Reversal of postprandial endothelial dysfunction by cyclooxygenase inhibition in healthy volunteers.
The aim of this study was to evaluate the role of cyclooxygenase (COX) in venous vascular reactivity changes after an oral lipid overload (OLO). Venous endothelial function (dorsal hand vein technique) was evaluated in fasting, 30 minutes after COX inhibition (aspirin-fasting), 2 to 4 hours after an OLO (1000 kcal, 58% fat), and again after COX inhibition (aspirin-OLO, 600 mg/200 mL water) in 10 healthy adults (age, 28.1 +/- 1.3 years; body mass index, 22.3 +/- 0.6 kg/m). Fasting, 2- to 4-hour post-OLO, and 60-minute postaspirin plasma glucose, insulin, and lipids were also evaluated. The OLO increased triglycerides and insulin, reduced low-density lipoprotein and high-density lipoprotein, but glycemia and total cholesterol remained unchanged. There were no metabolic differences between OLO and aspirin-OLO. In fasting, aspirin reduced acetylcholine-induced venodilation (107.0% +/- 14% versus 57.3% +/- 11%; P < 0.001). Vascular reactivity was blunted after the OLO (phenylephrine dose: 0.3 +/- 0.2 fasting versus 1.9 +/- 0.8 nmol/min after OLO; P < 0.001) and was partially corrected by aspirin (0.4 +/- 0.2; P < 0.001). Similar changes were observed in maximum venodilation after acetylcholine (107.0% +/- 14% fasting versus 60.4% +/- 9% after OLO, P < 0.001; aspirin-OLO: 95.9% +/- 6%; P < 0.001). The responses to sodium nitroprusside remained unchanged during the study. We conclude that the OLO reduction in the endothelium-dependent venoconstriction and venodilation is partially the result of the action of COX.
Signori
Luis Ulisses
LU
Institute of Cardiology of Rio Grande do Sul/University Foundation of Cardiology, 370-Santana-Porto Alegre, RS-Brasil-90620-000.
da Silva
Antônio Marcos Vargas
AM
Plentz
Rodrigo Della Méa
RD
Moreno
Heitor
H
Irigoyen
Maria Cláudia
MC
Schaan
Beatriz D'Agord
BD
D000109:Acetylcholine / Q000494:pharmacology; D000328:Adult; D001241:Aspirin / Q000494:pharmacology; D001786:Blood Glucose / Q000378:metabolism; D015992:Body Mass Index; D008076:Cholesterol, HDL / Q000097:blood; D008078:Cholesterol, LDL / Q000097:blood; D016861:Cyclooxygenase Inhibitors / Q000494:pharmacology*; D004730:Endothelium, Vascular / Q000187:drug effects* / Q000502:physiology; D005215:Fasting; D006801:Humans; D007004:Hypoglycemic Agents / Q000097:blood; D007328:Insulin / Q000097:blood; D050356:Lipid Metabolism; D008055:Lipids / Q000097:blood*; D008297:Male; D010656:Phenylephrine / Q000494:pharmacology; D019518:Postprandial Period / Q000187:drug effects*; D013997:Time Factors; D014280:Triglycerides / Q000097:blood; D014664:Vasodilation / Q000187:drug effects; D014680:Veins / Q000187:drug effects / Q000502:physiology
D001786:Blood Glucose; D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D016861:Cyclooxygenase Inhibitors; D007004:Hypoglycemic Agents; D007328:Insulin; D008055:Lipids; D014280:Triglycerides; D010656:Phenylephrine; D000109:Acetylcholine; D001241:Aspirin