{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,15]],"date-time":"2026-10-15T02:04:20Z","timestamp":1792029860081,"version":"4.4.0"},"reference-count":61,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal of Applied Physiology"],"published-print":{"date-parts":[[2008,8]]},"abstract":"<jats:p> 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\u0307) 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-CO<jats:sub>2<\/jats:sub> reactivity, thereby altering ventilation. Ten men, resting supine in a water-perfused suit, underwent progressive hyperthermia [0.5\u00b0C increments in core (esophageal) temperature (T<jats:sub>C<\/jats:sub>) to +2\u00b0C] 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<jats:sub>CO<\/jats:sub><jats:sub>2<\/jats:sub>) and arterial blood pressure, Q\u0307 (flow model), and brachial and carotid blood flows (CCA) were measured continuously each 0.5\u00b0C change in T<jats:sub>C<\/jats:sub>. At each level, hypercapnia was achieved through 3-min administrations of 5% CO<jats:sub>2<\/jats:sub>, and hypocapnia was achieved with controlled hyperventilation. At baseline in Hypo, heart rate, MCAv and CCA were elevated ( P &lt; 0.05 vs. Euh). MCAv-CO<jats:sub>2<\/jats:sub> reactivity was unchanged in both groups at all T<jats:sub>C<\/jats:sub> levels. Independent of hydration, hyperthermic-induced hyperventilation caused a severe drop in Pet<jats:sub>CO<\/jats:sub><jats:sub>2<\/jats:sub> (\u22128 \u00b1 1 mmHg\/\u00b0C), which was related to lower MCAv (\u221215 \u00b1 3%\/\u00b0C; R<jats:sup>2<\/jats:sup> = 0.98; P &lt; 0.001). Elevations in Q\u0307 were related to increases in brachial blood flow ( R<jats:sup>2<\/jats:sup> = 0.65; P &lt; 0.01) and reductions in MCAv ( R<jats:sup>2<\/jats:sup> = 0.70; P &lt; 0.01), reflecting peripheral distribution of Q\u0307. Cerebral oxygenation was maintained, presumably via enhanced O<jats:sub>2<\/jats:sub>-extraction or regional differences in cerebral perfusion. <\/jats:p>","DOI":"10.1152\/japplphysiol.00010.2008","type":"journal-article","created":{"date-parts":[[2008,5,16]],"date-time":"2008-05-16T00:59:20Z","timestamp":1210899560000},"page":"433-445","source":"Crossref","is-referenced-by-count":90,"title":["Human cardiorespiratory and cerebrovascular function during severe passive hyperthermia: effects of mild hypohydration"],"prefix":"10.1152","volume":"105","author":[{"given":"Jui-Lin","family":"Fan","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"James D.","family":"Cotter","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rebekah A. 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