Nitric oxide (NO) is a free radical molecule with high reactivity, a s
hort half life and a variety of physiological activities. The role of
NO in tumor microcirculation, based on the data collected to date, can
be summarized as follows: 1) NO may partially mediate tumor angiogene
sis; 2) endogenous NO derived from tumor vascular endothelium and/or t
umor cells increases and/or maintains tumor blood flow via dilatation
of arteriolar vessels, decreases leukocyte-endothelial interaction, an
d increases vascular permeability; 3) exogenous NO can increase tumor
blood flow via vessel dilatation, and reduce vessel tone; and 4) NO pr
oduction rates and vascular response to NO are heterogeneous and tumor
-dependent. Modulation of NO level in tumor vessels can alter tumor he
modynamics and thus augment oxygen, drug, gene vector and effector cel
l delivery to solid tumors.