A. Cupisti et al., Responses of the skin microcirculation to acetylcholine and to sodium nitroprusside in chronic uremic patients, INT J CL L, 30(3), 2000, pp. 157-162
Citations number
37
Categorie Soggetti
Medical Research Diagnosis & Treatment
Journal title
INTERNATIONAL JOURNAL OF CLINICAL & LABORATORY RESEARCH
The aim of the present study was to assess the endothelial function of the
microcirculation in chronic renal failure. We investigated the responses of
the cutaneous blood flow to locally delivered acetylcholine and sodium nit
roprusside in uremic patients. The study included 60 chronic uremic patient
s: 40 patients with a creatinine clearance of 4-25 ml/min were on conservat
ive treatment and 20 patients were on maintenance hemodialysis. The changes
in skin blood flow following iontophoretic delivery of acetylcholine (an e
ndothelium-dependent vasodilator) and sodium nitroprusside (an endothelium-
independent vasodilator) were measured by laser Doppler flowmetry. Acetylch
oline induced a progressive increase in blood flow in both groups, reaching
approximately 100% of the maximal hyperemic response obtained by sodium ni
troprusside delivery. The percent increase in blood flow from baseline was
lower in hemodialysis patients than in patients on conservative treatment,
after both acetylcholine (550+/-44 vs. 718+/-61%, P<0.05) and sodium nitrop
russide (553+/-46 vs. 735+/-69%, P<0.05) delivery. In the hemodialysis grou
p, the hyperemic responses to acetylcholine and sodium nitroprusside did no
t improve after the hemodialysis session. Hence, the hyperemic responses of
the skin microcirculation are lower in hemodialysis patients than in patie
nts on conservative treatment, and did not ameliorate after hemodialysis. I
t seems to be independent of endothelial dysfunction, and associated with t
he severity of uremia and with the maintenance hemodialysis treatment. This
microcirculatory abnormality is in keeping with the arterial stiffness and
vascular wall damages described in dialysis patients, which contribute to
the cardiovascular morbidity of chronic uremia.