Components of Glucose Transport in the Host–Parasite System, Hymenolepis diminuta (Cestoda) and the Rat Intestine

1974 ◽  
Vol 52 (2) ◽  
pp. 183-197 ◽  
Author(s):  
R. B. Podesta ◽  
D. F. Mettrick

Glucose and fluid transport by the rat intestine and by the tapeworm Hymenolepis diminuta has been studied in vivo, using closed loops of the entire small intestine. The effect of pH, glucose concentration, and the presence of sodium on solute and solvent absorption has been determined in both host and parasite. The effect of the worms on intestinal absorption by the rat has also been evaluated. Three components of the glucose transport system, namely active transport, diffusion, and solvent drag, were determined by means of a model transport equation.Saturation kinetics for glucose absorption did not occur and the absence of sodium in the luminal fluid, while not affecting glucose absorption, markedly reduced fluid absorption by both the intestine and the worms. Lowering the pH of luminal fluids significantly reduced glucose transport by the intestine but increased absorption of fluid and glucose by H. diminuta. Irrespective of pH, fluid and glucose absorption were significantly reduced in the parasitized intestine.Active transport of glucose by normal or parasitized intestine and by H. diminuta was unaffected by the concentration of glucose in the lumen, or by changes in pH. The solvent drag and diffusion components of glucose transport were reduced by increasing the hydrogen ion concentration in uninfected and parasitized intestines. The solvent drag component of glucose absorption by the tapeworms was increased with increasing hydrogen ion concentration.The results are discussed in terms of the current hypotheses on the mechanism of glucose transport, sodium dependency, and the effect of hydrogen ions on transport mechanisms.

1975 ◽  
Vol 229 (2) ◽  
pp. 344-349 ◽  
Author(s):  
KM Riegle ◽  
RL Clancy

The effect of norepinephrine (NE) on the intracellular hydrogen ion concentration [H+]i of isolated rat hearts perfused with a modified Krebs-Henseleit solution (SHS) was determined. The [H+]i was calculated with the [14C]-dimethyloxazolidinedione method. Respiratory or metabolic acidosis was produced by equilibrating the KHS with 20% C02 or decreasing the [HC03-] of the KHS, respectively. Three types of experiments were carried out: 1) beta blockade--MJ 1999 (Sotalol) was added to the KHS; 2) control--no pharmacological treatment; and 3) NE-norepinephrine was added to the KHS. The effective CO2 buffer values (delta[HC03-]i/deltapHi) during respiratory acidosis were: beta blockade, 11; control, 35; and NE, 84. The production of metabolic acidosis resulted in the following [H+]i changes: beta blockade, 52 mM; control, 60 nM; and NE 7 nM. These results suggest that NE markedly attenuates the changes in [H+]i accompanying respiratory and metabolic acidosis and may account in part for previous observations that the effective C02 buffer value of cardiac muscle in vivo is greater than that in vitro.


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