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HC03, mmol/I. mm Hg. Blood pH. Dogs. Humans. Dogs Humans Dogs. 18. 18. 35. 35. 7.33. 13 ... Dogs respond to sustained hypocap- ... [HC031, the net change.
6. Holt DW, Johnston A, Marsden JT, et al. Monoclonal antibodies for radioimmunoassay of cyclosporine: a multicenter comparison of their performance with the Sandoe polyclonal RIA kit. Clin Chem 1988;34: 1091-6.

David W. Holt Atholl Johnson Analytical Unit, Card iol. Sci. St. George’s Hosp. Med. Sch. London, U.K. SW17 ORE Renal Response to Chronic Hypocapnia: Qualitative Differences between Dogs and Humans? To the Editor: Among its other requirements, the precise characterization and management of clinical disorders in acid-base balance require the knowledge of the quantitative response of body mechanisms regulating acid-base balance to a given single primary disturbance. This response includes the buffering process, which involves extracellular and complex intracellular mechanisms, and the so-called “physiological compensation,” that is, the secondary changes in the function of the organs regulating acid-base balance. The

method of studying physiological compensation consists of the induction of a single acid-base disorder and usual

of the changes in the function of the regulatory organs and in the acid-base parameters under controlled experimental conditions. The study of primary hypocapnia under this methodology has, on the surface, produced conflicting results between dogs and humans. Dogs respond to sustained hypocapma by base diure8is. In single primary hypocapnia, the base diuresis results in a decrease in serum bicarbonate concentration and consequent maintenance of blood pH close to normal (1); hence, the term “physiological compensation.” If primary hypocapnia is suobservation

perimposed on pre-existing metabolic acidosis, however, the decrease in serum bicarbonate secondary to base diuresis is sufficient to create a further decline in blood pH (2,3). Thus it appears that, in dogs, hypocapnia obligates base diuresis and a decrease in blood bicarbonate regardless of the effects on blood pH. It was recently reported that this “maladaptive” renal response to hypocapnia does not develop in humans (4). The matter is important, because primary hypocapnia superimposed on metabolic acidosis is encountered rather frequently in clinical practice. It is, therefore, appropriate to examine the data reported in dogs and humans and search for the differences and similarities between the two species. The experimental conditions were comparable between the two species (1-4). When a process affects both blood Pco2 and bicarbonate [HC031, the net change in blood pH is determined, according to the Henderson-Hasselbalch equation, by the change in the fraction [HCO3]/p02. Mathematically, this fraction decreases in hypo. capma when the i[HCO3]/,p02> ([HCO3]/p01, where ([HC03JJ Pco ) = the initial (pre-hypocapnia) fradion. A decrease in the fraction HCO3]/p determines an appropriate decrease in blood pH. Comparison of the dog and human experiments with hypocapnia (1-4) reveals two important qualitative similarities and one important quantitative difference. Qualitatively, the renal mechanisms of base excretion produced by hypocapnia appear to be similar between the two species. More importantly, the resulting ratio [HCO3i/ was the same, in each species, in solitary primary hypocapnia and in primary hypocapnia superimposed on metabolic acidosis. Quantitatively, the value of the computed ratio in dogs was greater (0.5 mmol/L per mmHg) than in humans (0.4 mmol/L pet mmllg).

For the [HCO3]/p02 values reported, the relationship [HCO3]/ Pco > ([HCO3}/p02)1 holds true for initial pH values