Arie Keynan

Dead sea water poisoning

A unique chemical intoxication by Dead Sea water and its resultant physiological effects of combined severe hypercalcemia and hypermagnesemia are described. Of 48 adult patients, 16 had at least one severe clinical manifestation of either disturbed sensorium or a syndrome similar to adult respiratory distress syndrome. The patients had tachyarrhythmias (11 of 38, 29%), conduction disturbance (nine of 37, 24%), and a normal QTc interval in the presence of severe hypercalcemia. Combined respiratory and metabolic acidosis and concomitant extreme hypercalcemia and hypermagnesemia, reaching serum levels up to 28.8 and 33 mg/dL, respectively, were responsible for most of the clinical findings. The adult mortality was 19%. Four pediatric patients with variable degrees of intoxication survived. Discriminant function analysis determined that admission serum calcium concentration of more than 15.5 mg/dL was the best predictor of mortality. In patients with severe intoxication, supportive medical treatment, including forced diuresis, was disappointing. Early dialysis for severe cases merits further study.

The erythrocyte membrane in essential hypertension. Modified temperature-dependence of Li+ efflux.

The rate of ouabain-resistant Li+-efflux was studied in erythrocytes of normal controls and of patients with essential hypertension. Despite variability in rate, erythrocytes from normotensive persons revealed a uniform pattern of temperature dependence of the efflux, with two slopes (K = 9.4 and 19.1 kcal/mol, respectively) and a transition at about 25 degrees C. Erythrocytes from the patients showed both a higher rate of Li+ efflux and significant changes in the temperature response, with essentially a single slope (Ka = 14 kcal/mol). The data indicate localized changes in the membrane organization of hypertensive erythrocytes, involving lipid-protein interaction.

Bromosulfophthalein disposition in chronically bile duct obstructed rats

The disposition of bromosulfophthalein was studied in chronically bile duct obstructed rats. In this model a catheter was inserted into the common bile duct and the distal tip was sealed. Resumption of bile flow was achieved with great ease. Obstruction of bile duct for 18 days in rats resulted in elevated bilirubin, ALT, AST, and alkaline phosphatase levels. Portal hypertension developed within this period (11.6 +/- 0.5 in obstructed rats vs. 8.6 +/- 0.6 mm Hg in sham-operated group). After the bile duct obstruction was opened, the half-life time for elimination of bromosulfophthalein (42.30 +/- 6.47 min) was longer than in sham-operated rats (21.23 +/- 3.34 min). Plasma clearance was reduced by 70% in bile duct obstructed rats. In spite of increased bile flow rate, biliary excretion of the dye was reduced by 40% in chronically bile duct obstructed rats. Hepatic glutathione levels were significantly reduced by 20% in this model. The specific activity of glutathione S-transferase with chlorodinitrobenzene and styrene oxide, as substrates, was reduced by 50% and 30%, respectively. However, the percent of conjugated bromosulfophthalein in bile was similar to that of sham-operated rats.