Human cardiovascular dose–response to supplemental oxygen

Bak, Zoltán; Sjöberg, Folke; Rousseau, Andréas; Steinvall, Ingrid; Janerot-Sjöberg, Birgitta

doi:10.1111/j.1748-1716.2007.01710.x

Cited by 74 publications

(71 citation statements)

References 54 publications

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“…Prolonged O 2 breathing causes minor hemodynamic changes, such as bradycardia, and slight decreases in stroke volume and cardiac output (55). After O 2 exposure, we observed nothing outside of the physiological range in terms of heart rate and cardiac output in HO-1(CM) -/-mice.…”

Section: Discussionmentioning

confidence: 76%

Mitochondrial quality-control dysregulation in conditional HO-1–/– mice

Suliman¹,

Keenan²,

Piantadosi

2017

JCI Insight

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Section: Discussionmentioning

confidence: 76%

Mitochondrial quality-control dysregulation in conditional HO-1–/– mice

Suliman¹,

Keenan²,

Piantadosi

2017

JCI Insight

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“…22 It has been demonstrated that hyperoxia may influence systemic vascular resistance, stroke volume and BP. 23,24 Thus, the lack of blood-pressure decrease during chemoreflex deactivation can be explained by local vasoconstricting effect of hyperoxia that could offset the sympathoinhibitory effect of chemoreceptor deactivation. To clarify the influence of carotid body deactivation on the circulatory parameters in hypertensive patients, a more detailed hemodynamic approach including cardiac output measurement would need to be applied.…”

Section: Discussionmentioning

confidence: 99%

“…The circulatory effects of hyperoxia were described in healthy subjects and patients with heart failure. 23,24 Long periods of breathing 100% oxygen increased systemic resistance, decreased stroke volume and impaired left ventricular relaxation. It has been shown in the animal model 27 that shorter periods of hyperoxia inhibit ventilatory and circulatory chemoreflex response.…”

Section: Discussionmentioning

confidence: 99%

Tonic activity of carotid body chemoreceptors contributes to the increased sympathetic drive in essential hypertension

et al. 2011

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Carotid chemoreceptors provoke an increase in muscle sympathetic nerve activation (MSNA) in response to hypoxia; they are also tonically active during normoxic breathing. The contribution of peripheral chemoreceptors to sympathetic activation in hypertension is incompletely understood. The aim of our study was to investigate the effect of chemoreceptor deactivation on sympathetic activity in untreated patients with hypertension. A total of 12 untreated hypertensive males and 11 male controls participated in this randomized, crossover, placebo-controlled study. MSNA, systolic blood pressure(BP), diastolic BP, heart rate (HR), electrocardiogram, hemoglobin oxygen saturation (Sat%) and respiratory movements were measured during repeated 10-min periods of respiration with 100% oxygen or 21% oxygen in a blinded fashion. Compared with controls, hypertensives had higher resting MSNA (38±10 vs. 29±0.9 burst per min, Po0.05), systolic BP (150±12 vs. 124±10 mm Hg, Po 0.001) and diastolic BP (92 ± 10 vs. 77 ± 9 mm Hg, Po0.005). Breathing 100% oxygen caused significant decrease in MSNA in hypertensive patients (38 ± 10 vs. 26 ± 8 burst per min and 100 ± 0 vs. 90 ± 10 arbitrary units, Po0.05) and no change in controls (29±9 vs. 27±7 burst per min and 100±0 vs. 96±11 arbitrary units). BP, respiratory frequency and end tidal CO 2 did not change during chemoreceptor deactivation with hyperoxia. HR decreased and Sat% increased in both the study groups. These results confirm the role of tonic chemoreceptor drive in the development of sympathetic overactivity in hypertension.

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“…Hemodynamic changes such as decrease in heart rate, cardiac output and stroke volume were reported in hyperoxic breathing (2,12,16,24,34). The lowering of heart rate in hyperoxic condition may be triggered by increased parasympathetic activity (24).…”

Section: Discussionmentioning

confidence: 99%

Hyperoxia-induced hypertrophy and ion channel remodeling in left ventricle

Panguluri

Tur

Fukumoto

et al. 2013

American Journal of Physiology-Heart and Circulatory Physiology

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In the present study we investigated cardiac hypertrophy and cardiac complications in mice subjected to hyperoxia. Results demonstrate that there is a significant increase in average heart weight to tibia length (22%) in mice subjected to hyperoxia treatment vs. normoxia. Functional assessment was performed in mice subjected to hyperoxic treatment, and results demonstrate impaired cardiac function with decreased cardiac output and heart rate. Staining of transverse cardiac sections clearly demonstrates an increase in the cross-sectional area from hyperoxic hearts compared with control hearts. Quantitative real-time RT-PCR and Western blot analysis indicated differential mRNA and protein expression levels between hyperoxia-treated and control left ventricles for ion channels including Kv4.2 (Ϫ2 Ϯ 0.08), Kv2.1 (2.54 Ϯ 0.48), and Scn5a (1.4 Ϯ 0.07); chaperone KChIP2 (Ϫ1.7 Ϯ 0.06); transcriptional factors such as GATA4 (Ϫ1.5 Ϯ 0.05), Irx5 (5.6 Ϯ 1.74), NFB1 (4.17 Ϯ 0.43); hypertrophy markers including MHC-6 (2.17 Ϯ 0.36) and MHC-7 (4.62 Ϯ 0.76); gap junction protein Gja1 (4.4 Ϯ 0.8); and microRNA processing enzyme Drosha (4.6 Ϯ 0.58). Taken together, the data presented here clearly indicate that hyperoxia induces left ventricular remodeling and hypertrophy and alters the expression of Kv4.2 and MHC6/7 in the heart. ion channel regulation; hyperoxia; heart; hypertrophy; potassium channel; redox PATIENTS in critical or intensive care units (ICU) with acute lung injury or cardiac disease are often administered 100% O 2 for treatment. Recent studies indicate that hyperoxia induces cardiac injury due to dysfunctional lung and compromised pulmonary functioning (37), even though the exact nature of this problem remains unknown. Here, we evaluated changes in expression of the ion channel and key transcriptional factors in the heart that occur with hyperoxia and likely play a role in cardiovascular remodeling.Potassium channels and their auxiliary subunits such as potassium channel interacting protein-2 (KChIP2) are abundantly expressed in the heart (5, 7, 35). It is established that the potassium channels Kv4.2 and Kv1.5 are responsive to oxygen changes (29, 39). In the present study, we investigate whether hyperoxia alters expression of the transcription factors Irx5 and Mef2c, which are implicated to play a direct role in regulating Kv4.2 expression (7,15,22). Cardiac-specific markers used to identify hypertrophy and transcriptional changes (9, 22) were also evaluated by assessing myosin heavy chain-6, and -7 (MHC6, MHC7), zinc finger transcription factor (GATA4), histone-lysine N-methyltransferase (Ezh2), and Six-1 expression levels with hyperoxia.Key inflammatory mediators such as TNF␣ and NFB are central regulators or master switches for many pathological processes (10,20,30). Recent evidence indicates that NFB regulates KChIP2, which in turn regulates Kv4.2 expression (26). Therefore we assessed the levels of Kv4.2, KChIP2, and NFB in the mouse heart subjected to hyperoxia. We hypothesized that hyperoxia induces cardi...

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Human cardiovascular dose–response to supplemental oxygen

Cited by 74 publications

References 54 publications

Mitochondrial quality-control dysregulation in conditional HO-1–/– mice

Mitochondrial quality-control dysregulation in conditional HO-1–/– mice

Tonic activity of carotid body chemoreceptors contributes to the increased sympathetic drive in essential hypertension

Hyperoxia-induced hypertrophy and ion channel remodeling in left ventricle

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