Effects of sodium concentration and osmolality on water and electrolyte absorption form the intact human colon.

The influence of sodium concentration and osmolality on net water and monovalent electrolyte absorption from or secretion into the intact human colon was studied in healthy volunteers. WHEN ISOTONIC SOLUTIONS CONTAINING NACL AND/OR MANNITOL WERE INFUSED INTO THE COLON: (a) a direct linear relationship between luminal sodium concentration (in the range of 23-150 mEq/liter) and rate of net water, sodium, and chloride absorption was found. No water absorption was found when sodium concentration in the luminal fluid was below 20 mEq/liter; (b) water and sodium absorption from the isotonic test solutions was not enhanced by addition of 80-250 mg/100 ml of glucose; and (c) the rate of water and sodium absorption was decreased markedly when chloride was replaced by bicarbonate in the test solution. WHEN THE COLON WAS PERFUSED WITH HYPERTONIC TEST SOLUTIONS CONTAINING NACL AND MANNITOL OR UREA: (a) water was absorbed from hypertonic NaCl solutions against a lumen-to-blood osmotic gradient of 50 mOsm/kg; (b) when the osmolality of the mannitol solution was increased, water entered the colonic lumen at a more rapid rate. The relationship between the rate of water entering the colon and the osmolality of the test solution was a parabolic one; (c) sodium and chloride entered the colonic lumen at a rate that was lineraly related to that of water entrance when the lumen-to-blood osmotic gradient exceeded 150 mOsm/kg; (d) water flow into the colonic lumen was identical when equimolar urea or mannitol solutions were infused; (e) neither urea nor mannitol was absorbed in significant amounts from the hypertonic solutions; and (f) our results suggest that the equivalent pore radius of the human colon is smaller than the molecular radius of urea (2.3 A).

Alveolar epithelium permeability to small solutes: developmental changes.

To determine whether alveolar epithelium permeability to small lipid-insoluble solutes changes during development we measured transport across the blood-gas barrier in isolated Ringer-perfused lungs from prenatal, 1-day-old, 4-wk-old, and adult rabbits. Radioactive test molecules, one of which was always sucrose, were dissolved in Ringer solution and instilled into the trachea of degassed lungs. Samples taken from recirculating perfusate were used to calculate permeability-surface area (PS) products. Results were expressed as the ratio (PS)/(PS)sucrose, and as absolute permeability. Lungs from 4-wk-old rabbits were studied most thoroughly; the (PS)/(PS) sucrose ratios obtained are urea 4.0, erythritol 1.3, mannitol 0.98, L-glucose 1.4, and D-glucose 5.6. These and other data imply that the most lipid-insoluble molecules (erythritol, mannitol, L-glucose, and sucrose) are transported by a nonselective bulk process. Urea transport is primarily through lipid membranes; D-glucose seems to involve a special process. Sucrose and L-glucose permeability decreased during development, but their relative permeabilities did not change. Small lipid-insoluble solutes apparently do not cross the alveolar epithelium through small water-filled pores, and their permeability decreases as the animal matures.

Effects of dimethylsulfoxide (DMSO) on the oxygen paradox in perfused rat hearts.

The effect of dimethylsulfoxide (DMSO) on the morphologic features of cells and cellular enzyme release was studied in Langendorf-perfused rat hearts at 37 C. Ten percent DMSO greatly reduced the magnitude of oxygen-induced creatine kinase release (O2-CK) after a 60-minute period of hypoxic perfusion. DMSO also protected cells from development of severe contracture with formation of contraction bands. A linear correlation was found between the magnitude of O2-CK release and the percentage of cells in hearts containing contraction bands. Hypertonic mannitol did not protect hearts from CK release due to the calcium paradox, although DMSO was effective in this regard. DMSO reduced contractile force of hearts and tensions caused by hypoxic contracture as measured by an intraventricular balloon. This study suggests that DMSO affords protection from O2-CK release by actions on cells other than its osmotic effects. DMSO may alter the response of injured cells to the effects of calcium ions.