Background. Impaired vasomotor function has been suggested as playing a rol
e in the pathophysiology of atherosclerosis and it may also affect the late
patency of bypass grafts. We evaluated, in vitro, the influence of risk fa
ctors of atherosclerosis on saphenous vein endothelial function in patients
with cardiovascular diseases. Methods. Forty-five saphenous vein rings wit
h intact (E+) and denuded endothelium (E-) were studied. The following drug
s were used: norepinephrine (NE), acetylcholine (Ach), histamine (H) and se
rotonine (5-HT). Result. Contraction to norepinephrine (n=15) showed a maxi
mal tension of 783 +/- 115% that was increased in diabetics, smokers, and p
atients with hypertension. There was a wide range of response to acetylchol
ine in rings with intact endothelium (n=25), (mean relaxation 16.4 +/- 1.7%
, ranging from -22.2% to 45%) with relaxation (26 +/- 1.1%) and contraction
(-11 +/- 1.2%); relaxation was reduced in patients with hypertension and i
n diabetics (7.4 +/- 2.6% vs non diabetics 24.4 +/- 1.73%; p <0.01). Five o
f the 12 veins from diabetics exibited contraction (10 +/- 1.48%). Histamin
e (n=15) caused moderate relaxation at low doses (25 +/- 2.46%) followed by
contraction at higher concentrations (184 +/- 5.7%). This was greater in d
iabetics (193 +/- 6.8% vs non diabetics 157 +/- 5.3%; p=0.045) while in pre
parations without endothelium (n=10) only relaxation was obtained (45 +/- 2
.89%). Contraction (242 +/- 7.4%) was observed in response to serotonine (n
=15) that was not affected by endothelial removal. In this study saphenous
vein: (1) exhibited a wide range of responses to acetylcholine; (2) evoked
marked contraction to norepinephrine and serotonine; (3) elicited contracti
on in response to histamine that was endothelium-dependent, suggesting the
production or the release of an endothelium-derived-contracting-factor (EDC
F). Conclusions. Saphenous vein is able to secrete a contracting factor in
patients with risk factors of atherosclerosis and above all diabetes. The m
echanisms that regulate the balance between the relaxing and contracting fa
ctors and how the endothelial cells become the source of the substances wit
h vasoconstrictor activity remain to be determined.