Abstract

Damage of the small intestinal mucosa (SMI) could result in different permeability to water and electrolytes, and, hence, produce an abnormal response to oral hydration solutions (OHS) of diverse sodium:glucose ratios and osmolality. This hypothesis was tested in an animal model of mucosal damage induced by exposure of the jejunum to 5 mM deoxycholate (Dch). Anesthetized rats were treated [+], or not [−], with Dch in buffered saline for 1 hr and perfused through the jejunum with OHS containing bicarbonate, potassium and Na:glucose ratios (mEq/l:mM) 30:55, 60:50, 60:111 and 90:111; and 146, 190, 258 and 324 mOsm/kg, respectively. In [−] rats, Na was retained in solutions with >60 mEq/l Na, but in the [+] group the balance was negative at all Na levels. The rate of water absorption in both groups of rats inversely correlated with OHS osmolality. Net water transport ranged from a mean of 3.68±0.21 to 1.36±0.25 μl/min x cm in [−] rats, and from 1.68 ±0.11 to 0.10±0.19 in [+] rats. By extrapolation, these data reveled that, at zero osmolality, the [+] rats would lose about half their water absorption capacity. Water influx and efflux data in [−] rats correlated inversely and directly with osmolality, respectively, but in [+] rats efflux rates were consistently higher than in [−] and independent of OHS osmolality. Therefore, if mucosal damage is suspected, the advantage of lower osmolality in terms of net water absorption is lost and high Na concentration is insufficient to avoid Na loss.

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