Key result
Indomethacin reduces peak forearm reactive hyperaemia conductance by ~34% in older vs. young adults.
Why the study?
Does an acute dose of indomethacin attenuate forearm vascular conductance during reactive hyperaemia in older adults compared with young adults?
Does an acute dose of indomethacin attenuate forearm vascular conductance during reactive hyperaemia in older adults compared with young adults?
Acute cyclo-oxygenase inhibition with indomethacin attenuates resistance vessel responses during reactive hyperaemia in older adults, suggesting potential adverse cardiovascular consequences of COX inhibition in this population.
May warrant caution with COX inhibitors in older adults; leaves open clinical cardiovascular risks and need for prospective confirmation.
New Findings What is the central question of this study? We aimed to investigate the effects of the cyclo‐oxygenase (COX) inhibitor indomethacin on resistance vessel function in young and older adults and to test the hypothesis that indomethacin will attenuate forearm vascular conductance during reactive hyperaemia. What is the main finding and its importance? Older adults demonstrated an attenuated vasodilator response to ischaemia after COX inhibition compared with their younger counterparts. This suggests that older adults do not compensate for the vascular changes induced by an acute dose of indomethacin. Long‐term use of indomethacin may increase vascular resistance and reduce the response to acute haemodynamic stress in older adults. The risk for potential adverse cardiovascular consequences of COX inhibition should be considered. We have previously shown that non‐selective cyclo‐oxygenase inhibition, via indomethacin, unfavourably increased central blood pressure in older adults, with little effect in young adults. In addition, the vasoactive prostaglandins have been shown to contribute to both peripheral vasodilator responses and large artery function; however, there is little information available in older adults and conflicting reports in young adults on the extent to which resistance vessel function is influenced by indomethacin. Thus, we tested the hypothesis that cyclo‐oxygenase inhibition using indomethacin would attenuate forearm vascular conductance during reactive hyperaemia in older adults compared with young adults. Forearm blood flow responses to 5 min of forearm ischaemia were measured in 26 healthy adults (13 young, 25 ± 5 years old; and 13 older, 65 ± 6 years old), using venous occlusion plethysmography before and after indomethacin. Baseline forearm blood flow and vascular conductance were not different between groups during either trial, and there were no age‐related differences prior to cyclo‐oxygenase inhibition. Peak forearm vascular conductance and blood flow were similar between groups before indomethacin, but lower in older adults after indomethacin compared with young adults (27 ± 4 versus 41 ± 4 ml (100 ml) −1 min −1 (100 mmHg) −1 , P = 0.02; and 23 ± 3 versus 33 ± 3 ml (100 ml) −1 min −1 , P = 0.02, respectively). These results, in conjunction with our previous findings in large arteries, suggest that ageing alters the effect of cyclo‐oxygenase inhibition on vascular responses, and specifically, the resistance vessel responses underlying reactive hyperaemia.
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Taylor et al. (2014) studied Healthy adults (n=26). Indomethacin vs. Young adults (age-based comparison) was evaluated on Peak forearm vascular conductance during reactive hyperaemia after indomethacin (p=0.02). Acute cyclo-oxygenase inhibition with indomethacin significantly attenuated peak forearm vascular conductance during reactive hyperaemia in healthy older adults compared with young adults.
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