The toxic oil syndrome: An example of an exogenously induced autoimmune reaction

The toxic oil syndrome (TOS) is a chemically induced autoimmune-like reaction in humans. The etiologic agent(s) have so far not clearly been identified. A short overview is given on this disease which is associated with a unique antibody specificity to cryptic epitopes of C-reactive protein in affected patients. In addition a murine model for TOS is described which suggests that genetic suscepbility might play a role in inducing a similar syndrome in mice. These differences are reflected in the immunological alterations and cytokine production caused by the toxicant.Abbreviations CRP C-reactive protein - OAA oleic acid anilide - PAP 3-phenylamino-1,2-propanediol - TOS toxic oil syndrome     

Pathogenesis of pulmonary edema associated with the adult respiratory distress syndrome.

Pulmonary edema is common cause of acute respiratory failure and can be seen in not only cardiac but also noncardiac diseases. The pathophysiologic mechanism for the development of acute pulmonary edema in any clinical situation can usually be explained alterations in the forces governing the transvascular flux of fluid in the pulmonary microvasculature, according to the Starling equation. "Cardiac" pulmonary edema is primarily due to an increase in the capillary hydrostatic pressure of sufficient magnitude to overcome the forces maintaining fluid within the vessel and the ability of the lymphatics to drain the transudated fluid. On the other hand, pulmonary edema occurring in association with noncardiac disease (e.g., sepsis, aspiration or shock) is secondary to an increase in the permeability of the pulmonary microvasculature and is referred to as noncardiogenic pulmonary edema or the adult respiratory distress syndrome. This article examines the mechanisms for the development of pulmonary edema and discusses the differences between the cardiac and noncardiac types.     

Effects of diverse regimes of artificial respiration on the course of experimental toxic pulmonary edema

In acute experiments on cats with closed chest the author studied the influence of artificial ventilation of increased frequency or volume on the pulmonary edema degree, foam formation intensity, pulmonary gas exchange and the animals survival in experimental pulmonary edema caused by intravenous infusion of mixture fatty acids. It was shown, that artificial ventilation of increased frequencies or volumes in pulmonary edema reduces the increase of the pulmonary coefficient and edema liquid quantity at the beginning of edema and it does not become stronger in following stages. Artificial ventilation of increased regimes decreases the foam formation, increases survival of the animals, delays the arterial pressure decrease, improves the pulmonary gas exchange. Artificial ventilation of increased frequency is more effective then ventilation of increased volume decreases foam formation and improves gas exchange in the lungs.     

The production of toxic shock syndrome toxins and enterotoxins by Staphylococcus aureus]

The production of toxins of the toxic shock syndrome and enterotoxins by S. aureus of clinical origin was studied by means of commercial standard antisera and standard toxins. The study revealed that among 511 strains isolated in Russia toxigenic ones constituted 41%, and among 592 strains isolated in Czechia toxigenic ones constituted 63%. The capacity for producing toxins may be used as an epidemiological marker.     

Effectiveness of artificial ventilation in oil microembolism followed by pulmonary edema]

In experiments on sodium pentobarbital (40 mg/kg, i.p.) anesthetized mongrel cats of either sex weighting from 2.0 to 4.0 kg, it was found, that in conditions of oil pulmonary microembolization, followed by pulmonary edema, the most suitable is rapid and shallow pattern of ventilation, ensuring optimal ventilation/perfusion interrelation. The oil microembolization was introduced with intravenous administration (1 mg per kg of body weight during 2 min) of olive oil. It is necessary to provide flexible regimens of artificial ventilation and conformity of respiratory pattern and body's demands can be controlled according to pHa and PaO2. It is desirable that pH and pO2 can be evaluated continuously.     

Pathogenic mechanisms of acute pulmonary edema of hemodynamic origin in rats]

In normal anaesthetized rats (pentobarbital, 40 mg/kg i.p.), intravenous injection of a bolus of vasopressin (0.3 micrograms/kg) provoked a large increase in pulmonary and in systemic blood pressures. About three minutes later, some rats (60%) developed an acute pulmonary edema (OPA), froth appearing at the trachea. Other animals presented no OPA at the 4th minute following the injection, but OPA appeared immediately when bilateral vagotomy was performed at that time. Factors explaining the appearance of OPA are mechanical ones, circulatory or respiratory, without interferences with autonomous nervous processes.     

Methadone-induced pulmonary edema.

A patient with methadone-induced pulmonary edema had increased extravascular water in the lungs and a reduced total vascular albumin space. Diuresis resulted in hypotension. These observations suggest that the appropriate treatment of this condition should be ventilatory support and restoration of plasma oncotic pressure with albumin. Diuretic therapy should be used with caution.     

Pheochromocytoma presenting with pulmonary edema and hyperamylasemia.

A 28-year-old woman was admitted to hospital with acute pulmonary edema, mild abdominal discomfort and hyperamylasemia. From the 2nd hospital day hypertensive episodes occurred daily. The furosemide screening test for renovascular hypertension revealed elevated plasma renin activity (PRA) but an intravenous pyelogram revealed a right suprarenal mass and no evidence of renovascular compression. Elevated values of plasma and urinary catecholamines indicated a pheochromocytoma, and a single chromaffin tumour was resected. It is important to monitor left ventricular filling pressure during operative removal of a pheochromocytoma. Postoperatively the patient had normal blood pressure and PRA. Decreased urinary amylase clearance and abnormal pancreatic and salivary amylase isoenzymes were found.