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Final Program


Final Congress Guide

Biomedical Sciences

100 Section - Cardiovascular response to acute hypotension during hypoxia

Tuesday, May 19, 2026
6:00 PM - 7:30 PM PT

    Presenting Author/Autor expositor(s)

  • AT

    Atsuhiro Tsubaki, PhD

    Professor
    Niigata University of Health and Welfare
    Niigata-city, Niigata, Japan

    • Co-Author/Coautor(s)

  • KK

    Kei Konno, n/a

    Student
    Niigata University of Health and Welfare
    Niigata-city, Niigata, Japan

  • AH

    Asuto Hashimoto, n/a

    Student
    Niigata University of Health and Welfare
    Niigata-city, Niigata, Japan

  • SK

    Sho Kojima, PhD

    Assistant professor
    Niigata University of Health and Welfare
    Niigata-city, Niigata, Japan

  • EO

    Erika Omori, n/a

    Student
    Niigata University of Health and Welfare
    Niigata-city, Niigata, Japan

  • HT

    Hajime Tamiya, PhD

    Assistant professor
    Niigata University of Health and Welfare
    Niigata-city, Niigata, Japan

Objectives : We previously studied the cardiovascular response to acute hypotension under normoxic conditions. Acutely, hypoxia may occur because of impaired gas exchange; however, the response to blood pressure changes in such cases is poorly understood. This study aimed to elucidate the cardiovascular responses to acute hypotension during hypoxia.

Design: Seven healthy volunteers performed acute hypotension maneuvers using digital tourniquets before and after the inhalation of hypoxic air (fraction of inspired O2 = 15%) for 10 min. Cuffs placed on both thighs were inflated to 250 mmHg for 2 min after a 5-min baseline measurement. Following sudden deflation, heart rate (HR) and beat-to-beat mean arterial pressure (MAP) were recorded using photoplethysmography, the maximum change after cuff deflation was measured, and reactive changes and recovery speed were calculated using the slope and time constant, respectively. All participants provided written informed consent. This study was approved by the Ethics Committee of Niigata University of Health and Welfare and conformed to the standards outlined in the Declaration of Helsinki.

Results: Neither HR nor MAP changes differed before and after hypoxia (HR: 14.0 ± 6.6 bpm and 17.4 ± 5.6 bpm, respectively, p = 0.28), (MAP:-23.4 ± 5.0 mmHg and -22.9 ± 3.9 mmHg, respectively, p = 0.76). The slope of recovery shortened after hypoxia for HR (1.9 ± 0.5 and 2.7 ± 0.7, respectively, p = 0.02), but not for MAP (-4.1 ± 1.0 and -3.8 ± 0.9, respectively, p = 0.31). Although the time constant of HR changes did not differ before and after hypoxia (7.5 ± 4.6 s, 7.3 ± 2.8 s, respectively, p = 0.94), that of MAP shortened (before: 6.4 ± 1.6 s and after: 4.6 ± 1.8 s, p = 0.03).

Conclusion: This study showed that hypoxia accelerated the increase in HR and recovery of MAP after acute hypotension in healthy people.