Parker Vanamee

Renal oxalosis and azotemia after methoxyflurane anesthesia.

Abstract Renal biopsies performed in seven patients after methoxyflurane anesthesia followed by renal failure disclosed a striking degree of oxalate precipitation. The extent of the precipitation paralleled, but could not fully account for, the corresponding degree of azotemia. Urinary oxalate, determined in six patients, was elevated (96 to 480 mg per 24 hours). Methoxyflurane thus appears to cause secondary hyperoxaluria, and intrarenal oxalate precipitation may occur when renal function is compromised for any reason during or immediately after surgery. Oxalate deposition, when extensive, may contribute to the severity of the renal failure.

The importance of the etiology of hypokalemic alkalosis in determining replacement therapy.

Abstract Fifteen patients with potassium depletion were studied during the development and/or correction of their depletion. Alkalosis occurred in all these subjects. In every instance the alkalosis was associated with a positive cation excess: sodium was retained in excess of chloride in those patients depleted by sodium cycle exchange resins, and chloride was lost in excess of sodium in those patients depleted with diuretics. In every instance correction of the alkalosis was associated with a negative cation excess: chloride was retained in excess of sodium in those patients depleted with diuretics, and sodium was lost in excess of chloride in those patients depleted by sodium cycle exchange resins. Potassium depletion and particularly hypokalemia may be corrected independently of the alkalosis. Chloride is necessary for the correction of metabolic alkalosis only when there has been chloride loss during the development of alkalosis.

The effect on pancreatic flow of acetylated secretin preparations.

Summary Secretin was treated with acetic anhydride and the resulting preparation (Sa) was tested in dogs with Thomas duodenal cannulas for its effect on pancreatic flow. Sa caused pancreatic secretion when given as a constant infusion or as a single intravenous injection. A single injection of a large dose of Sa was apparently less stimulatory than a comparable amount of secretin. When a large dose of Sa in the form of a single injection was superimposed on a constant infusion of either secretin or Sa, there was a significant suppression of pancreatic flow. It is postulated that acetylated secretin competes with secretin for receptor sites in the pancreas. The failure to suppress pancreatic flow completely may be related to deacetylation or to residual secretory activity of the acetylated material.