Gas exchange and respiratory mechanics in moderate and severe pulmonary oedema in dogs.
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Biomedical subjects
Publications and source records attributed to D Jacobovitz-Derks.
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Twenty-two adult dogs were each given a single, 30-minute injection of 1.5 ml/kg body weight of pure triolein, and their pulmonary, hepatic, renal, and cerebral morphology was observed for 1, 2, 3, 4, 5, 6, 15, 24, and 48 hours; 3,4, and 5 days; 1 and 2 weeks; and 1 month after the injection. A picture of massive capillary occlusion by lipid droplets was followed by rapidly resolvable inflammatory pneumopathy of granulomatous type, leaving a normal lung at the end of the experiment. The cleaning of the capillaries may be attributed to the mechanical action of the blood flow and to the inflammatory reaction with evacuation of necrotic cells via the bronchial route. Transient pulmonary edema is attributed to increased pulmonary arterial pressure. There was no intravacular coagulation. The few pulmonary lesions observed after the triolein injection suggest that the chemical theory of neutral fat hydrolysis by pulmonary lipase and the toxicity of free fatty acids that are released should be reconsidered.
Electron microscopy in an infant of 4 months with pulmonary alveolar lipoproteinosis showed filling of the alveoli with osmiophilic lamellar bodies. Similar structures were present in the cytoplasm of type I alveolar epithelial cells and to a lesser extent in the capillary endothelium and interstitium. These changes represent widespread degenerative processes in the lung caused by an unidentified cytotoxic agent. In this patient the disease is comparable to the drug-induced cytotoxic animal model and differs from the dust-induced hypersecretory animal model.
This paper presents a systematic study of acute and chronic pulmonary lesions resulting from a single intravenous injection of oleic acid and a new fibrosis lung model is proposed: pulmonary interstitial fibrosis is obtained by means of a number of oleic acid intravenous injections. Nineteen adult dogs received 0.045 g/kg or 0.09 g/kg of oleic acid. A systematic morphologic study was carried out after 1, 2, 3, 4, 6, 12, 24, and 48 hours and 1, 2 and 4 weeks. Eleven other adult dogs received weekly one injection of 0.09 g/kg of pure oleic acid over a period of 1 to 3 months. Examination of the lung was carried out by means of light and electron microscopy and morphometry. An early stage characterized by the formation of thrombosis and cellular necrosis was followed by a repair stage with the proliferation of Type 2 cells and fibrotic foci in the subpleural areas. Lipid staining with Sudan IV allowed the onset and disappearance of lipid-laden macrophages to be ascertained. The late stage showed pulmonary fibrosis. The extent of the lesions is related to the number of oleic acid injections. Since interstitial pulmonary fibrosis invariably appeared, and only 2 dogs out of 11 died, the model is satisfactory for pathologist and physiologist.
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A physiological (hemodynamics, gas exchange and respiratory mechanics) and morphometric evaluation has been undertaken on six normal dogs (N) and seven dogs (F) whose lungs showed variable degrees of fibrosis produced by successive injections of oleic acid. The correlation between the degree of fibrosis and the ratio of measured to predicted alveolar surface was --0.97 (alpha < 0.01). Moderate pulmonary hypertension was present in group F. The greater the fibrosis, the more the volume/pressure curve was displaced downward and to the right. There was a good (positive or negative) correlation between the degree of fibrosis and the following data: expired quasi-static compliance, DLCO, PAO2, (A--a)Do2 and the intrapulmonary shunt. Except for the increase in shunt, the VA/Q distribution was not disturbed.