Effects of hyperbaric oxygen on vascular endothelial function in patients with slow coronary flow

Li, Yuan; Zhang, Huiping; Liang, Yi; Wang, Wei; Xu, Tongshun; Zhang, Jifang; Xiao, Wenliang; Wang, Tao

doi:10.5603/cj.a2017.0132

Cited by 11 publications

(7 citation statements)

References 20 publications

(26 reference statements)

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“…Numerous studies have shown that HBOT improves systemic hemodynamics and microcirculation, 95,96 accelerates angiogenesis, 97 stimulates the antioxidant protection, 98 increases fibroblast proliferation and collagen synthesis, 99 inhibits inflammation, 100,101 exerts antiatherogenic effects, 102 and reduces the atherosclerotic plaque area. 91 Increase in the pO 2 that remains for 4 to 6 hours after HBOT, provides mitochondrial respiration and cell survival in the state of hypoxia, 103 inhibits apoptosis of the pancreatic b-cells, 100,104 reduces leukocyte adhesion, 105 enhances bactericidal activity of leukocytes, 106 and reduces endothelial dysfunction, 107 thereby contributing to the reduction in inflammation and following vascular complications in patients with DM. 91 Chronic hyperglycemia is linked with the abnormal synthesis of nitric oxide (NO), which is associated with DM-related vascular complications.…”

Section: Risk Factors For the Development Of Vascular Complications Imentioning

confidence: 99%

Hyperbaric Oxygen Therapy and Vascular Complications in Diabetes Mellitus

et al. 2020

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Vascular complications in patients with diabetes mellitus (DM) are common. Since impaired oxygen balance in plasma plays an important role in the pathogenesis of chronic DM-associated complications, the administration of hyperbaric oxygen therapy (HBOT) has been recommended to influence development of vascular complications. Hyperbaric oxygen therapy involves inhalation of 100% oxygen under elevated pressure from 1.6 to 2.8 absolute atmospheres in hyperbaric chambers. Hyperbaric oxygen therapy increases plasma oxygen solubility, contributing to better oxygen diffusion to distant tissues and preservation of the viability of tissues reversibly damaged by atherosclerosis-induced ischemia, along with microcirculation restoration. Hyperbaric oxygen therapy exerts antiatherogenic, antioxidant, and cardioprotective effects by altering the level and composition of plasma fatty acids and also by promoting signal transduction through membranes, which are impaired by hyperglycemia and hypoxia. In addition, HBOT affects molecules involved in the regulation of nitric oxide synthesis and in that way exerts anti-inflammatory and angiogenic effects in patients with DM. In this review, we explore the recent literature related to the effects of HBOT on DM-related vascular complications.

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Section: Risk Factors For the Development Of Vascular Complications Imentioning

confidence: 99%

Hyperbaric Oxygen Therapy and Vascular Complications in Diabetes Mellitus

et al. 2020

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“…Evidence of fibromuscular hyperplasia, medial hyperplasia, myointimal proliferation, as well as edema at the electron microscopic level validated this hypothesis ( 19 ). Decreased flow-mediated dilation (FMD) of brachial coronary arteries, a mechanism reliant on endothelium, was also reported in participants with CSFP, highlighting the possibility that endothelial dysfunction contributes to CSFP etiology ( 20 , 21 ). Other factors including inflammatory status ( 22 , 23 ), subclinical atherosclerosis ( 24 , 25 ), and geometric irregularities in major coronary arteries ( 26 , 27 ) were also reported to be involved in this regard.…”

Section: Discussionmentioning

confidence: 91%

Alprostadil vs. isosorbide dinitrate in ameliorating angina episodes in patients with coronary slow flow phenomenon: A randomized controlled trial

Zhang

Dai

Shen

et al. 2022

Front. Cardiovasc. Med.

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BackgroundThe optimum therapy for coronary slow flow phenomenon (CSFP) stays debatable. This study compared the effectiveness of alprostadil with isosorbide dinitrate in alleviating angina episodes in CSFP patients.MethodsIn this prospective, randomized controlled study, 102 patients with CSFP without severe coronary artery stenosis that exhibited stable angina were allocated randomly in a ratio of 1:1 to either the alprostadil group (40 μg, three times per day, n = 51) or the isosorbide dinitrate group (5 mg, three times per day, n = 51). Frequency of angina events, intensity of suffering, and the Canadian Cardiovascular Society (CCS) grading of angina pectoris were evaluated at baseline and one month after. Additionally, the Seattle Angina Questionnaire (SAQ) was assessed.ResultsBaseline characteristics were comparable between the two groups. At 1-month follow-up, patients administered with alprostadil experienced fewer angina episodes [episodes per week, 1 (2) vs. 2 (2), P < 0.001] and less pain intensity [self-evaluated pain score, 2 (3) vs. 3 (4), P < 0.001] than those with isosorbide dinitrate. In the alprostadil group, 78.4% of patients were classified as CCS class I, significantly higher than the 47.1% seen in the isosorbide dinitrate group (P = 0.001). Furthermore, treatment of alprostadil led to a significant improvement in the SAQ score (7.09 U, 95% CI: 4.22–9.96, P < 0.001) compared to isosorbide dinitrate. Additionally, fewer patients suffered headaches when receiving alprostadil (7.8% vs. 19.6%, P = 0.084).ConclusionAlprostadil was more effective in ameliorating angina symptoms in CSFP patients than isosorbide dinitrate.Clinical trial registration[www.chictr.org.cn], identifier [ChiCTR2000033233].

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“…As lMVEC are exposed to wider oscillations of O2 due to their close proximity to air, they should be inherently more tolerant to higher O2 levels and oxidative stress. Most studies regarding the effects of oxygen in microvascular cells, specifically hyperoxia, are restricted to the lung (Ahmad et al, 2004;Ma et al, 2018;Mach et al, 2011;Narula et al, 1998), and occasionally arterial EC (Li et al, 2018;Suzuki et al, 1997;Wang et al, 2015), when microvascular networks from less oxygenated tissues are likely to be much more susceptible.…”

Section: Discussionmentioning

confidence: 99%

Microvascular Endothelial Cell Adaptation to Hypoxia Is Organ-Specific and Conditioned by Environmental Oxygen

Reiterer

Eakin

Burke

et al. 2020

Preprint

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Microvascular endothelial cells (MVEC) are plastic, versatile and highly responsive cells, with morphological and functional aspects that uniquely match the tissues they supply. The response of these cells to oxygen oscillations is an essential aspect of tissue homeostasis, and is finely tuned to maintain organ function during physiological and metabolic challenges. Primary MVEC from two continuous capillary networks with distinct organ microenvironments, those of the lung and brain, were pre-conditioned at normal atmospheric (~ 21 %) and physiological (5 and 10 %) O2 levels, and subsequently used to compare organ-specific MVEC hypoxia response. Brain MVEC preferentially stabilise HIF-2α in response to hypoxia, whereas lung MVEC primarily accumulate HIF-1α ; however, this does not result in significant differences at the level of transcriptional activation of hypoxia-induced genes. Glycolytic activity is comparable between brain and lung endothelial cells, and is affected by oxygen pre-conditioning, while glucose uptake is not changed by oxygen pre-conditioning and is observed to be consistently higher in brain MVEC. Conversely, MVEC mitochondrial activity is organ-specific; brain MVEC maintain a higher relative mitochondrial spare capacity at 5% O2, but not following hyperoxic priming. If maintained at supra-physiological O2 levels, both MVEC fail to respond to hypoxia, and have severely compromised and delayed induction of the glycolytic shifts required for survival, an effect which is particularly pronounced in brain MVEC. Oxygen preconditioning also differentially shapes the composition of the mitochondrial electron transport chain (ETC) in the two MVEC populations. Lung MVEC primed at physioxia have lower levels of all ETC complexes compared to hyperoxia, an effect exacerbated by hypoxia. Conversely, brain MVEC expanded in physioxia display increased complex II (SDH) activity, which is further augmented during hypoxia. SDH activity in brain MVEC primed at 21 % O2 is ablated; upon hypoxia, this results in the accumulation of near-toxic levels of succinate in these cells. Our data suggests that, even though MVEC are primarily glycolytic, mitochondrial integrity in brain MVEC is essential for metabolic responses to hypoxia; these responses are compromised when cells are exposed to supra-physiological levels of oxygen. This work demonstrates that the study of MVEC in normal cell culture environments do not adequately represent physiological parameters found in situ, and show that the unique metabolism and function of organ-specific MVEC can be reprogrammed by external oxygen, significantly affecting the timing and degree of downstream responses.

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Effects of hyperbaric oxygen on vascular endothelial function in patients with slow coronary flow

Cited by 11 publications

References 20 publications

Hyperbaric Oxygen Therapy and Vascular Complications in Diabetes Mellitus

Hyperbaric Oxygen Therapy and Vascular Complications in Diabetes Mellitus

Alprostadil vs. isosorbide dinitrate in ameliorating angina episodes in patients with coronary slow flow phenomenon: A randomized controlled trial

Microvascular Endothelial Cell Adaptation to Hypoxia Is Organ-Specific and Conditioned by Environmental Oxygen

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