In skin lesions of chronic venous incompetence (CVI) transcutaneous oxygen
pressure (tcpO(2)) at the ankle is often reduced. However, in some CVI pati
ents the tcpO(2) during suprasystolic occlusion remains significantly highe
r than in healthy subjects. The aim of the present study was to investigate
which kind of CVI patients develop this phenomenon and whether the higher
tcpO(2) during occlusion is caused by a smaller oxygen consumption of the s
kin or by an increased local oxygen content. The oxygen consumption of the
skin was measured by the pO(2) decrease (Delta tcpO(2)/Delta t) after stopp
ing the arterial oxygen supply when the hemoglobin was saturated by oxygen
inhalation, i.e., at tcpO(2) values above 120-130 mmHg. By multiplying the
tcpO(2) with the mean oxygen solubility coefficient of the skin the content
of physically dissolved oxygen is obtained. The decrease of tcpO(2) in the
55- to 45-mmHg range indicates the consumption of oxygen physically dissol
ved and chemically bound to hemoglobin. It gave a parameter for estimating
the local hemoglobin content of the skin. These values and the minimal tcpO
(2) after a 5-min arterial occlusion were measured in 14 healthy subjects,
in 13 patients with varicose veins, but no skin lesions, in 10 patients wit
h CVI lesions like white atrophy and lipodermatosclerosis and in 16 CVI pat
ients with Open venous ulcers. During suprasystolic occlusion tcpO(2) at th
e ankle remained significantly higher in CVI patients with skin lesions tha
n in the healthy control subjects (25.6 +/- 18.9 versus 8.0 +/- 7.0 mmHg).
The steepness of the tcpO(2) decrease caused by cutaneous oxygen consumptio
n in healthy subjects was not significantly different from the CVI patients
. In contrast, the decrease of tcpO(2) at the ankle between 55 and 45 mmHg
was 1.9 +/- 2.0 mmHg/s in the control group and 0.7 +/- 0.5 mmHg/s in the g
roup with open venous ulcers. These results indicate a higher hemoglobin co
ntent in the skin of the CVI patients than in healthy subjects. Obviously,
the hemoglobin bound oxygen content in the skin of CVI patients is increase
d. Thus, a lack of oxygen is unlikely to be the primary reason for the deve
lopment of skin lesions in CVI. (C) 2000 Academic Press.