Contribution of hyperosmolality to glucose-induced intestinal hyperemia

To test the hypothesis that changes in tissue osmolality participate in glucose-induced absorptive hyperemia, the mucosa of the rat jejunum was suffused with isotonic or hypertonic glucose solutions. Blood flow was calculated from the product of a constant, arteriolar diameter, and red blood cell velocity, which were measured in the submucosal microcirculation. Isotonic glucose solutions (293 +/- 2 mosmol/kg) were prepared by diluting 5, 10, or 20 ml of 5% glucose, which is isotonic with plasma, to 100 ml with Ringer-bicarbonate buffer to concentrations of 250, 500, and 1,000 mg/100 ml. Glucose was added directly to Ringer-bicarbonate buffer to increase osmolality. The osmolalities of the 250, 500, and 1,000 mg/100 ml hypertonic solutions were 305 +/- 3,319 +/- 3, and 353 +/- 1 mosmol/kg, respectively. Glucose caused a concentration-related increase in estimated submucosal arteriolar blood flow that averaged 18-21% (n = 14), 24-27% (n = 14), and 34-45% (n = 14) at 250, 500, and 1,000 mg/100 ml glucose, respectively. There was no effect of solution osmolality on either the time course or the magnitude of the hyperemia at a given glucose concentration. Whereas the magnitude of the glucose-induced hyperemia averaged less than 50%, the application of 10(-2) M adenosine caused a fivefold increase in calculated blood flow (492 +/- 67%, n = 24). Thus, glucose caused relatively small increases in intestinal blood flow. If changes in luminal osmolality caused changes in intestinal tissue osmolality, then it is unlikely that hyperosmolality participates in the functional hyperemia associated with glucose absorption.