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Effect of Glucose and Galactose on Microcirculatory Flow in Normal and Neoplastic Tissues in Rabbits¹

Department of Chemical Engineering, Carnegie Mellon University, Pittsburgh, Pennsylvania 15213

Red blood cell (RBC) velocity and vessel lumen diameter were measured in individual microvessels of both normal (mature granulation) and neoplastic (VX2 carcinoma) tissues grown in a transparent ear chamber prior to and following glucose and galactose injections (6 g/kg i.v.) in anesthetized rabbits. RBC velocity was measured using the dual-slit photometric technique and the diameter of the vessels was determined using an image shearing device. From these measurements, the mean volumetric flow rates in the individual vessels were determined. Glucose produced a 90% decrease in RBC velocity and blood flow rate in the tumor at 65 min postinjection without modifying the flow in the normal tissue. Galactose, on the other hand, decreased RBC velocity and blood flow in the tumor and normal tissues by approximately 90 and 55%, respectively, at 65 and 5 min postinjection. Neither glucose nor galactose caused any statistically significant changes in vessel diameter, WBC adhesion to vessels, microvascular permeability, or systemic viscosity. Results suggest that the mechanism responsible for flow reduction in tumors due to glucose and galactose are both systemic and local. Systemic mechanisms include reduction and redistribution of the cardiac output. Local mechanisms for glucose include blockage of rigid RBC in the tortuous vasculature of tumor and increase in local blood viscosity also due to RBC rigidity. Increase in RBC rigidity is caused by glucose itself as well as by low pH in tumors. Results also show that the local mechanisms responsible for blood flow reduction following galactose injection differ from those responsible for the reduction following glucose injection.

¹ Financial assistance was furnished by grants from the National Cancer Institute (CA-36358 and CA-37239) and R. K. Mellon Foundation. Preliminary reports of this work were presented at the Radiation Research Society Meeting, May 1985, and the Microcirculatory Society Meeting, May 1985.

² Recipient of a NIH Predoctoral Training Grant (1981–1985) during the course of this work.

³ Recipient of the NIH Research Career Development Award (1980–1985) during the course of this work. To whom requests for reprints should be addressed.

Received 4/ 2/85. Revised 6/30/86. Accepted 10/15/86.

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