Heart rate variability in healthy volunteers during normobaric and hyperbaric hyperoxia

Lund, Victoria E.; Kentala, Erna; Scheinin, Harry; Klossner, J; Helenius, Hans; Sariola-Heinonen, K; Jalonen, J.

doi:10.1046/j.1365-201x.1999.00581.x

Cited by 81 publications

(83 citation statements)

References 17 publications

(24 reference statements)

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“…It is speculated that high pressure of HBA may influence the lipid metabolism. On the other hand, HBO increased parasympathetic activities in healthy volunteers (32)(33)(34) and significantly decreased cortisol levels (35). Dominance of sympathetic activities causes high FFA, because β receptor signal stimulates lypolysis.…”

Section: Discussionmentioning

confidence: 99%

Long-term treatment with hyperbaric air improves hyperlipidemia of db/db mice

et al. 2010

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Section: Discussionmentioning

confidence: 99%

Long-term treatment with hyperbaric air improves hyperlipidemia of db/db mice

et al. 2010

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“…Although both s-amylase and s-CgA are employed as biomarkers of autonomic excitability, they may not be regulated completely by the same autonomic nervous system. Hyperoxic inhalation reduces heart rate and causes hyperoxic bradycardia, which suggests that hyperoxia modulates the autonomic nervous system (2,12,14). Some spectral analysis studies on heart rate variability under hyperoxic conditions showed that hyperoxia activates the parasympathetic nervous system (13,14).…”

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confidence: 99%

Effects of hyperoxic inhalation on psychological stress-induced salivary biomarkers

et al. 2009

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This study examined the effects of hyperoxic inhalation on psychological stress-induced salivary biomarkers. To induce psychological stress, eight males (22-24 year old) were performed a simple mathematical calculation. After the task, the subjects inspired either normal air or 100% O 2 for 30 min. The control subjects (control trial) did not perform the calculation task and inspired normal air. These three trials were randomly performed at an interval of at least one week, and the two calculation trials with and without 100% O 2 inhalation were performed using a single-blinded design. A tendency for increase in salivary cortisol (s-cortisol) and chromogranin A (s-CgA) concentrations, and a significant increase in salivary α-amylase (s-amylase) activity were observed following the task. Hyperoxic inhalation did not affect s-cortisol and s-CgA secretion, but decreased the s-amylase activity. Changes in the increased rate of s-amylase activity and s-CgA concentration showed a significant negative correlation with each other, after the task. These results imply that hyperoxic inhalation attenuates a part of autonomic excitability resulting from psychological stress. Although both s-amylase and s-CgA are employed as biomarkers of autonomic excitability, the s-amylase and s-CgA do not appear to be regulated by the same autonomic nervous system.

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“…It is not clear if the precipitous reduction in _ V E was a consequence of lung injury or of changes in autonomic regulation of the pulmonary system. Short-term changes in parasympathetic activity during hyperbaric hyperoxia have been reported previously (17). However, there are no reports regarding the long-term implications of oxygen exposure on parasympathetic regulation of breathing.…”

Section: Discussionmentioning

confidence: 88%

Cardiac Physiologic and Genetic Predictors of Hyperoxia-Induced Acute Lung Injury in Mice

Howden

Cho²,

Miller-DeGraff³

et al. 2012

Am J Respir Cell Mol Biol

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Exposure of mice to hyperoxia produces pulmonary toxicity similar to acute lung injury/acute respiratory distress syndrome, but little is known about the interactions within the cardiopulmonary system. This study was designed to characterize the cardiopulmonary response to hyperoxia, and to identify candidate susceptibility genes in mice. Electrocardiogram and ventilatory data were recorded continuously from 4 inbred and 29 recombinant inbred strains during 96 hours of hyperoxia (100% oxygen). Genome-wide linkage analysis was performed in 27 recombinant inbred strains against response time indices (TIs) calculated from each cardiac phenotype. Reductions in minute ventilation, heart rate (HR), low-frequency (LF) HR variability (HRV), high-frequency HRV, and total power HRV were found in all mice during hyperoxia exposure, but the lag time before these changes began was strain dependent. Significant (chromosome 9) or suggestive (chromosomes 3 and 5) quantitative trait loci were identified for the HRTI and LFTI. Functional polymorphisms in several candidate susceptibility genes were identified within the quantitative trait loci and were associated with hyperoxia susceptibility. This is the first study to report highly significant interstrain variation in hyperoxia-induced changes in minute ventilation, HR, and HRV, and to identify polymorphisms in candidate susceptibility genes that associate with cardiac responses. Results indicate that changes in HR and LF HRV could be important predictors of subsequent adverse outcome during hyperoxia exposure, specifically the pathogenesis of acute lung injury. Understanding the genetic mechanisms of these responses may have significant diagnostic clinical value.

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Heart rate variability in healthy volunteers during normobaric and hyperbaric hyperoxia

Cited by 81 publications

References 17 publications

Long-term treatment with hyperbaric air improves hyperlipidemia of db/db mice

Long-term treatment with hyperbaric air improves hyperlipidemia of db/db mice

Effects of hyperoxic inhalation on psychological stress-induced salivary biomarkers

Cardiac Physiologic and Genetic Predictors of Hyperoxia-Induced Acute Lung Injury in Mice

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