Low Doses of Hyperbaric Oxygenation Effectively Decrease the Size of Necrotic Zone in Rats with Experimental Myocardial Infarction

Доценко, Э. А.; Nikulina, N. V.; Саливончик, Д. П.; Lappo, O. G.; Грицук, А. И.; Bastron, A. S.

doi:10.1007/s10517-015-2849-1

Cited by 7 publications

(3 citation statements)

References 6 publications

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“…The field of therapeutic IH is dominated by the use of HBO, and HBO therapy is approved by the FDA to treat 15 indications 24. Additionally, although not FDA approved for these indications, studies appear to suggest that HBO therapy may ameliorate other conditions including myocardial infarction,25 hip fractures,2627282930 stroke,331323334353637 peri-surgical healing,3839404142 and traumatic brain injury 33543444546…”

Section: Discussionmentioning

confidence: 99%

Effect of intermittent hyperoxia on stem cell mobilization and cytokine expression

et al. 2019

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Introduction Modern medicine has made enormous progress in the past 150 years including the development of vaccines and pharmaceutical therapies. However, to date there is little progress in developing therapies that speed the healing of injured tissues. Hyperbaric oxygen therapy (HBOT) is a FDA approved therapy for non‐healing wounds consisting of daily intermittent doses of elevated partial pressure of oxygen (PO2) above 1520 torr. The hypothetical mechanism is its influence on mobilizing stem cells via cell signaling and gene transcription at effector tissues. Preclinical research showed a regimen of HBOT resulted in mobilization of stem cells and increased vasculogenesis in a wound healing model. Our study sought to determine if partial pressures of oxygen less than 760 torr would also mobilize stem cells. Methods Twelve, 10‐week‐old Sprague Dawley rats were randomly divided into two groups. The treatment group was exposed to a hyperoxic environment with a PO2 = 319 torr. The control group was exposed to room air (PO2 = 159 torr). Treatments were performed 5 days per week for 2 hours daily for a total of 10 treatment days (20 hours). Animals were sacrificed and approximately 8 ml of venous blood was harvested from the inferior vena cava. Red blood cells were lysed and plasma was drawn off and frozen. Remaining cells were prepared for flow cytometry by exposing them to cell surface marker antibodies for CD34+and CD 133+. These cells were then analyzed on a BD LSRII flow cytometer using DIVA software. Analysis was completed using FlowJo software. Statistics were performed using an unpaired t‐test with a p<.05 to indicate significance. Results Animals treated with a PO2 = 319 torr showed an increase (p = 0.045) in mobilized CD133+/34 endothelial progenitor cells (EPC's), while no differences were seen in CD133−/34+ hematopoietic stem progenitor cells (HSPC's) when compared to the control group. Discussion We hypothesized that there would be an increase in the CD133+/34− EPC's and an increase in CD133−/34+ HSPC's. Although our hypothesis was correct regarding the EPC's we did not see an increase in HSPC's as expected. CD133+/34− EPC's are considered more primitive stem cells than the CD133−/34+ HSPC's. CD133+/34− EPC's are capable of differentiation into CD133−/34+ HSPC's as they progress along the oligopotent path to maturation. Future research should include a pathological condition to test for changes in stem cell populations and the effects of pathology on stem cell differentiation. Our data suggest that low doses of daily intermittent hyperoxia mobilize the population of CD133+/34− EPC's. These EPC's have been shown in vivo to increase vascular density in a skin graft model. Further study is needed to determine what amount of intermittent hyperoxia treatment results in the most efficacious treatment in an injury model (increased stem cell mobilization, vasculogenesis and functional recovery). Support or Funding Information DOD Navy ‐ N00024‐17‐C‐4318 This abstract is from the Experimental Biology 2018 Meetin...

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Section: Discussionmentioning

confidence: 99%

Effect of intermittent hyperoxia on stem cell mobilization and cytokine expression

et al. 2019

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“…Hyperbaric oxygenation (HBO 2 ) is commonly used to improve injuries related to hypoxia and ischemia, including infections, such as meningococcal sepsis and gaseous gangrene [ 1 , 2 ], myocardial infarction [ 3 ], cerebral ischemia [ 4 ], and even some neurodegenerative disorders [ 5 – 7 ]. Experimental [ 8 ] and clinical data suggest that intermittent HBO 2 [ 9 ] decreases tissue edema, increases nitric oxide (NO) synthesis, changes vascular reactivity to stimuli [ 10 ], and inhibits neuroinflammatory factors' expression and apoptotic pathways [ 11 ].…”

Section: Introductionmentioning

confidence: 99%

Acute Hyperbaric Oxygenation, Contrary to Intermittent Hyperbaric Oxygenation, Adversely Affects Vasorelaxation in Healthy Sprague‐Dawley Rats due to Increased Oxidative Stress

Mihaljević

Matić

Stupin

et al. 2018

Oxidative Medicine and Cellular Longevity

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The present study was aimed at assessing endothelium-dependent vasorelaxation, at measuring superoxide production in the aorta and femoral artery, and at determining antioxidative enzyme expression and activity in aortas of male Sprague-Dawley rats (N = 135), randomized to an A-HBO2 group exposed to a single hyperbaric oxygenation session (120′ of 100% O2 at 2.0 bars), a 24H-HBO2 group (single session, examined 24 h after exposure), a 4D-HBO2 group (4 consecutive days of single sessions), and a CTRL group (untreated group). Vasorelaxation of aortic rings in response to acetylcholine (AChIR) and to reduced pO2 (HIR) was tested in vitro in the absence/presence of NOS inhibitor L-NAME and superoxide scavenger TEMPOL. eNOS, iNOS, antioxidative enzyme, and NADPH oxidase mRNA expression was assessed by qPCR. Serum oxidative stress markers and enzyme activity were assessed by spectrometry, and superoxide production was determined by DHE fluorescence. Impaired AChIR and HIR in the A-HBO2 group were restored by TEMPOL. L-NAME inhibited AChIR in all groups. Serum oxidative stress and superoxide production were increased in the A-HBO2 group compared to all other groups. The mRNA expression of iNOS was decreased in the A-HBO2 and 24H-HBO2 groups while SOD1 and 3 and NADPH oxidase were increased in the 4D-HBO2 group. The expression and activity of catalase and glutathione peroxidase were increased in the 4D-HBO2 group as well. AChIR was NO dependent. Acute HBO2 transiently impaired vasorelaxation due to increased oxidative stress. Vasorelaxation was restored and oxidative stress was normalized 24 h after the treatment.

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“…4 HBO was shown to induce cardioprotection through anti-apoptotic effect and decreased infarct size in a rat model of MI. 5,6 Several small clinical trials also demonstrated the beneficial effect of HBO in patients with acute coronary syndrome by reducing the infarct size, and the risk of major cardiovascular events and death. 7 Exosomes are 40-90 nm-sized extracellular vesicles of endosomal origin that play a crucial role in intercellular processes.…”

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confidence: 99%

Hyperbaric oxygen‐induced long non‐coding RNA MALAT1 exosomes suppress MicroRNA‐92a expression in a rat model of acute myocardial infarction

Shyu¹,

Wang²,

Fang³

et al. 2020

J Cellular Molecular Medi

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Hyperbaric oxygen (HBO) improves angiogenesis. The effect of HBO on metastasis‐associated lung adenocarcinoma transcript 1 (MALAT1), a pro‐angiogenic long non‐coding RNA, in cardiac myocyte‐derived exosomes and acute myocardial infarction (AMI) is unknown. We aimed to investigate whether MALAT1 is altered in cardiac myocyte‐derived exosomes in response to HBO as well as the molecular regulatory mechanisms of MALAT1 in cardiac myocytes treated with HBO. Cardiac myocytes were cultured, and HBO was applied at 2.5 atmosphere absolute in a hyperbaric chamber. Exosomes were extracted from the culture media. A rat model of AMI generated by the ligation of the left anterior descending artery was used. HBO significantly increased MALAT1 expression in cardiac myocytes and HBO‐induced MALAT1 and exosomes attenuated miR‐92a expression after myocardial infarction. Expression of krüppel‐like factor 2 (KLF2) and CD31 was significantly decreased after infarction and HBO‐induced exosomes significantly reversed the expression. Silencing of MALAT1 using MALAT1‐locked nucleic acid GapmeR significantly attenuated KLF2 and CD31 protein expression after infarction induced by HBO‐induced exosomes. HBO‐induced exosomes also decreased infarct size significantly. HBO‐induced exosomes from cardiac myocytes up‐regulate MALAT1 to suppress miR‐92a expression and counteract the inhibitory effect of miR‐92a on KLF2 and CD31 expression in left ventricular myocardium after myocardial infarction to enhance neovascularization.

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Low Doses of Hyperbaric Oxygenation Effectively Decrease the Size of Necrotic Zone in Rats with Experimental Myocardial Infarction

Cited by 7 publications

References 6 publications

Effect of intermittent hyperoxia on stem cell mobilization and cytokine expression

Effect of intermittent hyperoxia on stem cell mobilization and cytokine expression

Acute Hyperbaric Oxygenation, Contrary to Intermittent Hyperbaric Oxygenation, Adversely Affects Vasorelaxation in Healthy Sprague‐Dawley Rats due to Increased Oxidative Stress

Hyperbaric oxygen‐induced long non‐coding RNA MALAT1 exosomes suppress MicroRNA‐92a expression in a rat model of acute myocardial infarction

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