Effect of acid–base status on plasma phosphorus response to lactate

1984 ◽  
Vol 62 (8) ◽  
pp. 939-942 ◽  
Author(s):  
James R. Oster ◽  
Helen C. Alpert ◽  
Carlos A. Vaamonde
Keyword(s):  
Lactic Acid ◽  
Lactic Acidosis ◽  
Sodium Bicarbonate ◽  
Sodium Lactate ◽  
Phosphorus Concentration ◽  
Acid Anion ◽  
Acid Base ◽  
Phosphorus Response ◽  
Acid Base Status ◽  
Plasma Phosphorus

The mechanism(s) underlying the hyperphosphatemia of lactic acidosis is uncertain. We assessed the interacting influence of the acid anion and acid–base status on plasma phosphorus concentration by administering lactic acid alone, lactic acid plus sodium bicarbonate, sodium bicarbonate alone, and sodium lactate alone to four different groups of dogs. The findings of (1) no increase in plasma phosphorus concentration with lactic acid plus sodium bicarbonate versus a marked increment with lactic acid alone, and (2) no difference in the plama phosphorus response to sodium lactate versus sodium bicarbonate indicate that acidemia is necessary for the expression of lactate-induced hyperphosphatemia. The apparent greater propensity for marked hyperphosphatemia in lactic acidosis than in other types of metabolic acidosis remains unexplained, but conceivably might relate to differences in intracellular pH and in the rate of glycolysis.

Pathogenesis of hyperphosphatemia in lactic acidosis: disparate effects of racemic (DL-) and levo (L-) lactic acid on plasma phosphorus concentration

1985 ◽  
Vol 63 (12) ◽  
pp. 1599-1602 ◽  
Author(s):  
James R. Oster ◽  
Helen C. Alpert ◽  
Carlos A. Vaamonde
Keyword(s):  
Lactic Acid ◽  
Lactic Acidosis ◽  
Acid Group ◽  
Phosphorus Concentration ◽  
Base Line ◽  
Acid Base Status ◽  
Group 3 ◽  
Group 2 ◽  
Plasma Phosphorus ◽  
Group 1

The mechanism(s) for the hyperphosphatemia associated with lactic acidosis is unknown. Experimental lactate-induced hyperphosphatemia appears to require acidemia because we have shown that prevention of acidemia with NaHCO3 obviates increases in plasma phosphorus concentration ([P]). Since the rate of lactate metabolism (by utilizing NAD or other mechanisms) might modulate transcellular movement of phosphorus, we assessed the plasma [P] response to 3-h infusions of DL-lactic acid versus L-lactic acid. The dog metabolizes primarily the L- moiety of DL-lactic acid (thereby consuming H+), so more L-lactic acid is needed to produce the degree of acidemia attained with DL-lactic acid. Group 1 (n = 6) mongrel dogs received 12 mequiv./kg DL-lactic acid; group 2 (n = 6) 12 mequiv./kg L-lactic acid, and group 3 (n = 7) 16–19 mequiv./kg L-lactic acid. Prior to acid loading, the plasma [P] and acid–base status of the three groups were similar. After 3 h, blood pH and [HCO3] and change from base line in plasma [P], in both milligrams per decilitre and percent, were as follows: group 1: 7.05 ± 0.02, 9 ± 2 mM, 1.9 ± 0.4 mg/dL, 38 ± 10%; group 2: 7.28 ± 0.02, 18 ± 1, 0.9 ± 0.3, 17 ± 6; group 3: 7.06 ± 0.04, 12 ± 1, 1.1 ± 0.3, 26 ± 10, respectively. Thus, there was a tendency for both infusion rates of L-lactic acid to increase [P] less than DL-lactic acid, suggesting the importance of other factors in addition to pH. Also, since presumably more lactate was metabolized in group 3 than in group 2 (but the change in [P] was approximately the same in both), the findings do not support the hypothesis that the rate of lactate utilization is a major modulator of plasma [P] in acute lactic acidosis.

The Effect of Long-Term Aerial Exposure on Heart Rate, Ventilation, Respiratory Gas Exchange and Acid-Base Status in the Crayfish Austropotamobius Pallipes

1981 ◽  
Vol 92 (1) ◽  
pp. 109-124
Author(s):  
E. W. TAYLOR ◽  
MICHÈLE G. WHEATLY
Keyword(s):  
Heart Rate ◽  
Lactic Acid ◽  
O2 Consumption ◽  
Aerial Exposure ◽  
Acid Base ◽  
Bicarbonate Buffer ◽  
Content Difference ◽  
Acid Base Status ◽  
Lactate Levels

1. When first removed into air, crayfish showed transient increases in heart rate (fH) and scaphognathite rate (fR) which rapidly recovered to submerged levels and were unchanged for 24 h. The rate of O2 consumption(Moo2) increased from an initially low level and was then maintained for 24 h in air at the same level as in settled submerged animals. 2. There was an initial acidosis in the haemolymph which was both respiratory and metabolic due to the accumulation of CO2 and lactate. Progressive compensation by elevation of the levels of bicarbonate buffer in the haemolymph and reduction of circulating lactate levels returned pH towards submerged levels after 24 h in air. 3. Exposure to air resulted in a marked internal hypoxia with haemolymph O2, tensions, both postbranchial Pa, oo2 and prebranchial Pv, oo2, remaining low throughout the period of exposure. The oxygen content or the haemolymph was initially reduced, with a - vOO2 content difference close to zero. Within 24 h both Ca, oo2 and Cv, OO2 had returned towards their levels in submerged animals. These changes are explained by the Bohr shift on the haemocyanin consequent upon the measured pH changes. 4. After 48 h in air, MO2 and fH were significantly reduced and ventilation became intermittent. There was a slight secondary acidosis, increase in lactic acid levels and reduction in a - vO2 content difference in the haemolymph. 5. When crayfish were returned to water after 24 h in air, MOO2, fHfR were initially elevated by disturbance and there was a period of hyperventilation. In the haemolymph there was an initial slight alkalosis, and an increase in Ca, OO2 lactic acid. All variables returned to their settled submerged levels within 8 h.

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