title: Tissue oxygen saturation during hyperthermic progressive central hypovolemia.
abstract: During normothermia, a reduction in near-infrared spectroscopy (NIRS)-derived tissue oxygen saturation (So2) is an indicator of central hypovolemia. Hyperthermia increases skin blood flow and reduces tolerance to central hypovolemia, both of which may alter the interpretation of tissue So2 during central hypovolemia. This study tested the hypothesis that maximal reductions in tissue So2 would be similar throughout normothermic and hyperthermic central hypovolemia to presyncope. Ten healthy males (means ± SD; 32 ± 5 yr) underwent central hypovolemia via progressive lower-body negative pressure (LBNP) to presyncope during normothermia (skin temperature ≈34°C) and hyperthermia (+1.2 ± 0.1°C increase in internal temperature via a water-perfused suit, skin temperature ≈39°C). NIRS-derived forearm (flexor digitorum profundus) tissue So2 was measured throughout and analyzed as the absolute change from pre-LBNP. Hyperthermia reduced (P < 0.001) LBNP tolerance by 49 ± 33% (from 16.7 ± 7.9 to 7.2 ± 3.9 min). Pre-LBNP, tissue So2 was similar (P = 0.654) between normothermia (74 ± 5%) and hyperthermia (73 ± 7%). Tissue So2 decreased (P < 0.001) throughout LBNP, but the reduction from pre-LBNP to presyncope was greater during normothermia (-10 ± 6%) than during hyperthermia (-6 ± 5%; P = 0.041). Contrary to our hypothesis, these findings indicate that hyperthermia is associated with a smaller maximal reduction in tissue So2 during central hypovolemia to presyncope.
authors.affiliation: Institute for Exercise and Environmental Medicine, Texas Health Presbyterian Hospital of Dallas, Dallas, Texas, and the University of Texas Southwestern Medical Center, Dallas, Texas;
authors.forename: Zachary J
authors.initials: ZJ
authors.lastname: Schlader
authors.affiliation: Institute for Exercise and Environmental Medicine, Texas Health Presbyterian Hospital of Dallas, Dallas, Texas, and the University of Texas Southwestern Medical Center, Dallas, Texas; Department of Kinesiology, Texas Woman's University, Denton, Texas;
authors.forename: Eric
authors.initials: E
authors.lastname: Rivas
authors.affiliation: Reflectance Medical Incorporated, Westborough, Massachusetts; Department of Anesthesiology, University of Massachusetts Medical School, Worcester, Massachusetts; and.
authors.forename: Babs R
authors.initials: BR
authors.lastname: Soller
authors.affiliation: U.S. Army Institute of Surgical Research, Fort Sam Houston, Texas.
authors.forename: Victor A
authors.initials: VA
authors.lastname: Convertino
authors.affiliation: Institute for Exercise and Environmental Medicine, Texas Health Presbyterian Hospital of Dallas, Dallas, Texas, and the University of Texas Southwestern Medical Center, Dallas, Texas; CraigCrandall@texashealth.org.
authors.forename: Craig G
authors.initials: CG
authors.lastname: Crandall
mesh_terms: D000328:Adult; D062186:Arterial Pressure; D005334:Fever / Q000378:metabolism* / Q000503:physiopathology; D005542:Forearm; D006339:Heart Rate; D006801:Humans; D020896:Hypovolemia / Q000378:metabolism* / Q000503:physiopathology; D008150:Lower Body Negative Pressure; D008297:Male; D018482:Muscle, Skeletal / Q000378:metabolism*; D010100:Oxygen / Q000378:metabolism*; D010101:Oxygen Consumption; D012039:Regional Blood Flow; D012867:Skin / Q000098:blood supply*; D012881:Skin Temperature; D019265:Spectroscopy, Near-Infrared; D013575:Syncope / Q000378:metabolism* / Q000503:physiopathology; D013997:Time Factors
chemical_list: D010100:Oxygen
keywords: heat stress; lower body negative pressure; simulated hemorrhage; syncope