Failure of corticosteroid therapy for experimental acid aspiration

Early death after acid aspiration results from hypoxia and hypovolemic shock. Pharmacologic doses of methylprednisolone sodium succinate (CS) are alleged to be beneficial in the early therapy of aspiration. Aspiration pneumonia was simulated in 27 mongrel dogs. Hydrochloric acid 0.1 N (pH ≤ 1) was instilled intratracheally (1.0 ml/kg). Controls (N = 7) received acid alone. Group 1 dogs (N = 10) received acid followed 5 min later by methylprednisolone sodium succinate (CS) (30 ml/kg iv). Group 2 (N = 10) received CS 20 min before aspiration. Femoral artery and pulmonary artery catheters were inserted for pressure and cardiac output monitoring and for blood sampling. Dogs received saline solution (4 ml/kg/hr iv) for the 6 hr of the experiment. Systemic and pulmonary arterial and wedge pressures were monitored and cardiac index (CI) was calculated. Intrapulmonary shunt ($\text{Q}{}_{\mathrm{<mtext>s</mtext>}}\text{Q}{}_{\mathrm{<mtext>t</mtext>}}$) was calculated with Berggren's equation. Lung water as a percentage of lung weight (%LW) was calculated for excised lungs. Baseline and 6-h values were tabulated. Depression of CI and increased $\text{Q}{}_{\mathrm{<mtext>s</mtext>}}\text{Q}{}_{\mathrm{<mtext>t</mtext>}}$ were observed in controls. Treated animals maintained CI but shunting was not improved. Increased %LW indicated pulmonary edema in all animals. Even when given before acid aspiration, CS failed to control shunting and edema.     

Erythrocyte sodium-potassium-stimulated adenosine triphosphatase activity is not related to obesity

Altered erythrocyte sodium potassium (Na,K)-stimulated adenosine triphosphatase (ATPase) activity has been cited as having pathophysiologic significance in morbidly obese man. Previous studies have failed to consider obese patients after weight loss and, therefore, did not clarify the role of ATPase deficiency as a cause or effect of the obese state. To define more completely the possible alteration of cellular thermogenesis in obesity, a study was made of three groups of people: (1) normal weight controls; (2) morbidly obese; and (3) formerly morbidly obese patients who had lost over 100 pounds after gastric bypass surgery. Erythrocyte ATPase activity was determined by use of an assay that coupled ATPase activity with NADH oxidation in the presence of excess pyruvate kinase, lactic dehydrogenase, and phosphoenolpyruvate. This coupled assay produced a continuous slope so that activity could be calculated from the initial, maximal, linear portion of the decay trace. Results did not demonstrate any statistically significant differences in Na,K-ATPase activity between groups by analysis of variance. A nonsignificant correlation of 0.086 was seen between obesity index and Na,K-ATPase activity. It is concluded that (1) erythrocyte Na,K-ATPase activity is similar in both normal and obese individuals, (2) erythrocyte Na,K-ATPase does not change with weight loss, and (3) therefore, disordered erythrocyte thermogenesis does not have a role in the development or maintenance of obesity.