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Biomedical subjects

C Albers

Publications and source records attributed to C Albers.

At least 37 records · Page 2Linked to original sources
PubMed1983

Effect of acclimation temperature on oxygen transport in the blood of the carp, Cyprinus carpio.

The temperature dependence of the O2 equilibrium in whole blood was measured in carp acclimated for more than 3 weeks at 10 degrees C or 20 degrees C water temperature. O2 combining curves were obtained for the same samples at 10 degrees C or 20 degrees C using blood from the 10 degrees C or 20 degrees C acclimated fish (group A) or only at the acclimation temperature (group B). Whereas in group B the P50 was about the same at both temperatures, in group A P50 was higher at 20 degrees C than at 10 degrees C, yielding an apparent heat of oxygenation delta H = -9.9 kcal/mol at pH = 8.0. The CO2 Bohr effect in group A was delta log P50/delta pH = -0.93 at 20 degrees C and -1.17 at 10 degrees C, whereas in group B no temperature effect was seen (-0.98 and -0.97). The acclimation temperature had no effect on the electrophoretic Hb pattern. As expected, the in vivo pH changed inversely with temperature from 8.06 at 10 degrees C to 7.73 at 20 degrees C, enhancing the temperature-induced shift in P50. Acclimation reverses partly the changes in O2 affinity, thereby improving the uptake of oxygen in the gills.

Acclimatization↗
PubMed1983

Effect of acclimation temperature on intraerythrocytic acid-base balance and nucleoside triphosphates in the carp, Cyprinus carpio.

In carp acclimated to 20 degrees C or 10 degrees C intraerythrocytic pH (pHi) and plasma pH (pHe) were determined in vitro after equilibration with CO2 in either O2 or N2. ATP and GTP were determined with an enzymatic assay described in detail. The relationship between pHi, pHe and oxygen saturation was not affected by the acclimation temperature and was (pHi-6.10) = (0.853-0.159 X S) X (pHe-6.21) There was a slight but significant decrease in ATP at 20 degrees C. Apparent buffer values were affected by oxygenation and temperature. It is concluded from the recalculated CO2 Bohr factor and from the temperature effect on the buffer value that carp hemoglobin forms carbamate which decreases at a higher temperature. These changes in ATP and carbamate can partly account for the increase in whole blood oxygen affinity in carp acclimated at a high temperature.

Acid-Base Equilibrium↗
PubMed1981

Effect of CO2 and lactic acid on intracellular pH of ascites tumor cells.

The effect of CO2 and of lactic acid (L.A.) on the extracellular (pHe) and intracellular pH (pHi) of ascites tumor cells (DS-carcinosarcoma) in rats was studied by in vitro equilibration of ascites with CO2 and alteration of lactic acid concentration. pHi was determined by the distribution of DMO. The effects of lactic acid and CO2 on pH were additive and could be expressed as pHe = 8.872 - 0.745 logPCO2 - 0.0355 (L.A.) (R = 0.867, n = 201) pHi = 8.218 - 0.436 logPCO2 - 0.0275 (L.A.) (R = 0.812, n = 143) delta pHi/delta pHe was dependent on the way pHe was changed: If the change in pHe was due to lactic acid, delta pHi/delta pHe was 0.91; if it was due to CO2 delta pHi/delta pHe was 0.625. pHi exceeded pHe if either PCO2 and/or the concentration of lactic acid was raised above a critical level. The results render it questionable to predict intracellular pH values within solid tumor from pH measurements within the extracellular fluid.

Animals↗
PubMed1981

Non-bicarbonate buffering of ascites tumor cells in the rat as titrated by strong acids.

Buffer equations originally derived for blood were applied to the in vitro system "ascites tumor cells and ascitic fluid'. Non-bicarbonate buffer values beta(mmol x pH(-1) x 1(-1)) were determined experimentally by titration of ascites, cell free ascitic fluid and cell homogenates with NaOH in the absence of CO2. beta in ascitic fluid, in native ascites and in cell homogenate were beta (F) = 5.9, beta (A) = 16.4 and beta (H) = 24.9, respectively. Intracellular beta value beta (C) calculated from buffer equations depended on the ratio delta pHi/delta pHe. With delta pHi/delta pHe = 1, beta (C) was 38.8. The difference between beta (C) and beta (H) could be partly accounted for by differences in the cellular protein content. With delta pHi/delta pHe = 0.62 as in the presence of CO2, beta (C) becomes 62.6. In the presence of CO2 (see Albers et al., 1981), the extracellular buffering was higher and the intracellular buffering lower than the values titrated in the absence of CO2. It is concluded that in the presence of CO2 and/or HCO3- the apparent intracellular buffering of intact tumor cells results from non-bicarbonate buffering by cell proteins as well as from active or passive ionic exchanges with the extracellular fluid.

Acid-Base Equilibrium↗
PubMed1981

Oxygen transport and acid-base balance in the blood of the sheatfish, Silurus glanis.

Oxygen binding and buffer properties of the blood of the sheatfish, Silurus glanis, were investigated in vitro at 20 and 10 degrees C. The O2 binding curves were hyperbolic with P50 = 10.1 mm Hg (20 degrees C, pH = 7.5) and 4.6 (10 degrees C, pH = 7.5). There was a very large Bohr effect with an average delta log P 50/delta pH of - 1.14. At 20 degrees C this value tended to be higher than at 10 degrees C. As a consequence the apparent heat of oxygenation depended on pH. The mean value of delta H was -10.4 kcal/mol. The Haldane effect was pronounced too (delta pH/delta S = -0.14) as was the Root effect. Isoelectric focussing revealed 3 major hemoglobin fractions with isoionic points in a more alkaline region than in carp hemoglobin. The non-bicarbonate buffer value was -10 mmol . 1-1. pH -1. The intraerythrocytic pH depended on the extracellular pH and the O2 saturation: pH = (0.87 - 0.14 S) (pHe -6.68 + 6.48). Delta pH/delta t for a constant CO2 content was -0.0166.

Acid-Base Equilibrium↗
PubMed1978

Mean whole body intracellular pH in unanesthetized dogs: a revised method.

An improved method of calculating the mean whole body intracellular pH (pHi) by means of DMO in unanesthetized dogs is described. The elemination of DMO from the body fluid is assumed to follow a simple exponential decay with a time constant k1. The distribution of DMO into the extracellular and intracellular water is described by an exponential function (1-exp(-k2t)). From experiments in 9 unanesthetized dogs it was found that k1 = 0.008 h-1 and k2 = 1.325 h-1. Mean pHi was 7.08 +/- 0.05 at Pa(c02) = 4.1 kPa (31 mm Hg). The average difference between arterial blood and pHi was 0.35. No statistically different pHi values were found with data from arterial or mixed venous blood. Even after 24 h the method still yields reasonable values for pHi.

Acid-Base Equilibrium↗
PubMed1977

Respiratory control of body temperature: a theoretical model.

The two-compartment model of a ventilatory CO2 chemostat of Grodins et al. (1954) is modified to describe a ventilatory thermostat fitting the requirements of panting. Allowance for the extra heat production during panting leads to a second order third degree differential equation which by introducing the ventilation/perfusion ratio can be reduced to the second degree. From the steady-state solutions calculated for dogs using experimentally determined constants it is concluded that: (1) the ventilation/perfusion ratio has no influence; (2) the ambient temperature leads to a marked panting only above 30 degree C; (3) the relative humidity of the air increases the panting; (4) due to the oxygen cost of panting, the regulation of the body temperature is possible only within limits. The limitation depends upon the energy requirements of the respiratory muscles, upon the set-point temperature and the controller gain. The unsteady-state solution is given by approximation. The ventilatory reaction to the heat stress appears to be slow with a half-time of about 15 min for a 20 kg dog. All properties of the model are mainly determined by the high specific heat of tissues relative to expired air.

Animals↗
PubMed1975

Determination of mean whole body intracellular pH in unanesthetized dogs.

In order to determine mean whole body pHi in unanesthetized dogs, assumptions on the urinary and intestinal excretion of DMO, the total loss of an injected single dose of [14C] DMO, and the distribution kinetics of DMO were tested experimentally. Urinary excretion of DMO was almost negligible. The best assumption on the total loss of DMO was based on the exponential decay observed over a period of 1 to 4 weeks. The biological half-life of DMO was 5 days, the time constant being --0.14 d-1. The extracellular distribution of DMO was considered to equal that of [3H] inulin. Between 1 and 7 hours after an injection of inulin in nephrectomized dogs the distribution volume increased linearly from 16% of the body weight after 2 hours to 21% after 6 hours. Based on these experimental results, pHi was determined in 16 unanesthetized dogs. 120 min after the injection of DMO pHi was 7.05 and 430 min after the injection pHi was 7.11. It is concluded that the assumption made allow the estimation of pHi in unanesthetized dogs over a period of 1 to 7 hours.

Acid-Base Equilibrium↗
PubMed1975

Intracellular pH in unanesthetized dogs during panting.

Intracellular pH, arterial blood gases and several plasma enzymes were estimated in unanesthetized dogs during a 3-hour exposure to 30 degrees C/50% relative humidity, and 40 degrees C/50% relative humidity. No change occurred during mild heat stress, whereas during severe heat stress a profound respiratory alkalosis developed together with an increase in intracellular pH from 7.03 to 7.29. Most plasma enzymes increased by about 300% or more. In spite of extreme panting body temperature rose to 42.2 degrees C. Exposure to 40 degrees C/50% relative humidity with 4% CO2 in the climatic chamber inhibited the respiratory alkalosis and the increase of plasma enzymes. Though the panting frequency was lower the ventilatory heat dissipation was more efficient. Body temperature rose to only 39.8 degrees C. It is concluded that the intracellular buffering is not able to prevent marked changes of the intracellular pH during panting.

Acid-Base Equilibrium↗
PubMed1975

The effect of temperature and mechanical work load on the intracellular pH and buffer capacity of cardiac muscle in rats.

The effect of temperature on hydrogen ions and buffer capacity in extracellular fluid differs from the effects in intracellular fluid. In our experiments cardiac hypertrophy was achieved by increasing the mechanical work load. It could be demonstrated that there is a certain correlation between buffering of hydrogen ions and mechanical activity of heart muscle.

Animals↗
PubMed1975

[Intracellular pH of cardiac muscle after administration of potassium-magnesium-aspartate (author's transl)].

27 Sprague-Dawley rats were anesthetized with pentobarbital. Artificial ventilation was given by a Starling pump respirator via a tracheal tube. Intracellular pH of cardiac muscle was determined by means of the indirect procedure of measuring the distribution of 5,5-dimethyl-2,4-oxazolidinedione (DMO) in intra- and extracellular spaces (DMO-method). 12 rats were injected i.p. with 0.33 mval potassium-magnesium-aspartate/100 g body weight and 15 rats served as controls. Using a regression analysis, the following relationships were obtained: 1. animals injected with potassium-magnesium-aspartate pHa = --0.75 log PaCO2 + 8.535, PHi = --0.30 log PaCO2 + 7.509, pHi = 0.41 pHa + 4.036; 2. control animals pHa = --0.59 log PaCO2 + 8.308, pHi = --0.27 log PaCO2 + 7.381, pHi = 0.47 pHa + 3.503. At a pCO2 of 40 torr a pHa of 7.33 (7.36) and a pHi of 7.03 (6.95) was obtained. At an arterial pH of 7.40 the pHi was 7.07 (6.98). The results of the control group are written in brackets. -- The experiments demonstrate an increase in the intracellular buffer bases after administration of potassium-magnesium-aspartate. This effect can be recognized by a concomitant increase in the intracellular pH of 0.09 compared to the control group.

Animals↗