Effect of renal sympathetic nerve stimulation on proximal water and sodium reabsorption

The renal responses to sympathetic nerve stimulation were studied in saline-expanded rats. The left kidney was partially denervated by crushing the left greater splanchnic nerve. Then the distal portion of the nerve was stimulated with square wave pulses of 0.5 ms duration, voltage twice threshold, and 1 or 2 Hz frequency while monitoring the compound action potential. Fibers with conduction speeds of 13-17 m-s-1 and of 0.7-1 m-s-1 were identified. Only stimulation of the latter appeared to produce changes in renal Na and water excretion. Whole kidney and individual nephron studies were performed alternating control and nerve stimulation periods. Nerve stimulation produced approximately a 25% reduction of the left kidney urine volume and sodium excretion. Glomerular filtration rate and renal plasma flow remained unchanged. Right kidney Na and water excretion, glomerular filtration rate, and renal plasma flow remained constant. In the left kidney, during nerve stimulation, the tubular fluid to plasma inulin concentration ratio increased significantly in the late proximal tubule. We conclude that the antidiuresis and antinatriuresis seen during sympathetic nerve stimulation were caused by increased sodium and water reabsorption in the proximal tubule, probably mediated by the stimulation of slowly conducting unmyelinated fibers. These responses appeared to be unrelated to systemic or intrarenal hemodynamic changes.     

Increasing polyunsaturation of milk fats by feeding formaldehyde protected sunflower-soybean supplement

A practical means of protecting fats of a feed concentrate containing high polyunsaturated fatty acids is described. A ground mixture of 30% soybeans and 70% sunflower seeds was treated with 1% formaldehyde to protect the unsaturated lipids from microbial hydrogenation in the rumen. This was fed as a supplement to two Holstein cows in amounts that were doubled weekly. These ranged from 524 to 8384 g/day and provided successively increasing intakes of 100, 200, 400, 800, and 1600 g of linoleic acid daily. Percent milk fat increased by more than one, and linoleic acid (C18:2) of milk fat increased from 2.5 to 20% with compensatory declines in myristic (C14:0) and palmitic (C16:0) acids. Cholesterol and vitamin E of plasma both doubled at the highest supplementation. Milk yield, solids-not-fat, protein and milk cholesterol were unaltered. Fat in feces doubled from about 3 to 6%. Daily linoleic acid content of feces increased from 25 g to 120 g, indicating a dietary loss of 7 to 10% of this polyunsaturated acid. These cheaper feed ingredients elevated the polyunsaturated fats in milk as effectively as the expensive purified casein and safflower oil supplements in previous experiments.     

Immunology and adjuvant chemoimmunotherapy of breast cancer

Antibody against a breast carcinoma antigen was present in patients with breast carcinoma and other cancer more often (P less than .05) than in normal women. The incidence of antibody in women with breast carcinoma correlated with the presence or absence of gross tumor, and the titer of antibody paralleled the clinical course. These results suggest importance of a host-immune response to breast carcinoma. Fifty-seven patients with stage II carcinoma of the breast were entered into a prospective randomized adjuvant chemoimmunotherapy program of cyclophosphamide, methotrexate, and fluorouracil, and BCG vaccine +/- an irradiated allogeneic tumor cell vaccine. After 24 months of study, metastases occurred in two patients (3.5%) and a new primary carcinoma developed in the contralateral breast in two others, for an overall treatment failure rate of 7%. Adjuvant chemoimmunotherapy can delay early recurrence. Long-term follow-up is needed to assess the significance of these results.     

Electrolyte transport by gallbladders of rabbit and guinea pig: effect of amphotericin B and evidence of rheogenic Na transport

Ion transport and electrical properties of rabbit and guinea pig gallbladders were investigated to gain further information about the active transport mechanism that mediates fluid absorption. The intracellular and transepithelial electrical potentials were measured simultaneously using the microelectrode technique. Exposure of the mucosal surface to Amphotericin B resulted in the prompt development of a serosa-positive electrical potential difference (PD) which could not be attributed to an alteration in ion diffusion potentials across either the cell membrane or across the tight junction. Because the Amphotericin B-induced PD was immediately dependent on warm temperatures and O2, and was independent of NA and K concentration gradients across the cell membrane, it is suggested that active ion transport is directly responsible for the PD. Since the PD was abolished in the absence of Na in the bathing solutions, a rheogenic Na pump is postulated; this pump also appears to be operative in tissues not exposed to Amphotericin B. The specific tissue properties altered by Amphotericin B to produce a serosa-positive PD remain incompletely defined. The results of the present study indicate that ion transport by rabbit gallbladder in vitro is a consequence of a rheogenic active Na transport mechanism at the basolateral membranes which, in conjunction with a coupled NaC1 influx process at the mucosal border, ultimately results in absorption of NaC1 and water.     

Treatement of excessive weight gain in patients taking lithium

Six female primary affective disorder patients who had gained an average of 9.5 kg while taking lithium lost an average of 2.9 kg on a 10-day 900 calorie a day hospital diet containing 100 mEq of sodium per day. No evidence of lithium toxicity was observed on this regimen. There was no evidence that fluid retention played a major role in the weight gain.     

Longitudinal sliding of the median nerve during movements of the upper limb

Repeated transfusion of small increments of blood are frequently required for the sick and premature newborn infant to correct endogenous hypovolemia and/or to replace blood obtained for laboratory monitoring purposes. Previously fresh group and type specific whole blood was used. To eliminate waste of fresh whole blood, maintain fresh red blood cell properties, eliminate the hazards of transfusing plasma and to provide a more efficient system, a pediatric frozen red cell pack (PFRCP) has been developed. Units of group O rr red blood cells are glycerolized using a high glycerol method. The glycerolized red blood cells are separated into three equal aliquots and frozen. When needed, the PFRCP are deglycerolized by a modified procedure using the IBM Cell Processor. During a six month period, 71 infants were given 153 separate transfusions of deglycerolized red blood cells using 102 PFRCP prepared from 34 units of red blood cells. Red blood cell recovery, hematocrit, white blood cell removal, residual glycerol, total protein, and supernatant hemoglobin levels were measured. Clinical response was followed and found to be excellent.     

Morphometric analysis of rat hepatocytes after total billary obstruction

Using light and electron microscopic morphometric techniques, the effects of 48 hr of extrahepatic biliary obstruction on hepatocyte structure were examined in the rat. Liver cells near the portal area were compared to those in the centrilobular regions of the hepatic lobule. Observations on the normal animals confirm earlier evidence of quantitative differences in the surface density of organelles in hepatocytes located within different regions of the lobule. A striking difference in the quantity of the Golgi complex in the two areas of the lobule was noted for the first time, with the portal cells containing a significantly greater quantity of this organelle than centrolobular hepatocytes. After 48 hr of total obstruction, most of the previously reported qualitative changes in the canalicular and pericanalicular regions were confirmed. Morphometric analysis at the light-microscopic level showed an increase in the number of cells and a decrease in cell size in those cells near the portal area were compared to those in the centrolobular regions of the helar level demonstrated a significant decrease in both rough and smooth surfaced endoplasmic reticulum in cells of both zones, a finding in marked contrast to the hypertrophy of smooth endoplasmic reticulum suggested by other investigators on the basis of qualitative assessments. There was also a striking decrease in the amount of the Golgi complex, limited to cells in the portal regions. In addition, in all zones a decrease in the volume density of mitochondria and lysosomes was noted, whereas the volume of microbodies was increased. It is suggested that this loss in total membrane material within the cell may be secondary to the degranulation and decrease in total surface area of rough surfaced endoplasmic reticulum, an organelle thought to be responsible in part for the synthesis of new cellular membranes. These observations suggest that present concepts concerning the pathogenesis of cholestatic liver disease require reappraisal.     

Gastrointestinal metabolism of cadmium in experimental iron deficiency;

The average gastrointestinal uptake 4 h after an intragastric dose of 400 nmol of cadmium chloride labeled with 109CdCl2 in iron-deficient mice, 25%, was significantly greater than the result, 16%, in iron-normal animals, and more cadmium entered the body of the former, 3.8%, than the latter, 2% (P less than 0.05). Between 4 and 72 h, gastrointestinal radioactivity declined without further increase in body activity; however, more radiocadmium remained in the duodenum of iron-deficient than iron-normal animals (P less than 0.05). The radiocadmium sequestered in the duodenum was bound to a protein with a molecular weight of about 12,000. After subcutaneous injection of radiocadmium, the rate of excretion of radioactivity from the body was similar in iron-normal and iron-deficient mice; however, a greater proportion of the injected dose accumulated in the duodenum of the iron-deficient animals (P less than 0.05). Thus, the intestinal adapative response to iron deficiency may enhance cadmium toxicity, whereas sequestration and subsequent excretion of cadmium by the intestinal mucosa serves to protect the body against toxic effects. The duodenum, particularly in iron-deficient mice, is especially vulnerable to the toxic effects of cadmium.