title: Human cardiorespiratory and cerebrovascular function during severe passive hyperthermia: effects of mild hypohydration.
abstract: The influence of severe passive heat stress and hypohydration (Hypo) on cardiorespiratory and cerebrovascular function is not known. We hypothesized that 1) heating-induced hypocapnia and peripheral redistribution of cardiac output (Q) would compromise blood flow velocity in the middle cerebral artery (MCAv) and cerebral oxygenation; 2) Hypo would exacerbate the hyperthermic-induced hypocapnia, further decreasing MCAv; and 3) heating would reduce MCAv-CO2 reactivity, thereby altering ventilation. Ten men, resting supine in a water-perfused suit, underwent progressive hyperthermia [0.5 degrees C increments in core (esophageal) temperature (TC) to +2 degrees C] while euhydrated (Euh) or Hypo by 1.5% body mass (attained previous evening). Time-control (i.e., non-heat stressed) data were obtained on six of these subjects. Cerebral oxygenation (near-infrared spectroscopy), MCAv, end-tidal carbon dioxide (PetCO2) and arterial blood pressure, Q (flow model), and brachial and carotid blood flows (CCA) were measured continuously each 0.5 degrees C change in TC. At each level, hypercapnia was achieved through 3-min administrations of 5% CO2, and hypocapnia was achieved with controlled hyperventilation. At baseline in Hypo, heart rate, MCAv and CCA were elevated (P<0.05 vs. Euh). MCAv-CO2 reactivity was unchanged in both groups at all TC levels. Independent of hydration, hyperthermic-induced hyperventilation caused a severe drop in PetCO2 (-8+/-1 mmHg/ degrees C), which was related to lower MCAv (-15+/-3%/ degrees C; R2=0.98; P<0.001). Elevations in Q were related to increases in brachial blood flow (R2=0.65; P<0.01) and reductions in MCAv (R2=0.70; P<0.01), reflecting peripheral distribution of Q. Cerebral oxygenation was maintained, presumably via enhanced O2-extraction or regional differences in cerebral perfusion.
authors.affiliation: Department of Physiology, Otago School of Medical Science, University of Otago, Dunedin, New Zealand.
authors.forename: Jui-Lin
authors.initials: JL
authors.lastname: Fan
authors.forename: James D
authors.initials: JD
authors.lastname: Cotter
authors.forename: Rebekah A I
authors.initials: RA
authors.lastname: Lucas
authors.forename: Kate
authors.initials: K
authors.lastname: Thomas
authors.forename: Luke
authors.initials: L
authors.lastname: Wilson
authors.forename: Philip N
authors.initials: PN
authors.lastname: Ainslie
mesh_terms: D000328:Adult; D001831:Body Temperature / Q000502:physiology; D002245:Carbon Dioxide / Q000494:pharmacology; D002560:Cerebrovascular Circulation / Q000502:physiology*; D003681:Dehydration / Q000503:physiopathology*; D004947:Esophagus / Q000502:physiology; D005334:Fever / Q000503:physiopathology*; D006801:Humans; D006985:Hyperventilation / Q000503:physiopathology; D016857:Hypocapnia / Q000378:metabolism; D017078:Laser-Doppler Flowmetry; D008297:Male; D020768:Middle Cerebral Artery / Q000503:physiopathology; D010101:Oxygen Consumption / Q000502:physiology; D011659:Pulmonary Gas Exchange / Q000502:physiology; D012039:Regional Blood Flow / Q000502:physiology; D012867:Skin / Q000098:blood supply; D016683:Supine Position / Q000502:physiology
chemical_list: D002245:Carbon Dioxide