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H C Alpert

Publications and source records attributed to H C Alpert.

7 recordsLinked to original sources
PubMed1989

Phlorizin-induced glycosuria does not prevent gentamicin nephrotoxicity in rats.

Because rats with streptozotocin-induced diabetes mellitus (DM) have a high solute diuresis (glycosuria of 10 to 12 g/day), we have suggested that this may in part be responsible for their resistance to gentamicin-induced acute renal failure (ARF). The protection from gentamicin nephrotoxicity was studied in non-diabetic rats with chronic solute diuresis induced by blockage of tubular glucose reabsorption with phlorizin (P). DM rats with mild glycosuria (similar in degree to that of the P treated animals) were also studied. Unanesthetized adult female, Sprague-Dawley rats were divided in four groups and studied for 15 days. Group 1 (P alone) received P, 360 mg/day, for 15 days; Group II (P + gentamicin); Group III (gentamicin alone) and Group IV (mild DM + gentamicin). Nephrotoxic doses (40 mg/kg body wt/day) of gentamicin were injected during the last nine days of study to the animals of groups II to IV. In Group I, P induced a moderate and stable glycosuria (3.9 +/- 0.1 g/day, SE), and no functional or morphologic evidence of renal dysfunction (baseline CCr 2.1 +/- 0.1 ml/min, undetectable lysozymuria) or damage (tubular necrosis score [maximum 4], zero). In Group II, P did not prevent gentamicin-ARF (maximal decrease in CCr at day 9.89%, P less than 0.001; peak lysozymuria, 1863 +/- 321 micrograms/day; and tubular necrosis score, 3.9 +/- 0.1). These values were not different from those of Group III: maximal decrease in CCr 73% (P less than 0.001); lysozymuria, 2147 +/- 701 micrograms/day; tubular necrosis score, 3.8 +/- 0.1.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Kidney Injury↗
PubMed1988

Effect of acute reversal of experimentally-induced ketoacidosis with sodium bicarbonate on the plasma concentrations of phosphorus and potassium.

To determine if ketoacidosis per se, or its reversal with NaHCO3, predisposes to hypophosphatemia, six conditioned dogs were infused for two hours with 3.0 mmol/kg body wt/hour of beta-hydroxybutyric acid, followed by 1.5 mmol/kg/hour of NaHCO3 for two hours. Acid infusion caused moderate decrements in blood pH and [HCO3], a 23 +/- 4% increase in plasma [P] (p less than 0.005), and a 15 +/- 3% decrease in plasma [K] (p less than 0.005). NaHCO3 administration returned blood pH and [HCO3] levels to or slightly greater than baseline. Plasma [P] decreased, but not below baseline, whereas plasma [K] remained below baseline, and underwent an additional small decline (p less than 0.01). We conclude that acute correction of experimental ketoacidosis with NaHCO3 reverses the characteristic hyperphosphatemia but does not induce hypophosphatemia. On the other hand, NaHCO3 administration appeared to contribute to the perpetuation of hypokalemia.

3-Hydroxybutyric Acid↗
PubMed1985

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

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.(ABSTRACT TRUNCATED AT 250 WORDS)

Acid-Base Equilibrium↗
PubMed1985

Effect of potassium depletion on acidosis-induced changes in plasma potassium concentration.

It is unknown whether acute metabolic acidosis causes increases in plasma potassium concentration despite pre-existing potassium depletion. In fact, it has long been assumed clinically that acidosis-induced acute hyperkalemia may be masked by potassium depletion. In order to assess this question, moderate to severe potassium depletion was produced in 7 female mongrel dogs (potassium-depleted group) over a 12-day period with injections of desoxycorticosterone acetate (DOCA), NaCl added to the drinking water, and a potassium-free diet. Six dogs (control group) received regular chow, identical NaCl supplements, and sham injections of DOCA. The achievement of potassium depletion was documented by significant differences between the two groups in urinary potassium and in muscle and plasma potassium levels (potassium-depleted group: 0.9 +/- 0.2 mEq/24 h, 19 +/- 3 mEq/100 g dry weight, 1.9 +/- 0.1 mEq/1; control group: 44 +/- 11 mEq/24 h [p less than 0.025], 30 +/- 1 mEq/100 g [p less than 0.005], 3.5 +/- 0.1 mEq/l [p less than 0.005]). There were no statistically significant differences between the groups in blood pH or [HCO3]. On day 13, an NH4Cl acid-load was given (5 mEq/kg body weight i.v. over 3 h in 0.45% NaCl using pentobarbital anesthesia). Following acid-loading, the increases in plasma [K] were significantly greater in the control group than in the potassium-depleted group only at 90 and 120 min. There were no significant differences in the maximal increases from baseline in plasma [K] (potassium-depleted group: 0.6 +/- 0.1 mEq/l, 31 +/- 6%; control group: 1.5 +/- 0.4 mEq/l, 41 +/- 10%).(ABSTRACT TRUNCATED AT 250 WORDS)

Acidosis↗
PubMed1984

Effect of acid-base status on plasma phosphorus response to lactate.

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 plasma 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.

Acid-Base Equilibrium↗
PubMed1982

Plasma parathyroid hormone and divalent cation response to induction of acute metabolic acidosis.

Since the effect of acute administration of acid upon blood magnesium and parathyroid hormone (PTH) is unclear we infused anesthetized dogs with saline (controls), HCl, lactic, and methylmalonic acids for 3 h. In all groups but lactic acid, plasma magnesium decreased; ionized calcium levels were increased by all three acids. Nevertheless, PTH increased in each of six dogs following methylmalonic acid and decreased in four of six animals after lactic acid. The decrease in plasma magnesium concentration after methylmalonic acid appeared to be an important factor in explaining the disparate PTH changes in these two groups because concomitant magnesium administration obviated the increases in PTH in four of six additional methylmalonic acid-infused dogs.

Acidosis↗