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Oxygen deteriorates arterial function in type 1 diabetes

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Abstract

Aims

Although oxygen is commonly used to treat various medical conditions, it has recently been shown to worsen vascular function (arterial stiffness) in healthy volunteers and even more in patients in whom vascular function might already be impaired. The effects of oxygen on arterial function in patients with type 1 diabetes (T1D) are unknown, although such patients display disturbed vascular function already at rest. Therefore, we tested whether short-term oxygen administration may alter the arterial function in patients with T1D.

Methods

We estimated arterial stiffness by augmentation index (AIx) and the pulse wave velocity equivalent (SI-DVP) in 98 patients with T1D and 49 age- and sex-matched controls at baseline and during hyperoxia by obtaining continuous noninvasive finger pressure waveforms using a recently validated method.

Results

AIx and SI-DVP increased in patients (P < 0.05) but not in controls in response to hyperoxia. The increase in AIx (P = 0.05), systolic (P < 0.05), and diastolic (P < 0.05) blood pressure was higher in the patients than in the controls.

Conclusions

Short-term oxygen administration deteriorates arterial function in patients with T1D compared to non-diabetic control subjects. Since disturbed arterial function plays a major role in the development of diabetic complications, these findings may be of clinical relevance.

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Abbreviations

SBP:

Systolic blood pressure

DBP:

Diastolic blood pressure

PP:

Pulse pressure

MAP:

Mean arterial pressure

AIx:

Augmentation index

AIxHR :

Heart rate-adjusted augmentation index

AER:

Albumin excretion rate

T1D:

Type 1 diabetes

SI-DVP:

An index of large artery stiffness (SIDVP) derived from the digital volume pulse (DVP)

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Acknowledgments

This study was supported by grants from Folkhälsan Research Foundation, Academy of Finland (134379), Helsinki University Central Hospital Research Funds (EVO), the Wilhelm and Else Stockmann Foundation, the Perklén foundation, the Waldemar von Frenckell Foundation, the Liv och Hälsa Foundation, the Finnish Medical Society (Finska Läkaresällskapet), the Diabetes Research Foundation, the Paulo Foundation, the Paavo Nurmi Foundation, The Finnish Medical Foundation, the Biomedicum Helsinki Foundation, the Novo Nordisk Foundation, and the Signe and Ane Gyllenberg Foundation, Helsinki. The authors thank Jaana Tuomikangas, Tuula Soppela, Maikki Parkkonen, and Anna-Reetta Salonen from the Division of Nephrology, Department of Medicine, Helsinki University Central Hospital, and Institute of Genetics, Folkhälsan Research Center, Helsinki, Finland, for excellent technical assistance. D.G., L.B., M.R.-B., and A.N. researched data. D.G., L.B., V.-P.M., and P.-H.G. wrote the manuscript and researched data. D.G., L.B., M.R.-B., V.-P.M., A.S.-P., C.F., A.N., and P.-H.G. reviewed/edited the manuscript. P.-H.G. was responsible for the conception, design, and collection of the study and data, writing and editing of the manuscript, and final approval of the manuscript. P.-H.G. is the guarantor of this work and, as such, had full access to all the data in the study and takes responsibility for the integrity of the data and the accuracy of the data analysis.

Conflict of interest

P.-H.G. received lecture fees from Eli Lilly, Boehringer Ingelheim, Novartis, Genzyme, Merck Sharp & Dohme, and Novo Nordisk and is an advisory board member of Boehringer Ingelheim, Novartis, and Cebix. No other potential conflicts of interest relevant to this article were reported.

Human and Animal Rights disclosure

All procedures followed were in accordance with the ethical standards of the responsible committee on human experimentation (institutional and national) and with the Declaration of Helsinki 1975, as revised in 2008.

Informed consent disclosure

Informed consent was obtained from all patients for being included in the study.

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Correspondence to Per-Henrik Groop.

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Managed by Antonio Secchi.

On behalf of the FinnDiane Study Group.

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Gordin, D., Bernardi, L., Rosengård-Bärlund, M. et al. Oxygen deteriorates arterial function in type 1 diabetes. Acta Diabetol 53, 349–357 (2016). https://doi.org/10.1007/s00592-015-0775-3

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  • DOI: https://doi.org/10.1007/s00592-015-0775-3

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