Effect of norepinephrine on myocardial intracellular hydrogen ion concentration

1975 ◽  
Vol 229 (2) ◽  
pp. 344-349 ◽  
Author(s):  
KM Riegle ◽  
RL Clancy
Keyword(s):  
Metabolic Acidosis ◽  
Respiratory Acidosis ◽  
Hydrogen Ion ◽  
Ion Concentration ◽  
Beta Blockade ◽  
Hydrogen Ion Concentration ◽  
Rat Hearts ◽  
Buffer Value

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.

Adaptive changes in renal acidification in response to chronic respiratory acidosis

1985 ◽  
Vol 248 (4) ◽  
pp. F492-F499 ◽  
Author(s):  
R. L. Tannen ◽  
B. Hamid
Keyword(s):  
Metabolic Acidosis ◽  
Proton Transport ◽  
Respiratory Acidosis ◽  
Hydrogen Ion ◽  
Distal Nephron ◽  
Urine Ph ◽  
Chronic Metabolic Acidosis ◽  
Adaptive Changes ◽  
Secretory Capacity

To examine whether chronic respiratory acidosis results in adaptive changes in renal acidification, rats were housed for 3 days in an environmental chamber with an ambient CO2 content of 10% and their kidneys were perfused in vitro according to two protocols. To assess hydrogen ion secretory capacity of the distal nephron, perfusions were carried out with a low bicarbonate concentration, in the absence of ammoniagenic substrate, and with saturating quantities of the buffer creatinine. Under these conditions, the titration of creatinine at a pH less than 6.0 (TA pH 6.0) reflects the H+ secretory capacity of a discrete functional segment of the distal nephron. Kidneys from rats with chronic respiratory acidosis exhibited a significantly lower urine pH and higher rate of TA pH 6.0 than controls perfused in this fashion, indicative of an adaptive increase in the distal nephron capacity for proton transport. This adaptation was comparable with that reported previously for rats exposed to chronic metabolic acidosis. Furthermore, evidence of adaptation persisted in the presence of amiloride (10(-5) M), suggesting that it reflects, at least in part, a sodium-independent mechanism of proton transport. Hydrogen ion secretion by the proximal nephron was assessed by performing standard bicarbonate titration curves with kidneys from rats with chronic respiratory acidosis, chronic metabolic acidosis, and controls using a perfusate equilibrated with 95% O2/5% CO2.(ABSTRACT TRUNCATED AT 250 WORDS)

A physiological approach to acid–base disorders: The roles of ion transport and body fluid compartments

2020 ◽  
pp. 2182-2198
Author(s):  
Julian Seifter
Keyword(s):  
Metabolic Acidosis ◽  
Gas Analysis ◽  
Hydrogen Ion ◽  
Anion Gap ◽  
Ion Concentration ◽  
Hydrogen Ions ◽  
Acid Base ◽  
Hydrogen Ion Concentration ◽  
Arterial Blood Gas ◽  
Fluid Compartments

The normal pH of human extracellular fluid is maintained within the range of 7.35 to 7.45. The four main types of acid–base disorders can be defined by the relationship between the three variables, pH, Pco2, and HCO3 –. Respiratory disturbances begin with an increase or decrease in pulmonary carbon dioxide clearance which—through a shift in the equilibrium between CO2, H2O, and HCO3 –—favours a decreased hydrogen ion concentration (respiratory alkalosis) or an increased hydrogen ion concentration (respiratory acidosis) respectively. Metabolic acidosis may result when hydrogen ions are added with a nonbicarbonate anion, A−, in the form of HA, in which case bicarbonate is consumed, or when bicarbonate is removed as the sodium or potassium salt, increasing hydrogen ion concentration. Metabolic alkalosis is caused by removal of hydrogen ions or addition of bicarbonate. Laboratory tests usually performed in pursuit of diagnosis, aside from arterial blood gas analysis, include a basic metabolic profile with electrolytes (sodium, potassium, chloride, bicarbonate), blood urea nitrogen, and creatinine. Calculation of the serum anion gap, which is determined by subtracting the sum of chloride and bicarbonate from the serum sodium concentration, is useful. The normal value is 10 to 12 mEq/litre. An elevated value is diagnostic of metabolic acidosis, helpful in the differential diagnosis of the specific metabolic acidosis, and useful in determining the presence of a mixed metabolic disturbance. Acid–base disorders can be associated with (1) transport processes across epithelial cells lining transcellular spaces in the kidney, gastrointestinal tract, and skin; (2) transport of acid anions from intracellular to extracellular spaces—anion gap acidosis; and (3) intake.

Metabolic acidosis developing during cardiopulmonary bypass is related to a decrease in strong ion difference

Perfusion ◽  
2004 ◽  
Vol 19 (3) ◽  
pp. 145-152 ◽  
Author(s):  
R Peter Alston ◽  
Laura Cormack ◽  
Catherine Collinson
Keyword(s):  
Metabolic Acidosis ◽  
Lactate Concentration ◽  
Gas Analysis ◽  
Hydrogen Ion ◽  
Ion Concentration ◽  
Outcome Variable ◽  
Royal Infirmary ◽  
Strong Ion Difference ◽  
Hydrogen Ion Concentration ◽  
Arterial Blood

Metabolic acidosis is a frequent complication of cardio-pulmonary bypass (CPB). Commonly, its cause is ascribed to hypoperfusion; however, iatrogenic causes, related to the composition and volume of intravascular fluids that are administered, are increasingly being recognized. The aim of this study was to determine if metabolic acidosis during CPB was associated with hypoperfusion, change in strong ion difference (SID) or haemodilution. Forty-nine patients undergoing cardiac surgery using CPB in the Royal Infirmary of Edinburgh (RIE) or the HCI, Clydebank were included in the study. Arterial blood samples were aspirated before induction of anaesthesia and the end of CPB. Samples were subjected to blood gas analysis and measurement of electrolytes and lactate. Changes in concentrations were then calculated. Change variables that were found to be significant (p B-0.1) univariate correlates of the change in hydrogen ion concentration were identified and entered into a multivariate regression model with hydrogen ion concentra tion at the end of CPB as the outcome variable (r2=0.65, p<0.001). Change variance in hydrogen ion concentration was created by first entering the baseline hydrogen ion concentration into the model. Next, any variance resulting from the respiratory component of acidosis was removed by entering the change in arterial carbon dioxide tension (regression coefficient (β)=0.67, p<0.01). Change in SID (β=-0.34, p<0.01) and surgical institution (β=-0.40, p<0.01) were then found to be predictors of the remaining variance whilst change in concentration of lactate (β in=0.16, p=0.07) and volume of intravascular fluid that was administered (β=-0.07, p=0.52) were rejected from the model. These findings suggest that the metabolic acidosis developing during CPB is partially the result of iatrogenic decrease in SID rather than hypoperfusion, as estimated by lactate concentration, or haemodilution.

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
Keyword(s):  
Glucose Transport ◽  
Fluid Transport ◽  
Glucose Absorption ◽  
Hymenolepis Diminuta ◽  
Hydrogen Ion ◽  
Ion Concentration ◽  
Solvent Drag ◽  
Rat Intestine ◽  
Hydrogen Ion Concentration

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.

Effect of glucose and inosine triphosphate on seasonal variation of gastric acid production in Rana pipiens

1959 ◽  
Vol 196 (5) ◽  
pp. 975-978 ◽  
Author(s):  
Sherwin Mizell
Keyword(s):  
Seasonal Variation ◽  
Gastric Acid ◽  
Acid Production ◽  
Rana Pipiens ◽  
Hydrogen Ion ◽  
Ion Concentration ◽  
Hydrogen Ion Concentration ◽  
Total Chloride ◽  
Effect Of Glucose

The production of acid in vitro by the gastric mucosa of 375 Rana pipiens was studied over a period of 13 months. The frogs were kept at 21°C and histamine was used to induce secretion. Four conditions were studied: a) control, no substrate added to the nutrient solution; b) 10 mm glucose added; c) 0.6 µm inosine triphosphate (ITP) added and d) 10 mm glucose and 0.6 µm ITP added. For each mucosa the change in hydrogen ion concentration (ΔpH), titrable acidity and total chloride produced were measured. The results indicate that the seasonal variation in gastric acid production is due, in part, to a variation in the availability of substrate normally present.

Sign in / Sign up

Export Citation Format

Share Document