Reduction in tumor blood flow in skin flap tumor after hydralazine is not due to a vascular steal phenomenon

The purpose of this study was to evaluate whether a “vascular steal” mechanism (preferential arteriolar vasodilation in normal vs. tumor tissue concomitant with a reduction in blood pressure) is responsible for tumor blood flow reduction after hydralazine administration. Fischer‐344 rats, fitted with dorsal flap window chambers that allowed visualization of tumor and normal healing subcutaneous tissue vasculature, were the experimental subjects. Intravital microscopy of tumor and normal microvasculature was used to measure microvessel diameters and red cell velocities before and after hydralazine (0.4 mg/kg, i.v.) administration. Hydralazine caused an average drop in mean arterial pressure of 32 mmHg and a concomitant 70% drop in capillary and venous blood flow in central tumor regions in both 9‐ and 14‐day‐old tumors. Intermittent blood flow frequency increased in capillaries and veins from 3% prior to drug to 46% after drug administration. In contrast, capillary and venous flow increased in adjacent normal tissues by 30%. Normal and tumor arterioles showed no significant change in diameter after hydralazine administration. Since the reductions in tumor blood flow were not accompanied by preferential arteriolar dilation in normal arterioles, the hypothesis that a vascular steal phenomenon was responsible for the observed reduction in tumor blood flow in this model system was disproved. A more likely explanation is that the reduction in tumor vessel diameter and concomitant flow reduction are a passive effect related to the relative difference between intravascular pressure and interstitial fluid pressure and/or tissue pressures, the latter of which are known to be increased in tumors. The results suggest that reduction in tumor blood flow might be expected following blood pressure reduction, even when the tumor resides in normal tissue beds that are not actively vasodilated by an antihypertensive agent. © 1994 Wiley‐Liss, Inc.