Vandorpe D H, Nadler S P, Levine D Z
Department of Physiology, University of Ottawa, Ont., Canada.
Can J Physiol Pharmacol. 1991 Nov;69(11):1784-8. doi: 10.1139/y91-263.
Rebound metabolic alkalosis is a transient alkalemia that is seen during recovery from NH4Cl-induced metabolic acidosis. The persistent elevation of plasma bicarbonate concentration is the result of continuing excretion of net acid by the kidney. Bicarbonate transport by inner medullary collecting ducts has been reported by others to proceed normally (i.e., bicarbonate reabsorption continues in this segment) during rebound metabolic alkalosis. No other segmental responses have been evaluated. Since the surface distal tubule of the rat is known to both reabsorb and secrete bicarbonate in vivo, it was of interest to determine the response of this segment. Our results show that the distal tubule microperfused in vivo during rebound metabolic alkalosis continues to reabsorb significant amounts of bicarbonate, despite the presence of systemic alkalemia that we have previously shown to be associated with distal tubule bicarbonate secretion.
反弹性代谢性碱中毒是一种在氯化铵诱导的代谢性酸中毒恢复过程中出现的短暂性碱血症。血浆碳酸氢盐浓度持续升高是肾脏持续排泄净酸的结果。其他人曾报道,在反弹性代谢性碱中毒期间,髓质内集合管的碳酸氢盐转运正常进行(即该节段继续重吸收碳酸氢盐)。尚未评估其他节段的反应。由于已知大鼠的表层远曲小管在体内既能重吸收又能分泌碳酸氢盐,因此确定该节段的反应很有意义。我们的结果表明,在反弹性代谢性碱中毒期间体内微灌注的远曲小管继续重吸收大量碳酸氢盐,尽管存在我们之前已证明与远曲小管碳酸氢盐分泌相关的全身性碱血症。