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Ventilatory response to head-down-tilt in healthy human subjects. | LitMetric

Ventilatory response to head-down-tilt in healthy human subjects.

Exp Physiol

Centre for Human and Applied Physiological Sciences (CHAPS), Faculty of Life Sciences and Medicine, King's College London, London, UK.

Published: December 2024

AI Article Synopsis

  • The study investigates how postural changes, specifically a 50° head-down tilt (HDT), impact respiratory control in healthy individuals.
  • It involves two protocols measuring ventilation and blood flow responses under different gas conditions.
  • The findings show significant increases in ventilation during HDT in certain conditions, suggesting that alterations in cerebral venous pressure might influence respiratory response, despite no changes in cerebral blood flow.

Article Abstract

Postural fluid shifts may directly affect respiratory control via a complex interaction of baro- and chemo-reflexes, and cerebral blood flow. Few data exist concerning the steady state ventilatory responses during head-down tilt. We examined the cardiorespiratory responses during acute 50° head-down tilt (HDT) in 18 healthy subjects (mean [SD] age 27 [10] years). Protocol 1 (n = 8, two female) was 50° HDT from 60° head-up posture sustained for 10 min, while exposed to normoxia, normoxic hypercapnia (5% CO), hypoxia (12% inspired O) or hyperoxic hypercapnia (95% O, 5% CO). Protocol 2 (n = 10, four female) was 50° HDT from supine, sustained for 10 min, while breathing either medical air or normoxic hypercapnic (5% CO) gas. Ventilation ( , pneumotachograph), end-tidal O and CO concentration and blood pressure (Finapres) were measured continuously throughout each protocol. Middle cerebral artery blood flow velocity (MCAv; transcranial Doppler) was also measured during protocol 2. Ventilation increased significantly (P < 0.05) compared to baseline during HDT in both hyperoxic hypercapnia (protocol 1 by mean [SD] 139 [26]%) and normoxic hypercapnia (protocol 1 by mean [SD] 131 [21]% and protocol 2 by 129 [23]%), despite no change in or from baseline. No change in was observed during HDT with medical air or hypoxia, and there was no significant change in MCAv during HDT compared to baseline. The absence of change in cerebral blood flow leads us to postulate that the augmented ventilatory response during steep HDT may involve mechanisms related to cerebral venous pressure and venous outflow.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11607625PMC
http://dx.doi.org/10.1113/EP092014DOI Listing

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