Search

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.

Summary Suppression of external pancreatic secretion in dogs was produced by exogenous serotonin (serotonin creatinine sulfate) despite constant secretin stimulation and despite vagotomy or atropine. Attempts to modify this response, and attempts to modify the similar response to intraduodenal hypertonic feedings, by pretreatment with a number of serotonin antagonists were unsuccessful. Possible mechanisms involved in these pancreatic responses are discussed.

Changes in electrolyte metabolism in patients with neoplastic disease can be divided into three categories: 1. 1. Alterations resulting from mechanical interference by the tumor with the function of an organ. 2. 2. Abnormalities in electrolyte metabolism observed in patients with chronic disease, inanition and wasting. 3. 3. Alterations in electrolyte metabolism resulting from humoral or hormonal action of the tumor itself. Secretion of ACTH by tumors of various organs has been established and is responsible for the development of hypokalemic alkalosis. Secretion of ADH induced by tumors of the bronchus and the brain has been described in patients with hyponatremia and urinary sodium loss.

The renal transport of urate, phosphate and glucose was studied under conditions of glucose and phosphate loading in 2 patients with Fanconi syndrome and in a control subject. A definite relationship between the reabsorption of these 3 substances was established in the patients with Fanconi syndrome. Phosphate abolished the normally found uricosuric effect of glucose in the patients with Fanconi syndrome, but not in the control subject. In the absence of a glucose load, phosphate infusion had no effect on urate transport in either the patients with Fanconi syndrome or the control subject. Phosphate depressed the reabsorption of glucose during glucose loading in the patients with Fanconi syndrome, whereas little or no effect was observed in the normal subject. The administration of a phosphate load, with or without an additional glucose load, caused the complete inhibition of phosphate reabsorption in the patients with Fanconi syndrome. At similar phosphate load, phosphate reabsorption in the cont...

Sodium lactate was infused and urate clearance was measured under conditions of osmotic diuresis alone, as well as during simultaneous urate infusion. Urate clearance in the Dalmatian was not depressed by the administration of sodium lactate of 1.2–9.3 mEq/kg dl-sodium lactate, indicating that sodium lactate has no inhibitory effect on tubular secretion of urate. dl-Sodium lactate, 0.54–11.8 mEq/kg, was administered to four mongrel dogs in five experiments. In three experiments a significant drop of urate clearance in relation to filtration rate was observed. In two experiments in which urine flows exceeded 10 ml/min no significant decrease in urate clearance was recorded following dl-sodium lactate administration. The depression of urate clearance in the mongrel under conditions of moderate urine flow where reabsorption of solutes is more easily accomplished, and the absence of this effect in the Dalmatian as well as in the mongrel under conditions of vigorous diuresis where reabsorption of solutes is greatly diminished, lends support to the belief that sodium lactate depresses urate clearance by facilitating urate reabsorption in the mongrel.

SummaryRestraint-stress was induced in female CFE rats weighing between 150 and 200 g by stapling them in envelopes made of aluminum wire screening. Five mg of bovine growth hormone dissolved in 1 ml of buffer was administered subcutaneously immediately after stapling and again 10 hr later. Controls received injections of buffer or bovine serum albumin. The animals were sacrificed at 24 hr and the number of animals developing gastric erosions, the number per animal and the severity of erosions were determined with a dissecting microscope. Growth hormone provides partial but significant protection against the production of restraint-stress produced erosions, both in terms of incidence of erosions and their severity.

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.

The electrolyte abnormalities which have been described in hepatic failure include a decrease in plasma sodium, chloride, and carbon dioxide content and an elevation of lactic and pyruvic acid.* Elevation of the blood ammonia has also been reported, and, while there seems to be poor correlation between actual blood levels and symptoms of hepatic coma, there is increasing evidence that ammonia plays at least an indirect role in the production of coma.† The studies reported here were carried out in patients with liver coma in an attempt to evaluate these electrolyte alterations and to correlate the clinical symptomatology with alterations in blood ammonia levels. The results of these studies indicate that hepatic coma may in some cases be associated with a respiratory alkalosis, as evidenced by a high blood pH and a low pCO 2 level. Although there was poor correlation between blood ammonia levels per se and symptomatology, it

Human growth hormone was effective in healing erosions and controlling hemorrhage in six of eight patients with stress ulcers. This approach was based on known beneficial effects of growth hormone on nucleic acid and protein synthesis, demonstration of deleterious effects of stress on nucleic acid and protein synthesis, and demonstrated protective effects of growth hormone on animals subjected to stress. Bleeding cessation within 24 hours of its administration in two patients suggests the possible role of additional mechanisms involved in hemostasis. In a comparable group of eight patients with stress ulcer hemorrhage not treated with this agent, six died with continued bleeding. This high mortality represented the usual outcome in our patients with stress ulcer hemorrhage. These observations need to be extended to additional patients with stress ulcers in a larger randomized study.