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Effect of Galactose on Systemic Hemodynamics and Blood Flow Rate in Normal and Tumor Tissues in Rats¹

University of Texas Medical Branch, Galveston, TX 77550 [D. J. D., N. E. K., K. S.]; Department of Chemical Engineering, University of Kentucky, Lexington, KY 40506-0046 [K. A. W.]; and Department of Chemical Engineering, Carnegie Mellon University, Pittsburgh, PA 15213-3890 [R. K. J.]

The effect of galactose on systemic hemodynamics and blood flow rate of Walker 256 carcinomas and several normal tissues of unanesthetized, unrestrained female Sprague-Dawley rats was measured, using the radioactive microsphere technique, prior to and at 30 and 60 min after galactose administration (6 g/kg body weight, i.v.). Whereas heart rate remained unchanged following injection, cardiac output (CO) and cardiac index decreased by 35% (P < 0.05). Mean arterial pressure immediately decreased during the injection but then increased reaching a value 10% (P < 0.05) above the baseline 30 min following injection. Stroke volume (SV) decreased by 30% (P < 0.05) and total peripheral resistance increased by 65% (P < 0.05). Redistribution of blood flow, expressed as %CO, among normal tissues was seen to the brain, kidneys, liver, jejunum, and hindlimb muscle and away from the pancreas, stomach, and skin. Changes in %CO to the spleen, colon, forelimb muscle, and peritumor tissue were not significant. Blood flow rate in most normal tissues either decreased or remained constant following injection. An exception was in the liver where blood flow significantly increased. Blood flow significantly decreased in the tumor (60%) and this reduction in blood flow was larger than the reduction in CO. These results suggest that (a) the effect of galactose on systemic hemodynamics and blood flow rate are similar to those produced by glucose; (b) reduction in blood flow rate in tumors is due to both systemic and local effects; and (c) changes in blood flow to normal tissues should not be disregarded when using galactose in combination with hyperthermia and/or chemotherapy for cancer treatment.

¹ Supported by a grant from the NIH(CA-37239) and Cancer Center Grant, University of Texas Medical Branch, Galveston, TX (CA-17701). This work was presented at the 35th Annual Radiation Research Society Meeting and the 7th Annual North American Hyperthermia Meeting, Atlanta, GA, February 23, 1987.

² To whom requests for reprints should be addressed.

Received 5/28/87. Revised 12/ 1/87. Accepted 12/ 9/87.