Key result
Cyclooxygenase inhibition with aspirin partially corrected the reduction in maximum venodilation after acetylcholine induced by an oral lipid overload (95.9% vs 60.4%; P<0.001).
Why the study?
The role of cyclooxygenase in venous vascular reactivity changes after an oral lipid overload was not well understood.
Does cyclooxygenase inhibition with aspirin improve venous endothelial function after an oral lipid overload in healthy adults?
Does cyclooxygenase inhibition with aspirin improve venous endothelial function after an oral lipid overload in healthy adults?
Cyclooxygenase inhibition with aspirin partially reverses the acute endothelial dysfunction induced by an oral lipid overload in healthy adults.
Aspirin partially reverses lipid-induced venous endothelial dysfunction; hypothesis-generating for COX contribution in small healthy cohorts.
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.
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Signori et al. (2009) studied Healthy adults (n=10). Cyclooxygenase inhibition (aspirin) vs. Oral lipid overload alone was evaluated on Maximum venodilation after acetylcholine (p=<0.001). Cyclooxygenase inhibition with aspirin partially corrected the reduction in maximum venodilation after acetylcholine induced by an oral lipid overload (95.9% vs 60.4%; P<0.001).
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