PubMed · 3387694
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K Taniguchi. 1988. [Anaerobic threshold].. https://pubmed.ncbi.nlm.nih.gov/3387694/
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Acid-base disorders were investigated in 50 calves with chronic indigestion and metabolic acidosis. In the calves that were unable to stand up, the acidosis was significantly more severe than in the calves that could stand up. The anion gap and four different components of the base excess were calculated by the method described by Fencl. The anion gap was high in more than half of the calves, and it was significantly associated with the base excess due to unidentified anions. However, in seven of the calves, the excess of unidentified anions would not have been detected without the calculations, which made it possible to measure the effect of sodium, chloride, plasma protein and unidentified anions on the acid-base balance. Twenty-four of the calves had a combination of hyperchloraemic and high anion gap metabolic acidosis. Changes in sodium and plasma protein concentrations had a minor impact on the calves' acid-base status.
The mechanisms of intracellular pH (pH(i)) regulation were studied in hepatocytes isolated from three species of teleost: rainbow trout (Oncorhynchus mykiss), black bullhead (Ameiurus melas) and American eel (Anguilla rostrata). Intracellular pH was monitored over time using the pH-sensitive fluorescent dye BCECF in response to acid loading under control conditions and in different experimental media containing either low Na(+) or Cl(-) concentrations, the Na(+)-H(+) exchanger blocker amiloride or the blocker of the V-type H(+)-ATPase, bafilomycin A(1). In trout and bullhead hepatocytes, recovery to an intracellular acid load occurred principally by way of a Na(+)-dependent amiloride-sensitive Na(+)-H(+) exchanger. In eel hepatocytes, the Na(+)-H(+) exchanger did not contribute to recovery to an acid load though evidence suggests that it is present on the cell membrane and participates in the maintenance of steady-state pH(i). The V-type H(+)-ATPase did not participate in recovery to an acid load in any species. A Cl(-)-HCO(3)(-) exchanger may play a role in recovery to an acid load in eel hepatocytes by switching off and retaining base that would normally be tonically extruded. Thus, it is clear that hepatocytes isolated from the three species are capable of regulating pH(i), principally by way of a Na(+)-H(+) exchanger and a Cl(-)-HCO(3)(-) exchanger, but do not exploit identical mechanisms for pH(i) recovery. J. Exp. Zool. 284:361-367, 1999.
Rates of oxygen consumption (V(O)2), body temperatures and pulmonary blood temperatures, blood gases and blood pH were measured for seven 4.9+/-0.8 (SE) kg tammar wallabies (Macropus eugenii) during rest and during treadmill hopping. For animals resting on the treadmill V(O)2 averaged 0.030+/-0.003 L min(-1). During hopping V(O)2 increased linearly with speed up to 2.5 m sec(-1). Above 2.5 m sec(-1) V(O)2 was independent of hopping speed and averaged 0.340+/-0.004 L min(-1). At rest, rectal temperatures and pulmonary blood temperatures averaged 36 degrees C. During treadmill hopping, rectal temperatures and pulmonary blood temperatures increased similarly, to 39 degrees C. The Pv(CO)2 increased and pHv decreased in proportion to the increased V(O)2. The Pa(CO)2 and pHa were not significantly changed from values for animals resting on the treadmill. Cardiac output (Vb) averaged 0.97+/-0.04 L min(-1) when the wallabies were at rest on the treadmill and increased linearly with treadmill speeds up to 2.5 m sec(-1). Above 2.5 m sec(-1) Vb was independent of hopping speed and averaged 2.9+/-0.04 L min(-1). When data for all speeds were combined, Vb increased linearly with V(O)2. Thus, in spite of their unique mode of locomotion wallabies have maintained relationships between pulmonary ventilation and V(O)2 and between Vb and V(O)2 that are similar to those reported for eutherian mammals.