ABSTRACT
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.
Subject(s)
Hypertension, Pulmonary/etiology , Portasystemic Shunt, Transjugular Intrahepatic/adverse effects , Fatal Outcome , Humans , Hypertension, Pulmonary/pathology , Hypertension, Pulmonary/therapy , Male , Middle Aged , Pulmonary Artery/pathology , Time FactorsABSTRACT
OBJECTIVE: Development of a stable model of respiratory distress in pigs with oleic acid, fulfilling clinical criteria of the adult respiratory distress syndrome (ARDS). DESIGN: Eight pigs (9.1 +/- 0.7 kg) were anesthetized with pentobarbital, paralyzed with tubocurarine and mechanically ventilated with an FIO2 of 0.6, an I:E ratio of 2:3 and a PEEP of 0.2 kPa. Oleic acid (dissolved 1:1 in 96% alcohol) was administered in a series of multiple injections of 0.1 ml until PaO2 was lower than 8 kPa. MEASUREMENTS AND RESULTS: Careful titration of the oleic acid injections on guidance of the PaO2 established a reproducible respiratory distress (PaO2 = 7.3 +/- 0.8 kPa), in which gas exchange and hemodynamic variables were stable for at least 4 h. The number of oleic acid injections (22 +/- 11, mean and SD) varied between the animals. CONCLUSIONS: 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.
Subject(s)
Disease Models, Animal , Oleic Acids/administration & dosage , Respiratory Distress Syndrome/chemically induced , Swine , Animals , Blood Gas Analysis , Dextrans , Hemodynamics/physiology , Injections , Lung Volume Measurements , Oleic Acid , Pulmonary Gas Exchange , Respiratory Distress Syndrome/blood , Respiratory Distress Syndrome/physiopathologyABSTRACT
Distribution and severity of active vasoconstriction of muscular pulmonary arteries were morphometrically assessed in anaesthetized, paralysed and mechanically ventilated pigs with respiratory distress, induced by oleic acid. Vasoconstriction was deduced from the medial thickness which was measured and expressed as a percentage of external diameter. Six pigs received oleic acid (0.12 +/- 0.07 ml/kg), dissolved 1:1 in 96% alcohol, in multiple injections of 0.1 ml. Six pigs were used as controls. After the oleic acid injections a stable hypoxaemia (PaO2 = 57 +/- 8 mmHg, at an inspiratory oxygen fraction of 0.6) and pulmonary hypertension (mean Ppa = 36 +/- 2 mmHg) were obtained for several hours. Electron microscopy revealed swelling of endothelial cells with signs of degeneration. Medial thickness was far greater in the oleic acid group than in the control group; overall mean values were 8.1 +/- 3.2 and 3.8 +/- 1.7% respectively (P < 0.001). Arteries with prominent vasoconstriction were lying in clusters. This pattern was the same in dependent and non-dependent regions. We concluded that in oleic acid induced respiratory distress active vasoconstriction of muscular pulmonary arteries is an important factor in the development of pulmonary hypertension. Besides vasoconstriction, endothelial swelling and intravascular clotting may contribute to the development of pulmonary hypertension.
Subject(s)
Hypertension, Pulmonary/pathology , Oleic Acids , Pulmonary Artery/pathology , Respiratory Distress Syndrome, Newborn/pathology , Vasoconstriction , Animals , Disease Models, Animal , Female , Humans , Hypertension, Pulmonary/etiology , Infant, Newborn , Microscopy, Electron , Oleic Acid , Respiratory Distress Syndrome, Newborn/etiology , SwineABSTRACT
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 E(2) (PGE(2)) and isoprelanaline diminishes. The previously observed impairment of macrophage activity can then be explained at a subcellular level.
