Oxygen deteriorates arterial function in type 1 diabetes

Gordin, Daniel; Bernardi, Luciano; Rosengård-Bärlund, Milla; Mäkinen, Ville; Soro‐Paavonen, Aino; Forsblom, Carol; Sandelin, Anna; Groop, Per Henrik

doi:10.1007/s00592-015-0775-3

Cited by 3 publications

(4 citation statements)

References 36 publications

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“…These abnormalities have traditionally been attributed to anatomical changes involving neural degeneration 2 or atherosclerotic processes 3 . However, a functional –hence potentially reversible- component of autonomic and vascular abnormalities have been identified by our group, and others 4, 5 .…”

Section: Introductionmentioning

confidence: 60%

“…Nevertheless, in response to oxygen administration we also observed a transient increase in the blood pressure in patients with type 1 diabetes 4, 7 . Conversely, slow breathing did not increase or it even reduced the blood pressure 8 .…”

Section: Introductionmentioning

confidence: 64%

“…Because an excess of oxygen produces an excess of ROS, both of these might in concert have created a transient endothelial dysfunction, leading to an increase in arterial stiffness and blood pressure 4, 7 . Diabetic subjects already have a condition of oxidative stress, excess of free-radicals and endothelial dysfunction due to various reasons, including hyperglycaemia, low-grade inflammation 17 and pre-existing hypoxia 6 .…”

Section: Discussionmentioning

confidence: 99%

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Oxygen-induced impairment in arterial function is corrected by slow breathing in patients with type 1 diabetes

Bernardi

Gordin

Bordino

et al. 2017

Sci Rep

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Hyperoxia and slow breathing acutely improve autonomic function in type-1 diabetes. However, their effects on arterial function may reveal different mechanisms, perhaps potentially useful. To test the effects of oxygen and slow breathing we measured arterial function (augmentation index, pulse wave velocity), baroreflex sensitivity (BRS) and oxygen saturation (SAT), during spontaneous and slow breathing (6 breaths/min), in normoxia and hyperoxia (5 L/min oxygen) in 91 type-1 diabetic and 40 age-matched control participants. During normoxic spontaneous breathing diabetic subjects had lower BRS and SAT, and worse arterial function. Hyperoxia and slow breathing increased BRS and SAT. Hyperoxia increased blood pressure and worsened arterial function. Slow breathing improved arterial function and diastolic blood pressure. Combined administration prevented the hyperoxia-induced arterial pressure and function worsening. Control subjects showed a similar pattern, but with lesser or no statistical significance. Oxygen-driven autonomic improvement could depend on transient arterial stiffening and hypertension (well-known irritative effect of free-radicals on endothelium), inducing reflex increase in BRS. Slow breathing-induced improvement in BRS may result from improved SAT, reduced sympathetic activity and improved vascular function, and/or parasympathetic-driven antioxidant effect. Lower oxidative stress could explain blunted effects in controls. Slow breathing could be a simple beneficial intervention in diabetes.

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Section: Introductionmentioning

confidence: 60%

Section: Introductionmentioning

confidence: 64%

Section: Discussionmentioning

confidence: 99%

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Oxygen-induced impairment in arterial function is corrected by slow breathing in patients with type 1 diabetes

Bernardi

Gordin

Bordino

et al. 2017

Sci Rep

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“…It is noteworthy that potentially negative effects of hyperoxia have been demonstrated in some vascular beds, including the myocardium and brain (101,159), and O 2 breathing also contributes to vascular dysfunction (i.e., higher arterial stiffness) in individuals with diabetes (110). Given that cerebral perfusion is highly influenced by changes in arterial blood gases (316) and tissue ischemia is a major concern following myocardial infarct/cardiac arrest (48), blood flow to the brain and coronary circulation is of particular importance in hyperoxia.…”

Section: R5mentioning

confidence: 99%

Highs and lows of hyperoxia: physiological, performance, and clinical aspects

Brugniaux

Coombs

Barak

et al. 2018

American Journal of Physiology-Regulatory, Integrative and Comp

100

108

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Molecular oxygen (O) is a vital element in human survival and plays a major role in a diverse range of biological and physiological processes. Although normobaric hyperoxia can increase arterial oxygen content ([Formula: see text]), it also causes vasoconstriction and hence reduces O delivery in various vascular beds, including the heart, skeletal muscle, and brain. Thus, a seemingly paradoxical situation exists in which the administration of oxygen may place tissues at increased risk of hypoxic stress. Nevertheless, with various degrees of effectiveness, and not without consequences, supplemental oxygen is used clinically in an attempt to correct tissue hypoxia (e.g., brain ischemia, traumatic brain injury, carbon monoxide poisoning, etc.) and chronic hypoxemia (e.g., severe COPD, etc.) and to help with wound healing, necrosis, or reperfusion injuries (e.g., compromised grafts). Hyperoxia has also been used liberally by athletes in a belief that it offers performance-enhancing benefits; such benefits also extend to hypoxemic patients both at rest and during rehabilitation. This review aims to provide a comprehensive overview of the effects of hyperoxia in humans from the "bench to bedside." The first section will focus on the basic physiological principles of partial pressure of arterial O, [Formula: see text], and barometric pressure and how these changes lead to variation in regional O delivery. This review provides an overview of the evidence for and against the use of hyperoxia as an aid to enhance physical performance. The final section addresses pathophysiological concepts, clinical studies, and implications for therapy. The potential of O toxicity and future research directions are also considered.

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Arterial Stiffness and Type 1 Diabetes: The Current State of Knowledge

Kulecki

Uruska

Naskręt

et al. 2022

CDR

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: The most common cause of mortality among people with type 1 diabetes is cardiovascular diseases. Arterial stiffness allows predicting cardiovascular complications, cardiovascular mortality, and all-cause mortality. There are different ways to measure arterial stiffness; the gold standard is pulse wave velocity. Arterial stiffness is increased in people with type 1 diabetes compared to healthy controls. It increases with age and duration of type 1 diabetes. Arterial stiffness among people with type 1 diabetes has a positive association with systolic blood pressure, obesity, glycated hemoglobin, waist circumference, and waist to hip ratio. It has a negative correlation with estimated glomerular filtration rate, high-density lipoprotein, and the absence of carotid plaques. The increased arterial stiffness could be the result of insulin resistance, collagen increase due to inadequate enzymatic glycation, endothelial and autonomic dysfunction. The insulin-induced decrease in arterial stiffness is impaired in type 1 diabetes. There are not enough proofs to use pharmacotherapy in the prevention of arterial stiffness, but some of the medicaments have obtained promising results in single studies, for example, renin-angiotensin-aldosterone system inhibitors, statins, and SGLT2 inhibitors. The main form of prevention of arterial stiffness progression remains glycemic control and a healthy lifestyle.

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Oxygen deteriorates arterial function in type 1 diabetes

Abstract: 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.

Cited by 3 publications

References 36 publications

Oxygen-induced impairment in arterial function is corrected by slow breathing in patients with type 1 diabetes

Oxygen-induced impairment in arterial function is corrected by slow breathing in patients with type 1 diabetes

Highs and lows of hyperoxia: physiological, performance, and clinical aspects

Arterial Stiffness and Type 1 Diabetes: The Current State of Knowledge

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