The short-term influence of catecholamines on acid-base balance of rat soleus muscle in vitro

1984 ◽  
Vol 401 (3) ◽  
pp. 272-276
Author(s):  
F. Huguenin
Author(s):  
E. Boschetti ◽  
C. Minestrini ◽  
A. Scortecci ◽  
S. Cipolloni

1986 ◽  
Vol 64 (5) ◽  
pp. 1054-1057 ◽  
Author(s):  
B. L. Tufts ◽  
D. P. Toews

Specimens of Bufo marinus (L.) were cannulated in both ureters to partition between the regulatory contributions of the kidney and urinary bladder. These bladder-bypassed animals were then exposed to 10 h of dehydration in air and renal function and acid–base balance were assessed. The results indicated that the kidney showed an almost immediate response to dehydration which consisted of a large glomerular and smaller tubular component. Bypassing and emptying of the bladder and the removal of the ambient water had no effect on the animal's ability to maintain normal acid–base balance.


1987 ◽  
Vol 252 (2) ◽  
pp. F221-F225 ◽  
Author(s):  
S. Cheema-Dhadli ◽  
R. L. Jungas ◽  
M. L. Halperin

The purpose of this study was to clarify how changes in acid-base balance influence the rate of urea synthesis in vivo. Since ureagenesis was increased by an ammonium infusion into rats, regulation seemed to be a function of the blood ammonium concentration. The rate of urea synthesis was constant at a fixed rate of ammonium infusion and independent of the conjugate base infused, chloride or bicarbonate. The steady-state blood ammonium concentration was higher in the rats that developed metabolic acidosis. Thus it appeared that regulation was not directly mediated by this ammonium concentration per se. The rate of urea synthesis was also independent of the blood pH. Accordingly, the rate of urea synthesis was examined as a function of the plasma NH3 concentration. The rate of ureagenesis was found to be directly proportional to the plasma NH3 concentration. Assuming that plasma NH3 levels reflect those in mitochondria, the NH3 concentration yielding half-maximal rates of urea synthesis (close to 2 microM) was in the same range as Km for the rate-limiting step in ureagenesis, carbamoyl phosphate synthetase (EC 6.3.4.16). These results suggest that, at a constant ammonium concentration, the decreased rate of ureagenesis caused by a pH fall in vitro could reflect an acidosis-induced decline in the concentration of true substrate (NH3) for this pathway.


2003 ◽  
Vol 550 (2) ◽  
pp. 585-603 ◽  
Author(s):  
Charles T. Putman ◽  
Norman L. Jones ◽  
George J. F. Heigenhauser

1985 ◽  
Vol 17 (2) ◽  
pp. 226
Author(s):  
J. M. Kowalchuk ◽  
G. J. F. Heigenhauser ◽  
J. R. Sutton ◽  
N. L. Jones

Author(s):  
Hannah K. Marchant ◽  
Piero Calosi ◽  
John I. Spicer

The effect of short-term (5 days) exposure to CO2-acidified seawater (year 2100 predicted values, ocean pH = 7.6) on key aspects of the function of the intertidal common limpet Patella vulgata (Gastropoda: Patellidae) was investigated. Changes in extracellular acid–base balance were almost completely compensated by an increase in bicarbonate ions. A concomitant increase in haemolymph Ca2+ and visible shell dissolution implicated passive shell dissolution as the bicarbonate source. Analysis of the radula using SEM revealed that individuals from the hypercapnic treatment showed an increase in the number of damaged teeth and the extent to which such teeth were damaged compared with controls. As radula teeth are composed mainly of chitin, acid dissolution seems unlikely, and so the proximate cause of damage is unknown. There was no hypercapnia-related change in metabolism (O2 uptake) or feeding rate, also discounting the possibility that teeth damage was a result of a CO2-related increase in grazing. We conclude that although the limpet appears to have the physiological capacity to maintain its extracellular acid–base balance, metabolism and feeding rate over a 5 days exposure to acidified seawater, radular damage somehow incurred during this time could still compromise feeding in the longer term, in turn decreasing the top-down ecosystem control that P. vulgata exerts over rocky shore environments.


1970 ◽  
Vol 39 (2) ◽  
pp. 169-182 ◽  
Author(s):  
C. T. Kappagoda ◽  
R. J. Linden ◽  
H. M. Snow

1. The existing methods for assessing states of acidosis are discussed with particular reference to non-respiratory acidosis. Most of these methods are based either on the Henderson—Hasselbalch equation or on the direct extrapolation of in vitro studies on blood to the whole animal. The evidence available shows that these methods cannot be used to obtain an accurate assessment of disturbances of acid-base balance in the whole animal. 2. The experiments were designed to investigate the acid-base parameters of an animal when a respiratory acidosis was superimposed on a non-respiratory acidosis caused by the infusion of n HCl; from these experiments it was possible to construct CO2 titration curves at various levels of non-respiratory acidosis. 3. A scheme which is based upon the CO2 titration curves, has been proposed for assessing an acute acid-base disturbance in terms of its respiratory and non-respiratory components. 4. The use of sodium bicarbonate to correct a non-respiratory acidosis was investigated, and it was shown that the amount of sodium bicarbonate required varied with the rate of infusion. No firm predictions could be made regarding the dose of bicarbonate required, but from the results of the present experiments an infusion rate of 0·1 mEq kg−1 min−1 is recommended in dogs.


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