Varying Dialysate Bicarbonate Concentrations in Maintenance Hemodialysis Patients Affect Post-dialysis Alkalosis but not Pre-dialysis Acidosis.

This study aimed to assess the effects of different dialysate bicarbonate concentrations in correcting acid-base imbalance in 53 stable hemodialysis patients in a university-hemodialysis unit. Three different bicarbonate concentrations were assigned, i.e. 25 mEq/L in 10, 30 mEq/L in 30, and 35 mEq/L in 13 patients. Blood gas analyses from arterial line blood samples before and after dialysis in the mid-week were performed for the determination of pH and serum bicarbonate (HCO3 (-)) concentration. The mean values of predialysis arterial HCO3 (-) were mildly acidotic in all 3 groups, but not significantly different among them, whereas those of post-dialysis arterial HCO3 (-) were alkalotic, especially in the group of 35 mEq/L as compared with the other two groups. The mean blood pH was not significantly different among the 3 groups. As expected, there was a positive correlation between pre-dialysis pH and post-dialysis pH (r=0.45, p=0.001), and pre-dialysis HCO3 (-) and post-dialysis HCO3 (-) (r=0.58, p=0.000), but with a negative correlation between pre-dialysis HCO3 (-) and the increment of intradialytic HCO3 (-) following hemodialysis (r=-0.46, p=0.001). In conclusion, this study shows that the impact of conventional dialysate bicarbonate concentrations ranging from 25 to 35 mEq/L is not quite different on the mild degree of predialysis acidemia, but the degree of postdialysis alkalemia is more prominent in higher bicarbonate concentrations. Base supply by hemodialysis alone does not seem to be the main factor to determine the predialysis acidosis in end-stage renal disease patients on chronic maintenance hemodialysis.

Phototrophic transformation of phenol to 4-hydroxyphenylacetate by Rhodopseudomonas palustris.

Newly isolated and culture collection strains of Rhodopseudomonas palustris were able to transform phenol to 4-hydroxyphenylacetate under phototrophic conditions in the presence of acetate, malate, benzoate, or cinnamate as growth substrates. The reaction was examined with uniformly (14)C-labelled phenol and the product was identified by HPLC retention time, UV-scans, and (1)H- and (13)C-NMR analysis. The transformation reaction was detectable in cell-free extracts in the presence of NAD(+) and acetyl-CoA. For further degradation of 4-hydroxyphenylacetate by R. palustris, low partial pressures of oxygen were essential, presumably for aerobic aromatic ring fission reactions by mono- and di-oxygenases.

Glucagon acts in the liver to control spontaneous meal size in rats.

To determine the site of origin of pancreatic glucagon's inhibitory effect on spontaneous feeding in rats, glucagon was infused into either the hepatic portal vein or the inferior vena cava during spontaneous meals late in the dark phase. Hepatic portal infusion of 1.7-13.6 micrograms glucagon/meal reduced spontaneous meal size. In contrast, these doses did not significantly affect meal size when delivered via vena caval catheters that ended near the junction of the hepatic vein. This difference indicates that glucagon receptor sites in the liver initiate the satiating action of glucagon during spontaneous meals. The vagal dependency of glucagon satiety was also tested. Hepatic portal infusion of 13.6 micrograms glucagon/meal reduced the size of spontaneous meals both early and late in the dark in neurally intact rats, but not in hepatic-vagotomized rats. Finally, antagonism of endogenous glucagon with hepatic portal infusion of glucagon antibodies in a dose sufficient to neutralize 1 ng glucagon in vitro increased spontaneous meal size in intact rats, but not in hepatic-vagotomized rats. Thus the satiating effects of both exogenous and endogenous glucagon on spontaneous food intake appear to depend on the hepatic branch of the vagus. Taken together, these results are consistent with the hypothesis that glucagon acts in the liver to produce a satiety signal that is transmitted to the brain by the hepatic branch of the abdominal vagus.

Hepatic portal infusion of glucagon antibodies increases spontaneous meal size in rats.

Specific antibodies to pancreatic glucagon in a dose sufficient to neutralize 1.5 ng glucagon in vitro were intraportally infused during the first 2 min of spontaneous meals in ad libitum-fed male Sprague-Dawley rats. In separate tests, glucagon antibodies stimulated feeding during the first spontaneous meal of the dark phase (73% mean increase in meal size) and during spontaneous meals in the last quarter of the dark phase (58% increase). These results indicate that a glucagon-sensitive satiety mechanism has a physiological role in the control of nocturnal feeding in rats.