Shear stress induced by acute heat exposure is not obligatory to protect against endothelial ischemia-reperfusion injury in humans

Author:

Hemingway Holden W.1,Richey Rauchelle E.1ORCID,Moore Amy M.1,Shokraeifard Austin M.1,Thomas Gabriel C.1ORCID,Olivencia-Yurvati Albert H.12,Romero Steven A.1ORCID

Affiliation:

1. Human Vascular Physiology Laboratory, Department of Physiology and Anatomy, University of North Texas Health Science Center, Fort Worth, Texas

2. Department of Surgery, University of North Texas Health Science Center, Fort Worth, Texas

Abstract

Acute heat exposure protects against endothelial ischemia-reperfusion injury in humans. However, the mechanism/s mediating this protective effect remain unclear. We utilized arterial compression to inhibit the temperature-dependent increase in brachial artery blood velocity that occurs during acute heat exposure to isolate the contribution of shear stress to the protection of endothelial function following ischemia-reperfusion injury. Our findings demonstrate that shear stress induced by acute heat exposure is not obligatory to protect against endothelial I/R injury.

Funder

HHS | NIH | National Institute on Aging

American College of Sports Medicine

Publisher

American Physiological Society

Subject

Physiology (medical),Physiology

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