K．C．Wong教授生平

《中华麻醉学杂志》编委会第七届及第八届海外编委、《麻醉与镇痛》中文版创始人、国际麻醉研究学会（IARS）前主席K．C．Wong教授于2006年5月18日因癌症医治无效，在台北逝世。K．C．Wong教授于1936年11月12日出生于重庆市，8岁随父亲到美国檀香山，在那里接受教育并开始了事业生涯。他谦逊和蔼、学识渊博、医技精湛、医德高尚。不仅是美国麻醉学界一位领军人物，也是中国麻醉学界的良师益友。     

Effect of K depletion on renal K and Rb excretion: evidence for activation of K reabsorption.

Prolonged potassium depletion activates tubular transport mechanisms mediating potassium absorption. To study ion specificity and factors that modulate the activity of potassium transport pathways, fractional potassium excretion (FEK) was compared with that of rubidium (FERb) in control and potassium-depleted rats subjected to various experimental maneuvers. In control rats FEK considerably surpassed FERb (FEK/FERb 1.54 +/- 0.08; mean +/- SEM), whereas in potassium-depleted rats FEK was significantly lower than FERb (FEK/FERb 0.72 +/- 0.05). Preferential retention of potassium compared to rubidium in potassium-depleted rats was accentuated (FEK/FERb 0.33 +/- 0.01) when residual potassium secretion was inhibited by amiloride and K-H exchange stimulated by increased distal buffer delivery (metabolic alkalosis). When distal fluid and buffer delivery were increased in control animals by acetazolamide, FEK and FERb rose in parallel. In potassium-depleted rats only FERb but not FEK was enhanced by acetazolamide. These data demonstrate that both potassium secretory and potassium absorptive transport pathways prefer potassium to its congener rubidium. Prolonged potassium depletion activates a potassium absorptive mechanism which is stimulated by increased distal buffer delivery and which transports potassium more effectively than rubidium.     

K. H. Bauer zum 70. Geburtstag

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