With the use of multiple injections of oleic acid, a stable model of early respiratory distress in pigs can be achieved, in spite of individual differences in sensitivity. Such a stable model allows for a diversity of studies on early respiratory distress.

We reported the case of a patient in whom severe, and ultimately fatal, pulmonary hypertension developed 1.5 yrs after transjugular intrahepatic portosystemic shunt (TIPS).Pulmonary artery pressures were not affected by 100% oxygen, prostacyclin or nifedipine. Postmortem examinations showed pulmonary and vascular abnormalities typical of pulmonary hypertension.Pulmonary artery pressures should be measured in each patient with otherwise not readily explained dyspnoea following transjugular intrahepatic portosystemic shunt. Eur Respir J., 1996Respir J., , 9, 1562 Transjugular intrahepatic portosystemic shunt (TIPS) has recently been introduced as treatment for consequences of portal hypertension, such as variceal haemorrhage and refractory ascites [1,2]. Several complications in placement of TIPS have been reported, including stent dislodgement, haemobilia, liver capsule rupture, intraabdominal bleeding, encephalopathy, haemolysis, cholestasis, renal failure and sepsis [1][2][3]. We describe a patient who developed pulmonary hypertension 1.5 yrs after TIPS insertion. Case reportA 45 year old man with alcoholic liver cirrhosis was admitted to hospital due to bleeding from large gastric varices. After initial control of the bleeding with endoscopic sclerotherapy, a TIPS was inserted. After a year without medical problems, the patient was readmitted due to bleeding originating from a gastric varix. Recatheterization with phlebography revealed subtotal stent stenosis and a large coronary vein feeding gastric varices. A second stent was inserted inside the old one and embolization of the coronary vein was performed.Six months later, the patient presented with exertional dyspnoea and syncope. His medication consisted of spironolactone, furosemide, lactulose and ranitidine. At physical examination, arterial and central venous pressures were normal. Heart rate was 84 beats·min -1 . No jaundice, ascites, oedema, cyanosis or finger-clubbing was found. Normal heart sounds and a short ejection murmur at the left sternal border were noted. The lungs were normal on examination. The liver was felt 5 cm below the right costal margin.Laboratory investigation showed mild iron deficiency anaemia (haemoglobin 5.2 mmol·L -1 ). Arterial blood gas analysis was normal. Ventilatory function was normal: total lung capacity (TLC) 7.89 L, and forced expiratory volume in one second (FEV1) 3.67 L (95% predicted). Transfer factor of the lungs for carbon monoxide was normal. Doppler ultrasound examination suggested normal TIPS function. In contrast to the chest radiographic examination obtained before the first TIPS, the heart was increased in size and lung vessels were prominent. The lung parenchyma showed no abnormalities. Cardiac ultrasound showed dilation of right atrium and right ventricle, with insufficiency of the tricuspid valve. The function and dimensions of the left ventricle were considered normal. Pulmonary ventilation and perfusion scans were normal. Continuous registration of oxygen saturation during the night revealed ...

Alveolar macrophages have recently been postulated as being involved in the aetiology of adult respiratory distress syndrome (ARDS). To evaluate their role, basal cyclic AMP levels and responsiveness of adenylyl cyclase alveolar macrophages were determined at four intermediate stages of developing respiratory distress in piglets using a protocol with repeated lung lavage. Examination of alveolar cells recovered from the subsequent lavages reveals an influx of granulocytes (neutrophils and eosinophils) within 1 h of two intensive lung lavages. During the developing respiratory distress the basal cyclic AMPlevel of alveolar macrophages increases and adenylyl cyclase responsiveness to prostaglandin E2 (PGE2) and isoprelanaline diminishes. The previously observed impairment of macrophage activity can then be explained at a subcellular level.