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Human cardiorespiratory and cerebrovascular function during severe passive hyperthermia: effects of mild hypohydration

¹Department of Physiology, Otago School of Medical Science, University of Otago; and ²School of Physical Education, University of Otago, Dunedin, New Zealand

Submitted 6 January 2008 ; accepted in final form 6 May 2008

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 () 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°C increments in core (esophageal) temperature (T_C) to +2°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 (PET_CO2) and arterial blood pressure, (flow model), and brachial and carotid blood flows (CCA) were measured continuously each 0.5°C change in T_C. 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 T_C levels. Independent of hydration, hyperthermic-induced hyperventilation caused a severe drop in PET_CO2 (–8 ± 1 mmHg/°C), which was related to lower MCAv (–15 ± 3%/°C; R² = 0.98; P < 0.001). Elevations in 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 . Cerebral oxygenation was maintained, presumably via enhanced O₂-extraction or regional differences in cerebral perfusion.

cerebral perfusion; passive heating

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