Degree Of Pulmonary Edema Research Articles

Pulmonary edema induced by high intravenous doses of diatrizoate in the rat.

Using a simple, sensitive model, it has been demonstrated that intravenous administration of high doses of contrast medium can induce pulmonary edema in non-anesthetized rats. The degree of edema formation, which is dependent on the rate of injection as well as dose, is greatest immediately after injection and then decreases slowly. The amount of fluid accumulation in the lungs is related to the chemotoxicity of the medium as other solutions of equivalent hyperosmolality did not induce the same degree of pulmonary edema.

Effect of converting enzyme inhibition on pulmonary edema after microembolization.

We examined the effect of converting enzyme inhibition with captopril (SQ 14,225) on pulmonary hemodynamics and on accumulation of extravascular lung water after microembolization in dogs. Pulmonary microembolization, induced with glass beads (200 microns diam), increased the mean pulmonary arterial pressure to approximately 40 Torr in both control and captopril-treated animals. The increase in pulmonary vascular resistance (PVR) in control animals was sustained during the 75 min of study and was associated with an increase in the extravascular lung water content-to-bloodless dry lung weight ratio (W/D) from a normal value of 2.84 +/- 0.22 to 4.53 +/- 0.24 ml/g (P less than 0.01) after embolization. In the captopril-treated group, the PVR increased gradually, such that the value at 75 min postembolization was greater than in controls (P less than 0.05). The W/D in the captopril-treated group of 4.62 +/- 0.19 ml/g was greater than the value of 2.83 +/- 0.10 ml/g in nonembolized captopril-treated animals, but the degrees of edema in the control and captopril-treated animals were not different. A similar degree of embolization induced during infusion of 5 micrograms X kg-1 X h-1 of bradykinin also did not enhance the pulmonary edema, and there was also a greater increase in PVR than in control animals after embolization. These findings suggest that bradykinin does not contribute to the degree of pulmonary edema after microembolization.

Effect of Phosgene on Rat Lungs after Single High-Level Exposure

Rats were exposed under static conditions to phosgene at concentrations within the LCt50 range and above. Lungs were removed at various postexposure intervals. Degrees of pulmonary edema were estimated by increases in percentage of water in the lungs of exposed groups as opposed to control animals. Lungs were fractionated into four major subcellular organelle fractions: nuclear debris, mitochondrial-lysosomal, microsomal, and soluble (cytoplasmic). Activities of p-nitrophenyl phosphatase, cytochrome C oxidase, ATP'ase, and LDH within these fractions were decreased after phosgene exposure. There was a concomitant increase in serum LDH levels. One possible mechanism that may play a role in phosgene damage can be associated with either inhibition or loss of enzyme activities from the lung.

Pulmonary edema and ascorbic acid loss.

Loss of ascorbic acid from lung and pulmonary edema were produced in mice by intravenous injection of either adrenaline or noradrenaline (5 mumol/kg). While adrenalectomy performed before noradrenaline administration reduced the degree of pulmonary edema, a prior dose of hexamethonium accentuated this effect. Given alone, hexamethonium caused both loss of ascorbic acid and pulmonary edema. The results show that although endogenous catecholamines can potentiate the pulmonary edema produced by either adrenaline or noradrenaline, they play no specific role in the ascorbic acid loss. The evidence suggests that lung ascorbic acid levels are decreased following the development of pulmonary edema, irrespective of how it was caused.

Recurrent pulmonary edema induced by alpha 1-naphthyl thiourea.

The effects of repeated intraperitoneal injections of α-naphthyl thiourea on the pulmonary vascular bed were studied in rats. An initial injection of 2.5 or 3.5 mg of α-naphthyl thiourea per kg of body weight produced moderate pulmonary edema measured as an increase in the ratio of lung weight to body weight and large pleural effusions. Two additional doses of α-naphthyl thiourea at 2-day intervals produced lesser degrees of edema, and pleural fluid was minimal or absent. Repetition of the larger dose of α-naphthyl thiourea at daily intervals produced a constant degree of pulmonary edema. Histologically, with repeated injections, alveolar edema decreased and usually disappeared at a time when interstitial edema persisted, although in diminished amounts. Hemoconcentration and hypoproteinemia were generally found after the initial injection of α-naphthyl thiourea; various degrees of compensation were seen after subsequent doses. Tachyphylaxis to α-naphthyl thiourea was illustrated by the successive diminuti...

Mitral Stenosis and Pulmonary Fibrosis

Three patients had coexisting pneumoconiosis and mild mitral stenosis in which pulmonary edema was the presenting clinical manifestation. Hemodynamic abnormalities seemed quantitatively insufficient to account for the degree of pulmonary edema. In spite of the mild mitral stenosis, surgical relief produced a gratifying clinical response in all three patients. The discrepancy between symptoms and the hemodynamic abnormalities was consistent with a contributory role of pulmonary lymphatic obliteration. We have attempted to define the mechanism by which coexisting pulmonary lymphatic abnormalities might alter the course of heart diseases characterized by elevations of pulmonary capillary pressure. These patients also present the opportunity to review some recent concepts concerning the mechanisms of pulmonary edema.

Vagotomy-induced pulmonary edema in the guinea pig.

A method is described for measuring alterations in total thoracic mechanics during the development of vagotomy-induced lung edema in the unanesthetized guinea pig. Influences of restraint, tracheotomy, and positive-pressure ventilation on lung edema were determined prior to analysis of respiratory function. Volume-pressure relationship was obtained at inflation volumes from 2–8 ml delivered at a variety of frequencies and flow rates at intervals before and after bilateral vagotomy. Development of edema was characterized by a progressive upward shift in pressure with negligible change in compliance (ΔV/ΔP) above the tidal volume range. This shift was due mostly to an increase in the elastic component and scarcely at all to an increase in the resistive component of the volume-pressure function. Measurements revealed that the edema fulminates terminally. Good correlation was found between extent of pressure shift and increase of lung-to-body weight ratio, thereby substantiating the validity of the measurement for in vivo evaluation of degree of pulmonary edema. Attempt to use lung specific gravity as a postmortem criterion of lung edema failed because of inconstant trapping of air.

Lethal Factors in Experimental Infections of Trypanosoma equiperdum in Rats.

A biochemical and pathological study of experimental Trypanosoma equiperdum infections in laboratory-bred rats has disclosed that the animals died with a significantly reduced blood pH, lowered alkali reserve, and greatly diminished blood oxygen content, i. e., they finally succumbed to a condition of non-volatile, uncompensated acidosis. These findings are in harmony with the previously reported excessive lactic acid content and reduced oxygen content of the blood of trypanosome-infected rats (Kligler and Geiger;1 Kligler, Geiger and Comaroff2). A progressive hypoglycemia accompanied these terminal manifestations as has been demonstrated by a number of investigators.Tissue changes found at death were pronounced vasodilatation and congestion throughout the body, extreme enlargement of the spleen, varying degrees of pulmonary edema and occasionally emphysema, distension of the right heart and engorgement of the coronary vessels. The most significant development was the formation of intravascular blood clot...