Acid-base changes and acetate metabolism during routine and high-efficiency hemodialysis in children

Acid-base changes and acetate metabolism during routine and high-efficiency hemodialysis in children. Changes in acid-base status and plasma acetate concentrations were studied in eight children during 11 hemodialysis sessions. During dialysis, the blood bicarbonate concentration fell (20.5 ± 0.7 to 19.6 ± 0.8 mEq/liter), the PCO2 fell (33.4 ± 0.8 to 27.5 ± 1.4 mm Hg), and the pH rose (7.42 ± 0.01 to 7.48 ± 0.02). During the hour after dialysis, the bicarbonate concentration rose to normal (23.4 ± 0.7 mEq/liter), the PCO2 rose (32.8 ± 0.8 mm Hg), and the pH remained unchanged. The half-life of plasma acetate, measured after dialysis, was 8.7 min. During five “high-efficiency” dialysis sessions (urea clearance, > 3.0 ml/min/kg), blood bicarbonate concentration fell 3.2 mEq/liter, PCO2 fell 8.7 mm Hg, and plasma acetate rose to 7.51 mmoles/liter, whereas during six “routine efficiency” dialysis sessions (urea clearance, 1.5 to 3.0 ml/min/kg), blood bicarbonate rose 1.0 mEq/liter, PCO2 fell 36 mm Hg, and plasma acetate rose to 3.52 mmoles/liter. At 1 hour after the end of dialysis, blood bicarbonate, PCO2, and plasma acetate concentrations were similar in the two groups. Clinical problems occurred more frequently in the high-efficiency group during dialysis although the difference was not significant. The data indicate that (1) dialysis with acetate buffer effectively corrects pre-dialysis metabolic acidosis, (2) although children have a high rate of acetate metabolism, during high-efficiency dialysis this rate is exceeded by the influx of acetate, and acid-base abnormalities occur. These abnormalities are transient but may cause clinical problems.Modifications acido-basiques et métabolisme de l'acétate au cours de l'hémodialyse de routine ou à efficacité élevée chez l'enfant. Les modifications de l'état acido-basique et des concentrations plasmatiques d'acétate ont été étudiées chez huit enfants au cours de 11 séances d'hémodialyse. Au cours de la dialyse les bicarbonates diminuent (20,5 ± 0,7 à 19,6 ± 0,8 mEq/ litre), la PCO2 diminue (33,4 ± 0,8 à 27,5 ± 1,4 mm Hg), et le pH augmente (7,42 ± 0,01 à 7,48 ± 0,02). Au cours de l'heure qui suit la dialyse les bicarbonates s'élèvent à une valeur normale, 23,4 ± 0,07 mEq/litre, la PCO2 s'élève à 32,8 ± 0,8 mm Hg, et le pH est inchangé. La demi vie de l'acétate plasmatique, mesurée après la dialyse, était de 8,7 min. Au cours de cinq séances de dialyse à haute efficacité (clearance de l'urée, > 3,0 ml/min/kg) les bicarbonates baissent de 3,2 mEq/litre, la PCO2 de 8,7 mm Hg, et l'acétate plasmatique s'est élevé à 7,51 mmoles/litre alors qu'au cours de six séances de dialyse d'efficacité moyenne (clearance de l'urée, 1,5 à 3,0 ml/min/kg) les bicarbonates ont augmenté de 1,0 mEq/litre, la PCO2 a diminué de 3,6 mm Hg, et l'acétate plasmatique s'est élevé à 3,52 mmoles/litre. Une heure après la fin de la dialyse les bicarbonates, la PCO2 et l'acétate plasmatique étaient semblables dans les deux groupes. Des problèmes cliniques sont survenus plus souvent au cours de la dialyse dans le groups à haute efficacité bien que la différence ne soit pas significative. Ces résultats indiquent que (1) la dialyse avec le tampon acétate corrige efficacement l'acidose métabolique pré-dialytique, (2) bien que l'enfant ait une capacité élevée de métaboliser l'acétate, cette capacité est débordée, au cours de la dialyse à haute efficacité, par l'entrée d'acétate et des anomalies acidobasiques surviennent. Ces anomalies sont transitoires et peuvent déterminer des problèmes cliniques

Diesel Engine Exhaust Initiates a Sequence of Pulmonary and Cardiovascular Effects in Rats

This study was designed to determine the sequence of events leading to cardiopulmonary effects following acute inhalation of diesel engine exhaust in rats. Rats were exposed for 2 h to diesel engine exhaust (1.9 mg/m3), and biological parameters related to antioxidant defense, inflammation, and procoagulation were examined after 4, 18, 24, 48, and 72 h. This in vivo inhalation study showed a pulmonary anti-oxidant response (an increased activity of the anti-oxidant enzymes glutathione peroxidase and superoxide dismutase and an increase in heme oxygenase-1 protein, heme oxygenase activity, and uric acid) which precedes the inflammatory response (an increase in IL-6 and TNF-α). In addition, increased plasma thrombogenicity and immediate anti-oxidant defense gene expression in aorta tissue shortly after the exposure might suggest direct translocation of diesel engine exhaust components to the vasculature but mediation by other pathways cannot be ruled out. This study therefore shows that different stages in oxidative stress are not only affected by dose increments but are also time dependent

Metalloporphyrins – an update

Metalloporphyrins are structural analogues of heme and their potential use in the management of neonatal hyperbilirubinemia has been the subject of considerable research for more than three decades. The pharmacological basis for using this class of compounds to control bilirubin levels is the targeted blockade of bilirubin production through the competitive inhibition of heme oxygenase (HO), the rate-limiting enzyme in the heme degradative pathway. Ongoing research continues in the pursuit of identifying ideal metalloporphyrins, which are safe and effective, by defining therapeutic windows and targeted interventions for the treatment of neonatal hyperbilirubinemia