PubMed · 4988801
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G Saliou-Diallo, P Robitaille, G Lemieux. 1968. [Ascorbic acid and the kidney].. https://pubmed.ncbi.nlm.nih.gov/4988801/
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METHOD: Eighteen hospitalized patients with candiduria were treated with oral potassium-sodium-hydrogen citrate to alkalinize the urine. The results obtained were compared with those observed in an untreated retrospective control group. Dosage was adjusted in accordance with the pH of the urine measured immediately before treatment with the aim of achieving a pH of 7 to 7.5. RESULTS: All patients had an indwelling catheter, which is a predisposing factor for candiduria. In 16 out of 18 patients (89%) treatment with potassium-sodium-hydrogen citrate raised pH and resulted in the disappearance of candiduria. Duration of treatment varied between two days and one month (mean: seven days). In four patients the urine became completely sterile; during treatment 12 out of 18 patients developed significant bacteriuria (in eight cases of these the indwelling catheter had been left in place). CONCLUSIONS: Alkalinization of the urine is a simple and effective method of treating candiduria in patients with an indwelling catheter. An additional advantage is the metaphylaxis and prophylaxis of renal stone formation in immobilized patients.
The mechanisms involved in intracellular pH (pHi) recovery from an acid load have been investigated in enterocytes isolated from chicken. Following an intracellular acidification, by abrupt withdrawal of NH4Cl, pHi alkalinized in the nominally absence of Na+ and bicarbonate. This Na(+)- and bicarbonate-independent (NBI) regulatory cell alkalinization became negligible when the pHi has reached a value of approx. 6.85. Addition of Na+ induced a rapid pHi recovery to control values. Rotenone, DCCD, vanadate, NBD-Cl, SCH 28080 and EIPA inhibited the NBI cell alkalinization, whereas bafilomycin A1, ouabain and H2-DIDS were without effect. Na(+)-dependent pHi recovery from an acid load was inhibited by EIPA and unaffected by SCH 28080 or DCCD. The rate of NBI cell alkalinization was a linear function of the electrochemical proton gradient. In high external K+ buffer plus valinomycin the line goes through the origin. Gramicidin accelerated the rate of NBI cell alkalinization, whereas it was slightly reduced by low external potassium. The results demonstrate that in intestinal epithelial cells exist at least two mechanisms for proton secretion: a Na(+)-H+ exchanger and a Na(+)- and bicarbonate-independent proton transport system. This latter mechanism appears to be a proton conductance pathway.
Controversy has been raised about the effects of systemic carbon dioxide accumulation versus the intra-abdominal pressure on hemodynamics during laparoscopy. We compared the acid-base and hemodynamic changes during pneumoperitoneum in a randomized cross-over study between CO2 and nitrogen gases to test the hypothesis that the CO2 absorbed during laparoscopy, rather than the 15 mmHg intra-abdominal pressure created, accounted for these changes. Eight adult pigs were anesthetized and ventilated with a fixed minute ventilation. Metabolic function was measured from analysis of expired flow by a metabolic measurement cart. After baseline periods, animals were randomized into two groups, for 2 hr of either CO2 or nitrogen pneumoperitoneum at 15 mmHg intra-abdominal pressure, followed by 1 hr of recovery. After at least a 48-hr recovery period, the experiment was repeated with the other gas. Metabolic data revealed that there was a significant absorption of CO2 gas across the peritoneal epithelium during CO2 pneumoperitoneum. Animals insufflated with CO2 gas experienced a 75% increase in pulmonary CO2 excretion, with significant acidemia and hypercapnia, whereas there were no acid-base disturbances in those with nitrogen insufflation. Oxygen consumption remained essentially unchanged in both groups, even during pneumoperitoneum. CO2 pneumoperitoneum was also associated with systemic and pulmonary arterial hypertension and a reduction in stroke volume of up to 15%. Pneumoperitoneum alone did not compromise hemodynamics. Pneumoperitoneum using CO2 gas during laparoscopy resulted in systemic CO2 absorption across the peritoneum. This led to acidemia, hypercapnea, and depressed hemodynamics. The intra-abdominal pressure routinely used during laparoscopic surgery did not affect metabolic function, acid-base balance, or hemodynamics in the experimental model.