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This study investigated the contribution of cyclooxygenase (COX) dependent vasodilators to FMD before and after repeated IPC and RIPC.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>21 healthy participants underwent Radial artery FMD assessments before and after oral aspirin (600\u00a0mg) ingestion for COX inhibition. Participants then completed a one-weeklong alternate day unilateral IPC protocol (four repeated cycles of 5-minute ischemia and 5-minute reperfusion). 24\u00a0h after the final IPC session, FMD responses were reassessed before and after aspirin ingestion.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Prior to IPC treatment, aspirin failed to significantly reduce FMD in both Radial arteries. Following IPC treatment, the now significantly increased FMD of the ipsilateral arm (9.50\u2009\u00b1\u20094.58% (mean\u2009\u00b1\u2009standard deviation);\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.006) attenuated with aspirin (4.55\u2009\u00b1\u20092.68%;\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.002). Absolute difference in FMD % before and after aspirin ingestion increased from 1.48\u2009\u00b1\u20095.05% pre-IPC to 4.95\u2009\u00b1\u20094.96% (\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.016) post-IPC. In the contralateral (RIPC) arm, increased FMD % also attenuated with aspirin (\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.006) but this statistical significance was not seen following correction for shear rate. Nonetheless, absolute difference in FMD % before and after aspirin increased from 0.04\u2009\u00b1\u20094.05 pre-RIPC to 2.27\u2009\u00b1\u20093.60% (\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.043) post-RIPC.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>One week of alternate day IPC improves contribution of COX-derived vasoactive mediators to FMD. Contributions to RIPC driven improvements in FMD require further investigation.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1007\/s00421-026-06324-4","type":"journal-article","created":{"date-parts":[[2026,6,29]],"date-time":"2026-06-29T10:45:58Z","timestamp":1782729958000},"page":"5281-5291","update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Cyclooxygenase-dependent contribution to increased flow mediated dilatation following a week of repeated ischemic preconditioning"],"prefix":"10.1007","volume":"126","author":[{"ORCID":"https:\/\/orcid.org\/0009-0000-7315-5394","authenticated-orcid":false,"given":"Samuel","family":"Thomas","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sophia R.","family":"Murphy","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sultan E.","family":"AlSalahi","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-0670-8339","authenticated-orcid":false,"given":"Rehan T.","family":"Junejo","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2026,6,29]]},"reference":[{"issue":"5","key":"6324_CR1","doi-asserted-by":"publisher","first-page":"406","DOI":"10.1161\/01.RES.0000091074.33584.F0","volume":"93","author":"T Aizawa","year":"2003","unstructured":"Aizawa T, Wei H, Miano JM, Abe J-i, Berk BC, Yan C (2003) Role of Phosphodiesterase 3 in NO\/cGMP-Mediated Antiinflammatory Effects in Vascular Smooth Muscle Cells. 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