Hypocapnic but not metabolic alkalosis impairs alveolar fluid reabsorption.
نویسندگان
چکیده
Acid-base disturbances, such as metabolic or respiratory alkalosis, are relatively common in critically ill patients. We examined the effects of alkalosis (hypocapnic or metabolic alkalosis) on alveolar fluid reabsorption in the isolated and continuously perfused rat lung model. We found that alveolar fluid reabsorption after 1 hour was impaired by low levels of CO2 partial pressure (PCO2; 10 and 20 mm Hg) independent of pH levels (7.7 or 7.4). In addition, PCO2 higher than 30 mm Hg or metabolic alkalosis did not have an effect on this process. The hypocapnia-mediated decrease of alveolar fluid reabsorption was associated with decreased Na,K-ATPase activity and protein abundance at the basolateral membranes of distal airspaces. The effect of low PCO2 on alveolar fluid reabsorption was reversible because clearance normalized after correcting the PCO2 back to normal levels. These data suggest that hypocapnic but not metabolic alkalosis impairs alveolar fluid reabsorption. Conceivably, correction of hypocapnic alkalosis in critically ill patients may contribute to the normalization of lung ability to clear edema.
منابع مشابه
Injurious effects of hypocapnic alkalosis in the isolated lung.
Mechanical ventilation can worsen morbidity and mortality by causing ventilator-associated lung injury, especially where adverse ventilatory strategies are employed. Adverse strategies commonly involve hyperventilation, which frequently results in hypocapnia. Although hypocapnia is associated with significant lung alterations (e.g., bronchospasm, airway edema), the effects on alveolar-capillary...
متن کاملA novel target for diuretic therapy.
The reabsorption of salt in the distal nephron is predominantly mediated via the thiazide-sensitive sodium chroride cotransporter, NCC (SLC12A3), and the chloride-bicarbonate exchanger pendrin (SLC26A4, PDS), with pendrin working in tandem with the epithelial sodium channel and NCC working by itself. Single deletion of NCC or pendrin in genetically engineered mouse models does not cause salt wa...
متن کاملDepressed distal tubule acidification corrects chloride-deplete alkalosis in rats.
We investigated the relative contributions made by the proximal and distal tubule to the correction of Cl-deplete metabolic alkalosis induced by systemic administration of NaCl. Free-flow micropuncture was used to examine net bicarbonate reabsorption in superficial proximal and distal tubules of anesthetized Munich-Wistar rats during maintenance and correction of chronic furosemide-induced Cl-d...
متن کاملSegmental chloride and fluid handling during correction of chloride-depletion alkalosis without volume expansion in the rat.
To determine whether chloride-depletion metabolic alkalosis (CDA) can be corrected by provision of chloride without volume expansion or intranephronal redistribution of fluid reabsorption, CDA was produced in Sprague-Dawley rats by peritoneal dialysis against 0.15 M NaHCO3; controls (CON) were dialyzed against Ringer's bicarbonate. Animals were infused with isotonic solutions containing the sam...
متن کاملCorrection of metabolic alkalosis by the kidney after isomertric expansion of extracellular fluid.
Metabolic alkalosis was induced in dogs by administering ethacrynic acid and sustained by feeding a chloride-deficient diet. At the height of the alkalosis extracellular fluid was expanded "isometrically," i.e., with an infusion that duplicated plasma sodium, chloride, and bicarbonate concentrations. Correction of metabolic alkalosis promptly followed such expansion and was attributed to the se...
متن کاملذخیره در منابع من
با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید
عنوان ژورنال:
- American journal of respiratory and critical care medicine
دوره 171 11 شماره
صفحات -
تاریخ انتشار 2005