saline solution. Hypoxia was induced by bubbling with a nominally 0% O(2) gas mixture. RESULTS: A significant HPV response was observed above a baseline tension induced by phenylephrine (PE; 0.3 microm) or 5-hydroxytryptamine (5-HT; 0.1 microm). The HPV response in equine pulmonary vessels was approximately 33% less than the response observed in equivalent bovine vessels (equine 196 +/- 20%versus bovine 290 +/- 32%; p < 0.05). Removal of the endothelium (by rubbing the luminal surface) significantly reduced but did not abolish the HPV response. Incubation with the nitric oxide (NO) synthase inhibitor N-nitro-l-arginine methyl ester (L-NAME; 100 microm), or COX-1/COX-2 inhibitor indomethacin (10 microm) markedly attenuated the HPV response in equine vessels. CONCLUSIONS: These results suggest that a significant HPV response exists in isolated equine pulmonary vessels; a component of this response requires a functional endothelium. Inhibition of cyclooxygenase and NO synthase attenuated the response, suggesting the involvement of a COX product and/or NO in mediating this effect either directly or indirectly. Alternatively, a non-COX related action of the nonsteroidal anti-inflammatory drug, indomethacin, may be involved.     

Calcium antagonists,diltiazem and nifedipine,protect broilers against low temperature‐induced pulmonary hypertension and pulmonary vascular remodeling

This study was designed to determine whether calcium antagonists, diltiazem and nifedipine, can depress low temperature‐induced pulmonary hypertension (PH) in broilers (also known as ascites) and to characterize their efficacy on hemodynamics and pulmonary artery function. Chicks were randomly allocated into six experimental groups and orally administered with vehicle, 5.0 mg/kg body weight (BW)/12 h nifedipine or 15.0 mg/kg BW/12 h diltiazem from 16 to 43 days of age under low temperature. The mean pulmonary arterial pressure (mPAP), the ascites heart index (AHI), the erythrocyte packed cell volume (PCV) and the relative percentage of medial pulmonary artery thickness were examined on days 29, 36 and 43. The data showed that administration of diltiazem protected broilers from low temperature‐induced pulmonary hypertension and vascular remodeling. Although nifedipine prevented mPAP from increasing during the early stage, it did not suppress the development of PH during the late stage and did not keep heart rate (HR), PCV, AHI and the thickness of pulmonary small artery smooth muscle layer at the normal levels. Taken together, our results showed that diltiazem can effectively prevent low temperature‐induced pulmonary hypertension in broilers with fewer side‐effects and may be a potential compound for the prevention of this disease in poultry industry.     

Respiratory-induced variability of pulmonary arterial pressure measurements in cattle

The purpose of this study was to investigate the variability of the peak systolic (PAPs) and the end diastolic (PAPd) pulmonary arterial pressures induced by intrapleural pressure changes in cattle.The pleural pressure (Ppl), the electrocardiogram and the pulmonary arterial pressure (PAP) were simultaneously recorded in five healthy calves under three different conditions, i.e. normoxia (N), normoxia with an added airflow resistance (R) and hypoxia (H). PAPs, PAPd and their corresponding transmural pressures were measured and averaged over 10 successive regular cardiac cycles. The maximum Ppl changes (maxPpl) were measured on the same tracings. The variance and coefficients of variation were calculated for each set of vascular measurements.MaxPpl was significantly increased with regard to N values during R and H conditions. This increase in maxPpl induced a simultaneous rise in the variability of PAP measurements, while in each condition, this variability was greatly lowered by use of the corresponding transmural pressure.It was concluded that, in calves with high maxPpl, the influence of respiration on PAP becomes considerable. In such cases, the use of transmural pressures rather than luminal pressures can greatly reduce the variability of these pulmonary pressure measurements and therefore increase their sensitivity.     

Acute pulmonary edema after diazepam-ketamine in a dog

An 8-year-old mixed-breed dog was anesthetized for colonoscopy. Moderate sedation was produced by premedication with glycopyrrolate, acepromazine, and hydromorphone, and anesthesia was induced by IV injection of diazepam and ketamine. Frothy, reddish-colored fluid flowed from the endotracheal tube immediately after endotracheal intubation but ceased after several minutes. Furosemide was injected IV. Anesthesia was maintained by sevoflurane in oxygen. Ventilation and arterial blood pressure were satisfactory, however, after oxygen was administered to maintain normal hemoglobin saturation. Radiography revealed changes consistent with a diagnosis of pulmonary edema. The following day, ventricular premature contractions developed and atrial dissociation, valvular regurgitation, and pulmonary hypertension were diagnosed on echocardiography. The proposed etiology is either profound transient hypotension and/or pulmonary hypertension induced by ketamine. The cardiac abnormalities that were present the following day suggest that myocardial dysfunction after induction of anesthesia was more severe than was apparent as assessed by routine physical examination and monitoring methods.     

Growth-related changes in the pulmonary function of goats

Growth-related changes in pulmonary function values were investigated in 20 healthy French Alpine goats, aged between 20 and 550 days, weighing 7–55 kg. Pulmonary ventilation, mechanics of breathing and arterial oxyten tension were measured using standardized techniques and methods adapted for goats of different body sizes. The Ppl values and the tI/tTOT ratio showed no significant changes with age and body size. The ventilation values (Vt, Ve, mVI and mVE) increased linearly with growth. There was a significant correlation of age and body weight with dynamic lung compliance (Cdyn), total pulmonary resistance (RL), viscous work of breathing (Wvis tot) and minute viscous work (Wvis min) throughout the age range studied. Cdyn, Wvis tot and Wvis min increased and RL decreased with age and body weight. Arterial blood gases (PaO₂ and PaCO₂) did not show significant changes over the age range studied. Regression equations for each pulmonary function parameter are given with body weight as the independent variable. Data for the mechanics of breathing were compared with those elsewhere for cattle, horses, man and dogs.     

Post-anaesthetic pulmonary oedema in horses: a review

OBJECTIVES: To review information on the pathogenesis, diagnosis and treatment of post-anaesthetic pulmonary oedema in horses. DATABASES USED: Pubmed 1970-present, personal files.     

内皮素在肺动脉高压综合征肉鸡中的作用

通过急性试验确定内皮素（Endothelin，ET）对试验肉鸡肺动脉压的升压作用及其量效关系；在肉鸡快速生长期长时间给予ET，观察试验鸡发病率变化。结果表明：（1）在25ng／kg剂量静脉给予时，可引起肉鸡肺动脉压升高并达到与发病鸡相近的水平。（2）长期给予ET后，试验组30d发病率为6．7％，44d发病率13．3％，对照组发病率为0。同时，试验组红细胞压积（PCV）、腹水心脏指数（AHI）亦显著高于对照组。此结果表明，ET-1可通过缩血管效应引起肺动脉压升高，是致发肉鸡腹水综合征的一个重要因素。     

Post‐anesthetic pulmonary edema in two horses

Case 1 A two‐year old, 462 kg Standard bred horse was anesthetized for arthroscopy and castration. During anesthesia, hyperemia of the mucosal membranes and urticaria were noticed. During 5 hours of anesthesia subcutaneous edema of the eyelids and neck region developed. In the recovery box, the orotracheal (OT) tube was left in situ and secured in place with tape. Following initial attempts to stand, the horse became highly agitated and signs consistent with pulmonary edema developed subsequently. Arterial hypoxemia (PaO₂: 3.7 kPa [28 mmHg]) and hypocapnia (PaCO₂: 3.1 kPa [23 mmHg]) were confirmed. Oxygen and furosemide were administered. The horse was assisted to standing with a sling. Therapy continued with bilateral intra‐nasal oxygen insufflation. Ancillary medical therapy included flunixin meglumine, penicillin, gentamycin and dimethylsulfoxide. Following 7 hours of treatment the arterial oxygen tensions began to increase towards normal values. Case 2 An 11‐year old, 528 kg Paint horse was anesthetized for surgery of a submandibular mass. The 4‐hour anesthetic period was unremarkable. The OT tube was left in situ for the recovery. During recovery, the horse was slightly agitated and stood after three attempts. Clinical signs consistent with pulmonary edema and arterial hypoxemia (PaO₂: 5 kPa [37.5 mmHg]) subsequently developed following extubation. Respiratory signs resolved with medical therapy, including unilateral nasal oxygen insufflation, furosemide, flunixin meglumine and dimethylsulfoxide. The diagnosis of pulmonary edema in these horses was made by clinical signs and arterial blood‐gas analysis. While pulmonary radiographs were not taken to confirm the diagnosis, the clinical signs following anesthesia support the diagnosis in both cases. The etiology of pulmonary edema was most likely multifactorial.