AJP - Gastrointestinal and Liver Physiology, Vol 248, Issue 5 521-G525, Copyright © 1985 by American Physiological Society
Contribution of hyperosmolality to glucose-induced intestinal hyperemia
K. G. Proctor
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.
