Cardiopulmonary and arterial baroreceptor unloading during passive hyperthermia does not contribute to hyperthermia-induced hyperventilation

Rebekah A I Lucas, James Pearson, Zachary J Schlader, Craig G Crandall

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3 Citations (Scopus)

Abstract

This study tested the hypothesis that baroreceptor unloading during passive hyperthermia contributes to increases in ventilation and decreases in end‐tidal partial pressure of carbon dioxide (urn:x-wiley:09580670:media:eph1695:eph1695-math-0001) during that exposure. Two protocols were performed, in which healthy subjects underwent passive hyperthermia (increasing intestinal temperature by ∼1.8°C) to cause a sustained increase in ventilation and reduction in urn:x-wiley:09580670:media:eph1695:eph1695-math-0002. Upon attaining hyperthermic hyperventilation, in protocol 1 (n = 10; three females) a bolus (19 ± 2 ml kg−1) of warm (∼38°C) isotonic saline was rapidly (5–10 min) infused intravenously to restore reductions in central venous pressure, whereas in protocol 2 (n = 11; five females) phenylephrine was infused intravenously (60–120 μg min−1) to return mean arterial pressure to normothermic levels. In protocol 1, hyperthermia increased ventilation (by 2.2 ± 1.7 l min−1, P < 0.01), while reducing urn:x-wiley:09580670:media:eph1695:eph1695-math-0003 (by 4 ± 3 mmHg, P = 0.04) and central venous pressure (by 5 ± 1 mmHg, P <0.01). Saline infusion increased central venous pressure by 5 ± 1 mmHg (P < 0.01), restoring it to normothermic values, but did not change ventilation or urn:x-wiley:09580670:media:eph1695:eph1695-math-0004 (P > 0.05). In protocol 2, hyperthermia increased ventilation (by 5.0 ± 2.7 l min−1, P <0.01) and reduced urn:x-wiley:09580670:media:eph1695:eph1695-math-0005 (by 5 ± 2 mmHg, P < 0.01) and mean arterial pressure (by 9 ± 7 mmHg, P <0.01). Phenylephrine infusion increased mean arterial pressure by 12 ± 3 mmHg (P < 0.01), restoring it to normothermic values, but did not change ventilation or urn:x-wiley:09580670:media:eph1695:eph1695-math-0006 (P > 0.05). The absence of a reduction in ventilation upon reloading the cardiopulmonary and arterial baroreceptors to pre‐hyperthermic levels indicates that baroreceptor unloading with hyperthermia is unlikely to contribute to hyperthermic hyperventilation in humans.
Original languageEnglish
Pages (from-to)1309-1318
Number of pages10
JournalExperimental Physiology
Volume100
Issue number11
Early online date24 Aug 2015
DOIs
Publication statusPublished - 1 Nov 2015

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