Acipimox stimulates skin blood flow by a cyclo-oxygenase-dependent mechanism.
The blood flow in the skin and the urinary excretion of the PGI2 metabolite 2,3-dinor-6-keto-PGF1a (PGI-M) were determined in the nine healthy subjects randomly assigned to double-blind oral treatment with a) placebo and acipimox (AC) 500 mg, b) acetylsalicylic acid 1500 mg and AC 500 mg, or c) placebo and nicotinic acid (NIC) 500 mg, on three different occasions. After treatment with placebo and AC there was a transient increase in the skin blood flow, up to about four-times the basal level, and a concomitant increase in skin temperature. After acetylsalicylic acid and AC no increase in skin flow rate or temperature was found. Urinary excretion of PGI-M was insignificantly increased by AC, but fell after acetylsalicylic acid pretreatment. NIC elicited a more marked increase in skin blood flow than AC, and in parallel the urinary excretion of PGI-M was more than doubled. It is concluded that cutaneous flushing induced by AC is cyclo-oxygenase dependent. In comparison to NIC, however, AC appears as a weak stimulant of vascular prostacyclin formation.
Edlund
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Department of Clinical Physiology, Karolinska Institute, Huddinge Hospital, Sweden.
Musatti
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L
Wennmalm
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D015121:6-Ketoprostaglandin F1 alpha / Q000031:analogs & derivatives / Q000097:blood / Q000652:urine; D000328:Adult; D016861:Cyclooxygenase Inhibitors; D005260:Female; D006439:Hemodynamics / Q000187:drug effects; D006801:Humans; D000960:Hypolipidemic Agents / Q000494:pharmacology*; D008297:Male; D011719:Pyrazines / Q000494:pharmacology*; D012039:Regional Blood Flow / Q000187:drug effects; D012867:Skin / Q000098:blood supply*; D012881:Skin Temperature / Q000187:drug effects
D016861:Cyclooxygenase Inhibitors; D000960:Hypolipidemic Agents; D011719:Pyrazines; D015121:6-Ketoprostaglandin F1 alpha; C028290:2,3-dinor-6-ketoprostaglandin F1alpha; C027696:acipimox