Right ventricle dimensions and function in response to acute hypoxia in healthy human subjects.

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Title: Right ventricle dimensions and function in response to acute hypoxia in healthy human subjects.
Authors: Netzer, N. C., Strohl, K. P., Högel, J., Gatterer, H., Schilz, R.
Source: Acta Physiologica. Feb2017, Vol. 219 Issue 2, p478-485. 8p.
Subjects: Hypoxemia, Pulmonary circulation, Vasoconstriction, Human research subjects, Echocardiography, Physiology
Abstract: Aim Acute hypoxia produces acute vasoconstriction in the pulmonary circulation with consequences on right ventricular ( RV) structure and function. Previous investigations in healthy humans have been restricted to measurements after altitude acclimatization or were interrupted by normoxia. We hypothesized that immediate changes in RV dimensions in healthy subjects in response to normobaric hypoxia differ without the aforementioned constraints. Methods Transthoracic echocardiography was performed in 35 young, healthy subjects exposed to 11% oxygen, as well as six controls under sham hypoxia (20.6% oxygen, single blind) first at normoxia and after 30, 60, 100, 150 min of hypoxia or normoxia respectively. A subgroup of 15 subjects continued with 3-min cycling exercise in hypoxia with subsequent evaluation followed by an assessment 1 min at rest while breathing 4 L min−1 oxygen. Results During hypoxia, there was a significant linear increase of all RV dimensions ( RVD1 + 29 mm, RVD2 + 42 mm, RVD3 + 41 mm, RVOT + 13 mm, RVEDA + 18 mm, P < 0.01) in the exposure group vs. the control group. In response to hypoxia, right ventricular systolic pressure ( RVSP) showed a modest increase in hypoxia at rest (+7.3 mmHg, P < 0.01) and increased further with physical effort (+11.8 mmHg, P < 0.01). After 1 min of oxygen at rest, it fell by 50% of the maximum increase. Conclusion Acute changes in RV morphology occur quickly after exposure to normobaric hypoxia. The changes were out of proportion to a relatively low-estimated increase in pulmonary pressure, indicating direct effects on RV structure. The results in healthy subjects are basis for future clinically oriented interventional studies in normobaric hypoxia. [ABSTRACT FROM AUTHOR]
Copyright of Acta Physiologica is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
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  Data: Right ventricle dimensions and function in response to acute hypoxia in healthy human subjects.
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  Data: &lt;searchLink fieldCode=&quot;JN&quot; term=&quot;%22Acta+Physiologica%22&quot;&gt;Acta Physiologica&lt;/searchLink&gt;. Feb2017, Vol. 219 Issue 2, p478-485. 8p.
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  Data: Aim Acute hypoxia produces acute vasoconstriction in the pulmonary circulation with consequences on right ventricular ( RV) structure and function. Previous investigations in healthy humans have been restricted to measurements after altitude acclimatization or were interrupted by normoxia. We hypothesized that immediate changes in RV dimensions in healthy subjects in response to normobaric hypoxia differ without the aforementioned constraints. Methods Transthoracic echocardiography was performed in 35 young, healthy subjects exposed to 11% oxygen, as well as six controls under sham hypoxia (20.6% oxygen, single blind) first at normoxia and after 30, 60, 100, 150 min of hypoxia or normoxia respectively. A subgroup of 15 subjects continued with 3-min cycling exercise in hypoxia with subsequent evaluation followed by an assessment 1 min at rest while breathing 4 L min−1 oxygen. Results During hypoxia, there was a significant linear increase of all RV dimensions ( RVD1 + 29 mm, RVD2 + 42 mm, RVD3 + 41 mm, RVOT + 13 mm, RVEDA + 18 mm, P &lt; 0.01) in the exposure group vs. the control group. In response to hypoxia, right ventricular systolic pressure ( RVSP) showed a modest increase in hypoxia at rest (+7.3 mmHg, P &lt; 0.01) and increased further with physical effort (+11.8 mmHg, P &lt; 0.01). After 1 min of oxygen at rest, it fell by 50% of the maximum increase. Conclusion Acute changes in RV morphology occur quickly after exposure to normobaric hypoxia. The changes were out of proportion to a relatively low-estimated increase in pulmonary pressure, indicating direct effects on RV structure. The results in healthy subjects are basis for future clinically oriented interventional studies in normobaric hypoxia. [ABSTRACT FROM AUTHOR]
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  Data: &lt;i&gt;Copyright of Acta Physiologica is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites without the copyright holder&#39;s express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract.&lt;/i&gt; (Copyright applies to all Abstracts.)
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RecordInfo BibRecord:
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        Value: 10.1111/apha.12740
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      – Code: eng
        Text: English
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        PageCount: 8
        StartPage: 478
    Subjects:
      – SubjectFull: Hypoxemia
        Type: general
      – SubjectFull: Pulmonary circulation
        Type: general
      – SubjectFull: Vasoconstriction
        Type: general
      – SubjectFull: Human research subjects
        Type: general
      – SubjectFull: Echocardiography
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      – SubjectFull: Physiology
        Type: general
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      – TitleFull: Right ventricle dimensions and function in response to acute hypoxia in healthy human subjects.
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            NameFull: Netzer, N. C.
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            NameFull: Strohl, K. P.
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            NameFull: Högel, J.
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              Text: Feb2017
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              Y: 2017
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