IMAGING DIAGNOSIS—PULMONARY ALVEOLAR PROTEINOSIS IN A DOG

A young dog was presented for cyanosis and right heart failure. Radiographic and CT characteristics included right heart/pulmonary artery enlargement, hepatomegaly, abdominal effusion, and severe, generalized air‐space filling. Focal increased opacities were present in the peripheral lung, as were multiple pulmonary blebs and bullae. Echocardiographic findings were consistent with cor pulmonale and pulmonary hypertension. Bronchoscopic findings were consistent with chronic inflammation. Pulmonary alveolar proteinosis (PAP) was confirmed at necropsy. Pulmonary alveolar proteinosis is an interstitial lung disease that results in accumulation of phospholipoproteinaceous material and should be included as a differential diagnosis for dogs with these clinical and imaging characteristics.     

Effects of 12 and 17 cmH2O positive end-expiratory pressure applied after alveolar recruitment maneuver on pulmonary gas exchange and compliance in isoflurane-anesthetized horses

Objective

To compare static compliance (C_st) and alveolar–arterial oxygen tension difference [P(a–a)O₂] between positive end-expiratory pressures (PEEP) of 7, 12 and 17 cmH₂O applied after an alveolar recruitment maneuver (RM) in isoflurane-anesthetized horses.

Thrombosis of the median artery and its branches in a gelding: Clinical appearance,diagnosis and surgical management

This case report describes the clinical appearance, diagnosis and surgical management of thrombosis of the median artery and its branches in a gelding. The 4-year-old Danish Warmblood presented with acute severe progressive right front leg lameness, not responding to painkillers. Initial clinical examination including radiographs revealed no significant findings, and a scintigraphic examination showed decreased radiopharmaceutical uptake in the right front toe in comparison to the left limb. The following day, the temperature of the right front leg was significantly decreased, especially in the area distal to the carpus. No pulsation of the digital arteries could be detected. Ultrasonography showed partial thrombosis of the medial digital artery (A. digitalis palmaris medialis). Occlusion of this artery is a sporadic event with impressive clinical signs and might not be directly diagnosed due to it being a rare occurrence. Ultrasound is an excellent technique for diagnosing the presence of thrombosis and can also help delineate the extent. Our case did not respond to the initial treatment with phenylbutazone and acetylsalicylic acid. The ischaemia became even worse, requiring surgical intervention. A similar approach as for the aorta-iliac thrombosis in the hindlimb was undertaken in the front limb, which has not been described previously. The gelding recovered initially. Unfortunately, restenosis occurred and due to a poor prognosis for a second surgery, the gelding was euthanised.     

Effects of Rho kinase on p-Smad1 nuclear translocation in rat pulmonary artery smooth muscle cells

AIM: To explore the mechanism of bone morphogenetic protein (BMP) and Rho kinase signal pathways on the proliferation of pulmonary artery smooth muscle cells. METHODS: Pulmonary smooth muscle cells were isolated from the rat distal pulmonary artery and cultured. BMP and Rho kinase pathways were activated by BMP-2 and platelet-derived growth factor BB(PDGF-BB),respectively. Rho kinase inhibitor Y-27632 and MEK inhibitor U0126 were also used. Immunofluorescent staining was applied to observe p-Smad1 distribution across the nucleus, and the cells with positive p-Smad1 nuclear accumulation were counted and the nuclear translocation rate was calculated. The total p-Smad1 and its distribution across the nucleus were quantitatively determined by Western blotting. The cell proliferation was analyzed by CCK-8 assay. RESULTS: Exposure to BMP-2 significantly increased both the total amount of p-Smad1 and its nuclear accumulation in pulmonary smooth muscle cells. Pretreatment with PDGF-BB significantly decreased the nuclear accumulation of p-Smad1 induced by BMP-2 without decrease of total p-Smad1. However, pretreatment with Y-27632 or U0126 reversed the inhibitory effect of PDGF-BB on p-Smad1 nuclear accumulation. BMP-2 significantly inhibited the cell proliferation, but PDGF-BB blocked the effect of BMP-2 and significantly increased the cell proliferation. After pretreated with Y-27632 or U0126, the PDGF-BB-activated cell proliferation was suppressed.CONCLUSION: PDGF-BB-activated Rho kinase inhibits BMP-2-induced p-Smad1 nuclear translocation via MEK/ERK1/2, and increases pulmonary artery smooth muscle cell proliferation.     

40 ℃持续热应激对肉鸡股动脉压的影响

研究40 ℃持续热应激对肉鸡动脉压的影响,探讨肉鸡热应激发生发展规律.将60只25日龄商品代雄性AA肉鸡随机分为对照组(21～24 ℃,相对湿度(50±5)%)和试验组((40±0.5)℃,相对湿度(70±5)%),分组后自由采食和饮水,对肉鸡的股动脉压进行动态检测.结果显示热暴露使肉鸡平均股动脉压((16.66±0.47),(10.81±1.59) kPa)、股动脉收缩压((18.61±0.48),(12.00±1.49) kPa)和股动脉舒张压((15.68±0.47),(10.21±1.66)kPa)极显著下降(P<0.01);热暴露10 h时使股动脉收缩压最大变化速率((51.36±20.27),(32.72±4.85) kPa·s-1)显著下降(P<0.05);热暴露后2和5 h使股动脉舒张压最大变化速率((54.97±25.91),(31.88±5.49)和(53.49±22.94),(31.92±5.56) kPa·s-1)显著下降(P<0.05);热暴露后10 h股动脉舒张压最大变化速率((58.65±18.49),(18.09±4.66) kPa·s-1)极显著下降(P<0.01).平均股动脉压与呼吸频率、体温极显著负相关(r=-0.623,r=-0.642;P<0.01).结果表明,40 ℃持续热暴露,使肉鸡的股动脉压极显著下降;股动脉压短时间内极显著下降可能为肉鸡死亡的主要原因之一.     

肺动脉高压肉鸡和腹水肉鸡血清,肝,肺等组织NO含量及某些酶活性的变化

对肺动脉高压肉鸡、腹水肉鸡和正常肉鸡的血清、肺和肝的ＮＯ含量及某些酶活性的变化进行了比较。结果表明：肺动脉高压肉鸡的血清、肺和肝的ＮＯ含量显著高于正常肉鸡,差异显著（Ｐ〈０．０５）;腹水肉鸡肝ＮＯ含量显著高于正常肉鸡（Ｐ〈０．０５）,血清和肺的ＮＯ含量与正常肉鸡无差异（Ｐ〉０．０５）。肺动脉高压肉鸡血清的ＧＰＴ、ＬＤＨ－Ｌ的活性高于正常肉鸡（Ｐ〈０．０５）,腹水肉鸡与正常肉鸡无差异（Ｐ〉０．０５）;血清ＣＫ、ＡＫＰ的活性３组之间无差异。