Iacovitti M, Nash L, Peterson L N, Rochon J, Levine D Z
J Clin Invest. 1986 Dec;78(6):1658-65. doi: 10.1172/JCI112759.
We have performed microperfusion studies on distal tubules of normal and alkalotic rats in an attempt to demonstrate in vivo bicarbonate secretion. All perfusion solutions were free of phosphate and other nonbicarbonate buffers. In both normal and alkalotic rats, distal perfusions elicited significant tCO2 entry only at high flow (24 nl/min). Even when perfusate tCO2 concentration closely matched plasma tCO2 concentration (30 mM tCO2), significant tCO2 entry again occurred at high flow. This was associated with a rise of the perfusate tCO2 concentration, which indicated net entry of tCO2 against a concentration gradient. In this "symmetrical" perfusion situation, acetazolamide blockade prevented tCO2 entry. Accordingly: distal tubule tCO2 entry is demonstrable in both alkalotic and normal rats at high flow rates; increasing perfusate tCO2 concentration can suppress tCO2 entry; and entry can occur in the absence of a gradient and this effect can be blocked by acetazolamide.
我们对正常大鼠和碱中毒大鼠的远端小管进行了微灌注研究,以试图在体内证明碳酸氢盐的分泌。所有灌注溶液均不含磷酸盐和其他非碳酸氢盐缓冲液。在正常大鼠和碱中毒大鼠中,仅在高流量(24 nl/分钟)时,远端灌注才引起显著的总二氧化碳(tCO2)进入。即使灌注液tCO2浓度与血浆tCO2浓度紧密匹配(30 mM tCO2),在高流量时仍再次出现显著的tCO2进入。这与灌注液tCO2浓度的升高相关,这表明tCO2逆浓度梯度的净进入。在这种“对称”灌注情况下,乙酰唑胺阻断可防止tCO2进入。因此:在高流速下,碱中毒大鼠和正常大鼠的远端小管均可证明有tCO2进入;增加灌注液tCO2浓度可抑制tCO2进入;并且在没有梯度的情况下也可发生进入,且这种效应可被乙酰唑胺阻断。