No improvement in perfusion and oxygenation of experimental tumors upon application of vasodilator drugs

The oxygen deficiency seen in solid tumors is predominantly caused by an in sufficient O-2 supply as a result of inadequate tumor perfusion. The aim of this study was to analyze whether a number of vasodilator drugs might be s uitable to increase tumor perfusion and consequently improve the oxygenatio n status of experimental tumors. Rats with s.c. DS-sarcomas were treated wi th either Na+-nitroprusside (7-25 mug . min(-1). kg(-1) BW) or nifedipine ( 10 mug . min(-1). kg(-1) BW). Red blood cell (RBC) flux was assessed contin uously using laser-Doppler flowmetry and mean tumor pO(2) was measured pola rographically using O-2-sensitive catheter electrodes. Systemic application of the vasodilator drugs resulted in a dose-dependent decrease in MABP. In parallel, tumor perfusion was reduced linearly with failing MABP resulting in a decrease in RBC flux by approximately 40%. Resistance to flow did not change during the infusion indicating that these drugs have no impact on t umor vessel diameter. With decreasing tumor perfusion, tumor pO(2) was redu ced parallel to the MABP drop. This effect was more distinct with Na+-nitro prusside than with nifedipine due to the more pronounced fall in MABP. The vasodilator drugs studied are not suitable for dilation of tumor vessels ei ther because the tumor vasculature lacks contractile wall elements or becau se the vessels are already maximally dilated.