Hyperbaric Oxygen Administration Research Articles

Hyperbaric oxygen therapy in the ATLS/ACLS resuscitative management of acutely ill or severely injured patients with severe anemia: a review

For short periods, even without the presence of red blood cells, hyperbaric oxygen can safely allow plasma to meet the oxygen delivery requirements of a human at rest. By this means, hyperbaric oxygen, in special instances, may be used as a bridge to lessen blood transfusion requirements. Hyperbaric oxygen, applied intermittently, can readily avert oxygen toxicity while meeting the body's oxygen requirements. In acute injury or illness, accumulated oxygen debt is shadowed by adenosine triphosphate debt. Hyperbaric oxygen efficiently provides superior diffusion distances of oxygen in tissue compared to those provided by breathing normobaric oxygen. Intermittent application of hyperbaric oxygen can resupply adenosine triphosphate for energy for gene expression and reparative and anti-inflammatory cellular function. This advantageous effect is termed the hyperbaric oxygen paradox. Similarly, the normobaric oxygen paradox has been used to elicit erythropoietin expression. Referfusion injury after an ischemic insult can be ameliorated by hyperbaric oxygen administration. Oxygen toxicity can be averted by short hyperbaric oxygen exposure times with air breaks during treatments and also by lengthening the time between hyperbaric oxygen sessions as the treatment advances. Hyperbaric chambers can be assembled to provide everything available to a patient in modern-day intensive care units. The complication rate of hyperbaric oxygen therapy is very low. Accordingly, hyperbaric oxygen, when safely available in hospital settings, should be considered as an adjunct for the management of critically injured or ill patients with disabling anemia.

Hyperbaric Oxygen Upregulates Mst1 to Activate Keap1/Nrf2/HO-1 Pathway Resisting Oxidative Stress in a Rat Model of Acute Myocardial Infarction.

This study aimed to investigate the protective effects and mechanisms of hyperbaric oxygen (HBO) preconditioning in a rat model of acute myocardial infarction (MI) established by ligation of the left anterior descending (LAD) coronary artery. Microarray, real-time PCR, and western blotting (WB) results demonstrated that the Mst1 gene was downregulated in the heart tissue of the MI rat model. HBO preconditioning significantly increased Mst1 expression in cardiac tissues of rats after MI modeling. Lentiviral infection was used to silence the Mst1 gene in rats treated with HBO to probe the effect of Mst1 on HBO cardioprotection. HBO preconditioning decreased heart infarct size and ameliorated cardiac function in MI rats, whereas Mst1 silencing reversed the effect of HBO administration, as indicated after heat infarct size determination via TTC staining, histological examination via HE staining, and measurements of cardiac function. HBO preconditioning reduced oxidative stress and inflammation in cardiac tissue of MI rat model, evidenced by alteration of malondialdehyde (MDA), 8-hydroxy-2-deoxyguanosine (8-OHdG), and protein carbonyl contents, as well as production of inflammation-associated myeloperoxidase (MPO), IL-1β, and TNF-α. These findings provide a new signaling mechanism through which HBO preconditioning can protect against acute MI injury through the Mst1-mediating Keap1/Nrf2/HO-1-dependent antioxidant defense system.

HBO aftereffect on lipid peroxidation and enzyme antioxidants of the brain: prospective experiental study

OBJECTIVE. Study the effect of a single and multiple administration of hyperbaric oxygenation (HBO) in the therapeutic regime on the processes of lipid peroxidation (LPO) and enzyme of antioxidative defense in phylogenetically various structures of the brain in the period of the immediate and remote aftereffect of expositions.
 MATERIALS AND METHODS. Experiments were carried out on 87 nonlinear white male rats weighing 180-230 grams. Hyperbaric oxygenation was conducted by medical oxygen in the experimental pressure chamber in the “mild” mode (2 ata, 50 min isopression), 1 session per day in the morning. The study was carried out after 1, 5, 10 sessions, in 5 and 10 days after 1 session and in 5 days after 5 sessions of HBO. The content of malondialdehyde (MDA) was determined in the brain stem, cerebellum and large brain hemispheres. The state of an enzyme element of antioxidant defense was evaluated by superoxide dismutase (SOD) and catalase.
 RESULTS. It was found that exposure to oxygen under high pressure caused increased intensity of LPO processes in the brain that progresses from 1 to 5 sessions. While MDA changes in the brain stem were detected later than in the hemispheres and cerebellum. LPO intensification in the brain proceeded against the background of increased activity of SOD. After 10 sessions of HBO LPO intensity decreased that was confirmed by reduced MDA content and SOD activity in examined brain tissue. Catalase activity reduced in the stem after 5 sessions and increased in the cerebellum and hemispheres after 10 sessions of HBO. Aftereffect of 1 HBO session was characterized by persistent increase in MDA concentration in the brain regions, detected in 5 and 10 days after exposure and was accompanied by increased SOD activity against the background of reduced catalase activity. In 5 days after 5 sessions the increase in MDA content and SOD activation was observed only in the tissue of the cerebral hemispheres.
 DISCUSSION. The use of HBO in the mode 2 ata, 50 min stimulates reactions of free radical oxidation (FRO) in the brain. The dynamics of their development with continued exposure shows that there are enough resources of the brain antioxidant defense to compensate hyperoxic load, including 10-fold exposure and no depletion of the reserves of enzyme antioxidant element in the brain is observed. After a single exposure of hyperbaric oxygen FRO activation remains during 10 days that can be concluded from an increased level of MDA and an increased activity of SOD in all the brain regions against the background of reduced catalase activity of stem structures and cerebellum. Repeated 5-fold exposures have a shorter metabolic “footprint”: in 5 days LPO effect and SOD activation are less pronounced than in the period of 1 session aftereffect both in 5 and 10 days.
 CONCLUSION. The therapeutic “mild” mode of HBO (2 ata, 50 min, 1 session per day) causes FRO activation in the brain tissue of experimental animals. Its intensity is controlled by the activation of enzyme protection mechanisms that is enough to compensate FRO changes with this mode of hyperoxic load. After ending exposures more pronounced aftereffect of HBO in the brain regions is found after 1 session compared to 5 sessions.

Hyperbaric oxygen administration mitigates the expression of kidney injury molecule-1, inflammatory cytokines, and apoptotic markers during cold ischemic time in kidney transplantation

The aim of this study was to investigate the effect of hyperbaric oxygen (HBO2) administration applied during cold ischemic time to organs removed from donors before kidney transplantation. A total of 24 rats were divided into three groups: Group 1 was the control group, Group 2 received 60 minutes of HBO2 at 2.5 atmospheres absolute, and Group 3 received 120 minutes of 2.5 ATA HBO2. The renal artery was entered with a polyethylene catheter and perfused with a standard organ preservation solution. Falcon tubes containing organs obtained from rats in Groups 2 and 3 were placed in a box supported by ice blocks. The temperature was kept constant at 4 °C and the box was placed in a pressure tank with 2.5 ATA HBO2. HBO2 was applied for 60 and 120 minutes, respectively. Organ samples were harvested at the end of 24 hours for histopathological evaluation, immunohistochemical analysis of TNF-α and IL-18, TUNEL analysis for apoptosis, and gene expression levels of kidney injury molecule-1 (KIM-1) and caspase-3. In histopathological examinations, hematoxylin and eosin staining was performed and samples were evaluated for tubular necrosis and vacuolization criteria. Group 2 and Group 3 had significant decreases compared to Group 1 in this regard. Immunohistochemical staining was performed for TNF-α, IL-18, and apoptosis levels; significant decreases were found in Groups 2 and 3. There were significant decreases in Groups 2 and 3 for KIM-1 and caspase-3 gene expression levels compared to Group 1, as well. Thus, it was demonstrated that during the cold ischemic time before kidney transplantation, HBO2 administration to organs removed from donors can reduce apoptotic cell numbers, inflammatory cytokine release, and histopathological damage to the organs as well as decreasing the expression of the KIM-1 gene, which is an indicator of kidney damage.

Veno-venous extracorporeal blood phototherapy increases the rate of carbon monoxide (CO) elimination in CO-poisoned pigs.

Carbon monoxide (CO) inhalation is the leading cause of poison-related deaths in the United States. CO binds to hemoglobin (Hb), displaces oxygen, and reduces oxygen delivery to tissues. The optimal treatment for CO poisoning in patients with normal lung function is the administration of hyperbaric oxygen (HBO). However, hyperbaric chambers are only available in medical centers with specialized equipment, resulting in delayed therapy. Visible light dissociates CO from Hb with minimal effect on oxygen binding. In a previous study, we combined a membrane oxygenator with phototherapy at 623 nm to produce a "mini" photo-ECMO (extracorporeal membrane oxygenation) device, which improved CO elimination and survival in CO-poisoned rats. The objective of this study was to develop a larger photo-ECMO device ("maxi" photo-ECMO) and to test its ability to remove CO from a porcine model of CO poisoning. The "maxi" photo-ECMO device and the photo-ECMO system (six maxi photo-ECMO devices assembled in parallel), were tested in an in vitro circuit of CO poisoning. To assess the ability of the photo-ECMO device and the photo-ECMO system to remove CO from CO-poisoned blood in vitro, the half-life of COHb (COHb-t1/2 ), as well as the percent COHb reduction in a single blood pass through the device, were assessed. In the in vivo studies, we assessed the COHb-t1/2 in a CO-poisoned pig under three conditions: (1) While the pig breathed 100% oxygen through the endotracheal tube; (2) while the pig was connected to the photo-ECMO system with no light exposure; and (3) while the pig was connected to the photo-ECMO system, which was exposed to red light. The photo-ECMO device was able to fully oxygenate the blood after a single pass through the device. Compared to ventilation with 100% oxygen alone, illumination with red light together with 100% oxygen was twice as efficient in removing CO from blood. Changes in gas flow rates did not alter CO elimination in one pass through the device. Increases in irradiance up to 214 mW/cm2 were associated with an increased rate of CO elimination. The photo-ECMO device was effective over a range of blood flow rates and with higher blood flow rates, more CO was eliminated. A photo-ECMO system composed of six photo-ECMO devices removed CO faster from CO-poisoned blood than a single photo-ECMO device. In a CO-poisoned pig, the photo-ECMO system increased the rate of CO elimination without significantly increasing the animal's body temperature or causing hemodynamic instability. In this study, we developed a photo-ECMO system and demonstrated its ability to remove CO from CO-poisoned 45-kg pigs. Technical modifications of the photo-ECMO system, including the development of a compact, portable device, will permit treatment of patients with CO poisoning at the scene of their poisoning, during transit to a local emergency room, and in hospitals that lack HBO facilities.

The History and Development of Hyperbaric Oxygenation (HBO) in Thermal Burn Injury.

Background and Objectives: Hyperbaric oxygenation (HBO) denotes breathing of 100% oxygen under elevated ambient pressure. Since the initiation of HBO for burns in 1965, abundant experimental and clinical work has been done. Despite many undisputedly positive and only a few controversial results on the efficacy of adjunctive HBO for burn injury, the method has not yet been established in clinical routine. Materials and Methods: We did a retrospective analysis of the literature according to PRISMA—guidelines, from the very beginning of HBO for burns up to present, trying to elucidate the question why HBO is still sidelined in the treatment of burn injury. Results: Forty-seven publications (32 animal experiments, four trials in human volunteers and 11 clinical studies) fulfilled the inclusion criteria. Except four investigators who found little or no beneficial action, all were able to demonstrate positive effects of HBO, most of them describing less edema, improved healing, less infection or bacterial growth and most recently, reduction of post-burn pain. Secondary enlargement of burn was prevented, as microvascular perfusion could be preserved, and cells were kept viable. The application of HBO, however, concerning pressure, duration, frequency and number of treatment sessions, varied considerably. Authors of large clinical studies underscored the intricate measures required when administering HBO in severe burns. Conclusions: HBO unquestionably has a positive impact on the pathophysiological mechanisms, and hence on the healing and course of burns. The few negative results are most likely due to peculiarities in the administration of HBO and possibly also to interactions when delivering the treatment to severely ill patients. Well-designed studies are needed to definitively assess its clinical value as an adjunctive treatment focusing on relevant outcome criteria such as wound healing time, complications, length of hospital stay, mortality and scar quality, while also defining optimal HBO dosage and timing.

Cerebral arterial gas embolism proven by computed tomography following transthoracic echocardiography using bubble contrast

A 75 year-old male developed features of an acute stroke following bubble contrast echocardiography, which was shown on emergent computed tomography scanning to be a result of cerebral arterial gas embolism (CAGE) to the left middle cerebral artery. Ischaemic stroke symptoms have previously been reported as a rare complication of bubble contrast echocardiography. Radiologically proven CAGE from bubble contrast echocardiography had not been reported at the time this case occurred. Immediate provision of 100% oxygen and administration of hyperbaric oxygen are recommended treatments for CAGE and were associated with a substantial recovery for this patient.

Ghrelin system is involved in improvements in glucose metabolism mediated by hyperbaric oxygen treatment in a streptozotocin‑induced type1 diabetes mouse model.

Type 1 diabetes mellitus (T1DM) is an autoimmune disorder for which the only effective therapy is insulin replacement. Hyperbaric oxygen (HBO) therapy has demonstrated potential in improving hyperglycemia and as a treatment option for T1DM. Ghrelin and HBO have been previously reported to exert proliferative, anti-apoptotic and anti-inflammatory effects in pancreatic cells. The present study investigated the mechanism underlying HBO- and ghrelin system-mediated regulation of glucose metabolism. Male C57BL/6 mice were intraperitoneally injected with streptozotocin (STZ; 150 mg/kg) to induce T1DM before the diabetic mice were randomly assigned into the T1DM and T1DM + HBO groups. Mice in the T1DM + HBO group received HBO (1 h; 100% oxygen; 2 atmospheres absolute) daily for 2 weeks. Significantly lower blood glucose levels and food intake were observed in mice in the T1DM + HBO group. Following HBO treatment, islet β-cell area were increased whereas those of α-cell were decreased in the pancreas. In addition, greater hepatic glycogen storage in liver was observed, which coincided with higher pancreatic glucose transporter 2 (GLUT2) expression levels and reduced hepatic GLUT2 membrane trafficking. There were also substantially higher total plasma ghrelin concentrations and gastric ghrelin-O-acyl transferase (GOAT) expression levels in mice in the T1DM + HBO group. HBO treatment also abolished reductions in pancreatic GOAT expression levels in T1DM mice. Additionally, hepatic growth hormone secretagogue receptor-1a levels were found to be lower in mice in the T1DM + HBO group compared with those in the T1DM group. These results suggest that HBO administration improved glucose metabolism in a STZ-induced T1DM mouse model. The underlying mechanism involves improved insulin-release, glucose-sensing and regulation of hepatic glycogen storage, an observation that was also likely dependent on the ghrelin signalling system.

Current and research therapies for the prevention and treatment of delayed neurological syndrome associated with carbon monoxide poisoning: A narrative review.

Severe carbon monoxide (CO) poisoning causes fulminant deaths in common environment as well as neurological sequelae to survivors. Prevention of delayed neurological syndrome (DNS) after exposure to CO, the most important sequela, is based up to date on hyperbaric oxygen administration. Nevertheless, its use remains controversial due to the lack of evidence regarding its efficacy. The aim of this review is to report therapies under investigation for preventing or improving DNS, some of them with promising results in humans.

The myopic shift associated with hyperbaric oxygen administration is reduced when using a mask delivery system compared to a hood - a randomised controlled trial.

A temporary myopic shift is a well-recognized complication of hyperbaric oxygen treatment (HBOT). Oxidation of proteins in the crystalline lens is the likely cause. Direct exposure of the eye to hyperbaric oxygen may exacerbate the effect. Our aim was to measure the magnitude of the myopic shift over a course of HBOT when using two different methods of oxygen delivery. We conducted a randomised trial of oxygen delivery via hood versus oronasal mask during a course of 20 and 30 HBOT sessions. Subjective refraction was performed at baseline and after 20 and 30 sessions. We repeated these measurements at four and 12 weeks after completion of the course in those available for assessment. We enrolled 120 patients (mean age 57.6 (SD 11.2) years; 81% male). The myopic shift was significantly greater after both 20 and 30 sessions in those patients using the hood. At 20 treatments: refractory change was -0.92 D with hood versus -0.52 D with mask, difference 0.40 D (95% CI 0.22 to 0.57, P < 0.0001); at 30 treatments: -1.25 D with hood versus -0.63 with mask, difference 0.62 D (95% CI 0.39 to 0.84, P < 0.0001). Recovery was slower and less complete in the hood group at both four and 12 weeks. Myopic shift is common following HBOT and more pronounced using a hood system than an oronasal mask. Recovery may be slower and less complete using a hood. Our data support the use of an oronasal mask in an air environment when possible.

Calculated risk of pulmonary and central nervous system oxygen toxicity: a toxicity index derived from the power equation.

The risk of oxygen toxicity has become a prominent issue due to the increasingly widespread administration of hyperbaric oxygen (HBO) therapy, as well as the expansion of diving techniques to include oxygen-enriched gas mixtures and technical diving. However, current methods used to calculate the cumulative risk of oxygen toxicity during an HBO exposure i.e., the unit pulmonary toxic dose concept, and the safe boundaries for central nervous system oxygen toxicity (CNS-OT), are based on a simple linear relationship with an inspired partial pressure of oxygen (PO2) and are not supported by recent data. The power equation: Toxicity Index = t2 × PO2c, where t represents time and c represents the power term, was derived from the chemical reactions producing reactive oxygen species or reactive nitrogen species. The toxicity index was shown to have a good predictive capability using PO2 with a power c of 6.8 for CNS-OT and 4.57 for pulmonary oxygen toxicity. The pulmonary oxygen toxicity index (PO2 in atmospheres absolute, time in h) should not exceed 250. The CNS-OT index (PO2 in atmospheres absolute, time in min) should not exceed 26,108 for a 1% risk. The limited use of this toxicity index in the diving community, after more than a decade since its publication in the literature, establishes the need for a handy, user-friendly implementation of the power equation.

P11.14 The addition of hyperbaric oxygen to the treatment of T98G glioblastoma cell cultures with selected CK2 inhibitor TDB enhances its anti-tumour effect

Abstract BACKGROUND Glioblastoma (GBM) is the most aggressive glial neoplasm characterized by infiltrative cell growth in adults. The current standard of care for high-grade glioma patients includes surgery, radiotherapy and chemotherapy using temozolomide and other alkylating agents. Despite this, median survival of the patients with GBM is less than two years. One of the main factors related to the progression of neoplastic cells is hyperactivity of protein kinases, including CK2 kinase and a high level of tumor hypoxia, both of which also contribute to tumour resistance to treatment. Our previous study indicated that some CK2 inhibitors exhibit anti-proliferative effect on glioma cells. The aim of this study was to examine whether HBO may enhance the anti-tumour efficacy of 1-(β-D-2’-deoxyribofuranosyl)-4,5,6,7-tetrabromo-1H-benzimidazole (TDB) - CK2 inhibitor, under combination HBO/TDB therapy. MATERIAL AND METHODS Studies were performed on human glioblastoma T98G cell line (ATCC). Cells were cultured in MEM medium supplemented with 1-(β-D-2’-deoxyribofuranosyl)-4,5,6,7-tetrabromo-1H-benzimidazole in concentrations of 0.1 μM; 1 μM, 25 μM, 50 μM, 75μM, 100 μM. Cultures were sustained in various oxygen conditions: normoxia for 24 and 48 hours or1 hour of hyperbaric oxygen (HBO, 97,5% O2/2,5% CO2, pressure of 2 ATA) followed by 23 hours of normoxia (21% O2/5% CO2/78% N2). Control groups included the cultures sustained in normoxia conditions. The viability of glioma cell lines was established at 24 and 48 hours post TDB treatment by Cell Titer 96®A Queous One Solution Cell Proliferation Assay. RESULTS The study evidenced that TDB inhibited the viability of neoplastic cells at a concentration of 75 μM after 24 and 48 hours. Administration of hyperbaric oxygen alone also caused a reduction in viability of glioblastoma cells. The cytotoxic effect of the tested CK2 inhibitor was significantly enhanced when tested compound was combined with HBO. What’s more, under the influence of hyperbaric oxygen, TDB significantly reduced the viability of tumor cells already at a concentration of 25 μM after 24 hours. CONCLUSIONS Hyperbaric oxygen administration significantly reduces the viability of T98G line cells and increases their sensitivity to the tested CK2 kinase inhibitor. The beneficial cytotoxic effect of TDB/HBO can be obtained at lower concentrations of the tested compound and after shorter exposure time as compared to its administration without HBO. Acknowledgement: The research was supported by the Foundation for the Development of Diagnostic and Therapy, Warsaw

The National Brain Injury Rescue and Rehabilitation Study - a multicenter observational study of hyperbaric oxygen for mild traumatic brain injury with post-concussive symptoms.

The National Brain Injury Rescue and Rehabilitation Project was established as a preliminary study to test the safety and practicality of multi-center hyperbaric oxygen administration for the post-concussive symptoms of chronic mild traumatic brain injury as a precursor to a pivotal, independent, multi-center, controlled clinical trial. This report presents the results for 32 subjects who completed a preliminary trial of hyperbaric oxygen several years before the passage of the 21st Century Cures Act. This study anticipated the Act and its reassessment of clinical research. Subjects received 40–82 one-hour treatments at 1.5 atmospheres absolute 100% oxygen. Outcome measures included repeated self-assessment measures and automated neurocognitive tests. The subjects demonstrated improvement in 21 of 25 neurocognitive test measures observed. The objective neurocognitive test components showed improvement in 13 of 17 measures. Earlier administration of hyperbaric oxygen post injury, younger age at the time of injury and hyperbaric oxygen administration, military status, and increased number of hyperbaric oxygen administrations were characteristics associated with improved outcomes. There were no adverse events. Hyperbaric oxygen was found to be safe, inexpensive and worthy of clinical application in the 21st Century model of facile data collection provided by recent research regulatory shifts in medicine. The study was approved by the ethics review committee of the Western Institutional Review Board (WIRB® Protocol #20090761).

Do Late Phase Hyperbaric and Normobaric Oxygen Therapies have Effect on Liver Damage? An Experimental Sepsis Model

Background: Sepsis is fatal presentation which affects many systems with possible progression to organ dysfunction and organ failure. Among these organs liver plays an important role in the prognosis of this syndrome. This study investigated the effects of hyperbaric oxygen (HBO) and normobaric oxygen (NBO) therapies on liver damage and oxidative stress in an experimental sepsis model. Materials and Methods: Forty males Wistar rats were randomized into 4 groups as sham group (n=10), control (Sepsis+Cefepime) group (n=10), HBO (Sepsis+Cefepime+HBO) group (n=10), and NBO (Sepsis+Cefepime+NBO) group (n=10). Five days after sepsis induction, animals were sacrificed. The oxidative stress parameters, malondialdehyde (MDA) and superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) for antioxidant response were measured in liver tissue. Neutrophil migration using myeloperoxidase (MPO) activity and its contribution to liver damage was evaluated. Results: While MDA levels in HBO group were found to be lower than those in the control group, and comparable to those in the sham group, no difference was detected in the MDA levels between the control and NBO groups. SOD levels in NBO group were detected to be significantly higher than the control group. GSH-Px enzyme activity in HBO and NBO groups was at similar levels. Even though MPO levels in HBO group appeared to be lower than the control group, the difference did not reach statistical significance. When MPO levels and histopathological examination were evaluated, it was observed that neither HBO nor NBO administration in addition to antibiotherapy provided decrease in neutrophil infiltration which has an important role in liver damage. Conclusion: The benefit of HBO in the treatment of sepsis in addition to the use of antibiotics has also been confirmed to be successful in this study. Furthermore the data obtained from NBO applications in this study, is thought to be potentially useful for sepsis treatment.

Endothelial Dysfunction Improvement Mechanism By Hyperbaric Oxygen In Sprague Dawley By High-Cholesterol Diet

The purpose of this study was to investigate the mechanism of hyperbaric oxygen could improve endothelial dysfunction. In the experimental method, Sprague Dawley strains divided 3 groups : the normal control for p1, high cholesterol diet for p2, and high cholesterol diet with hyperbaric oxygen of 2.4 ATA with 98% O2 for 3 sessions with the duration of 30 minutes / session, and air break for 5 minutes between each session for the period of 10 days consecutively for p3. On the last day of treatment, serum was taken for heme oxygenase-1 (HO-1), Sirtuin (SIRT1), endothelial Nitric Oxide Synthase (eNOS) and lipoprotein-associated phospholipase A2 (Lp-PLA2) by ELISA method. The new findings of this study are hyperbaric oxygen could improve endothelial dysfunction which occurs due to an atherogenic diet, through two pathways. The first, hyperbaric oxygen therapy increased heme oxygenase1 (HO1) (p = 0,000), sirtuin-1 (SIRT1) (p = 0.025), endothelial nitric oxide synthase (eNOS) (p = 0,000) and decreased levels of lipoprotein-associated phospholipase A2 (Lp-PLA2) (p = 0,000). The second hyperbaric oxygen administration enhances sirtuin1 (SIRT1) (p=0,000) directly, endothelial nitric oxide synthase (eNOS) (p = 0,000) and decreased levels of lipoprotein-associated phospholipase A2 (Lp-PLA2) (p = 0,000).

Treatment with normobaric or hyperbaric oxygen and its effect on neuropsychometric dysfunction after carbon monoxide poisoning

Background:Carbon monoxide (CO) poisoning may result in acute neurological sequelae, cognitive sequelae, and delay neurological sequelae. The administration of hyperbaric oxygen (HBO) to prevent the development of delayed neurological sequelae in CO poisoning have extensively investigated but conflicting results have been reported. We performed a systematic literature review and meta-analysis of randomized controlled trials (RCTs) evaluating HBO treatment and its effect on neuropsychometric dysfunction after CO poisoning.Methods:We searched Medline, Embase, Pubmed, and the Cochrane Register of Controlled Trials from inception to December 2017. Eligible studies compared HBO therapy with normobaric oxygen (NBO) in patients with CO poisoning.Results:Six studies compared HBO with NBO in CO poisoning patients. Compared with patients treated with NBO, a lower percentage of patients treated with HBO reported headache (16.2% vs 16.5%, relative risk [RR] = 0.83, 95% CI = 0.38–1.80), memory impairment (18.2% vs 23.8%, RR = 0.80, 95% CI = 0.43–1.49), difficulty concentrating (15.0% vs 18.4%, RR = 0.86, 95% CI = 0.55–1.34), and disturbed sleep (14.7% vs 16.2%, RR = 0.91, 95% CI = 0.59–1.39). Two sessions of HBO treatment exhibited no advantage over one session.Conclusions:The meta-analysis indicated that compared with CO poisoning patients treated with NBO, HBO treated patients have a lower incidence of neuropsychological sequelae, including headache, memory impairment, difficulty concentrating, disturbed sleep, and delayed neurological sequelae. Taking into consideration the cost-effectiveness of one session of HBO, one session of HBO treatment could be an economical option for patients with CO poisoning with high severity.

Hyperbaric oxygen effects towards SIRT1 level in Sprague dawley with endothelial dysfunction by high-cholesterol diet

Introduction: Endothelial dysfunction is an early risk factor for cardiovascular disease and hypertension. Mechanisms that participate in endothelial dysfunction include the decrease of nitric oxide (NO) and the increase of endothelin-1 (ET-1). ATP-sensitive potassium channels (KATP channels) also participate in endothelial cells in the vascular system. This study aims to investigate whether energy / ATP / SIRT1 is involved in endothelial dysfunction after the administration of hyperbaric oxygen (HBO).Methods: This study was an experimental study, using a randomized post test only control group design using thirty white rats (Rattus norvegicus) Sprague dawley strains.There were 3 groups of p1, p2, and p3, and each group consists of 10 rats with the normal control for p1, high cholesterol diet for p2, and high cholesterol diet with hyperbaric oxygen of 2.4 ATA with 98% O2 for 3 sessions with the duration of 30 minutes / session, and air break for 5 minutes between each session for the period of 10 days consecutively for p3. The level of SIRT 1 was tested by using Elisa method. We applied statistical methods of investigation.Results: The SIRT1 from ELISA results tend to increase after the administration of hyperbaric oxygen (HBO). Decreased of SIRT1 occur at group was given by high-cholesterol diet (p1=0,188±0,017 ng/ml; p2=0,114±0,029 ng/ml; p3=0,252±0,027 ng/ml). Hypercholesterolemia and endothelial dysfunction affect energy metabolism and reduce ATP levels and nicotinamide adenine dinucleotide (SIRT1). HBO therapy increases ATP and nicotinamide adenine dinucleotide levels which affect the increase of silent mating type information regulation two homologs 1, resulting in the optimal endothelial cell function.Conclusion: Hyperbaric oxygen can significantly affect the endothelial dysfunction due to an high-cholesterol diet, by increasing the levels of Sirtuin-1.

The Role of Duration of Hyperbaric Oxygen Therapy on Lung Injury: An Experimental Study Lung Injury and Hyperbaric Oxygen Therapy.

We aim to histopathologically analyze the effect of hyperbaric oxygen (HBO) therapy in the lung tissue. A total of 21 rabbits were divided into three groups, with each containing seven rabbits. Group 1 was the control group. Group 2 underwent HBO of 3 atmosphere absolute (ATA) for 90 min/day for 7 days. In group 3, HBO at 3 ATA was administered 90 min/day for 28 days. Oxygen saturation (SpO2) was determined by pulse oximetry before and after administration of HBO. Rabbits were sacrificed, and the apex of the right lung was excised. SpO2 was 98-100% in all rabbits before HBO administration. After the procedure, the mean SpO2 was 92% and 83% in groups 2 and 3, respectively. As expected, histopathologic examination in group 1 was normal. In group 2, congestion in the lung vessels, mononuclear cell infiltration in the bronchial mucosa, interstitial edema, and alveolar dilation were evident. Histopathologic examination in group 3 indicated diffuse alveolar edema, peribronchial mononuclear cell infiltration, thickening of the alveolar and vessel wall, and intraalveolar hemorrhage. There is a strict relationship between duration of HBO administration and severity of lung injury.

Effect of Hyperbaric Oxygen on Proliferation and Gene Expression of Human Chondrocytes: An In Vitro Study.

The present study investigated the effects of hyperbaric oxygen (HBO) on human chondrocyte proliferation and gene expression patterns. Chondrocyte cultures were transferred to a HBO chamber and exposed to 100% oxygen for 7 consecutive days. Within groups, pressure was varied between 1 and 2 atm and duration of HBO administration was varied among 60, 90, and 120 minutes. Cell counts were performed using the WST-1 assay at 1, 3, 5, and 7 days after initiation of HBO treatment to obtain data to plot a growth curve. Gene expression of apoptosis markers PARP and caspase 3, as well as cartilage specific proteins collagen II and COMP, were detected by reverse transcription polymerase chain reaction. The experiments showed that in vitro administration of HBO inhibit chondrocyte growth. When applied compression was increased up to 2 atm, chondrocyte cell count was reduced by half at days 3 and 7 in association with an upregulation of the apoptosis markers PARP and caspase 3 as well as the cartilage specific proteins collagen II and COMP. No significant differences were monitored from varied duration of daily treatment. Chondrocyte growth was inhibited in vitro by treatment of HBO. This inhibitory effect was even increased by elevating the applied pressure, while molecular testing showed reduced chondrocyte growth. Higher levels of HBO inhibited cell growth even more, but up-regulation of apoptosis specific markers and cartilage specific proteins were seen during administration of high oxygen levels. Thus, it has to be evaluated that there is a critical level of hypo-/hyperoxia required to stimulate or at least maintain chondrocyte cell proliferation.

Increased Efficacy of Antivenom Combined with Hyperbaric Oxygen on Deinagkistrodon acutus Envenomation in Adult Rats.

Background:Snakebites are a neglected threat to global human health with a high morbidity rate. The present study explored the efficacy of antivenom with hyperbaric oxygen (HBO) intervention on snakebites, which could provide the experimental basis for clinical adjuvant therapy.Methods:Male Sprague–Dawley rats (n = 96) were randomized into four groups: the poison model was established by injecting Deinagkistrodon acutus (D. acutus) venom (0.8 LD50) via the caudal vein; the antivenom group was injected immediately with specific antivenom via the caudal vein after successful establishment of the envenomation model; and the antivenom + HBO group was exposed to HBO environment for 1 h once at predetermined periods of 0 h, 4 h, 12 h, and 23 h after antivenin administration. Each HBO time point had six rats; the control group was left untreated. The rats in the experimental group were euthanized at the corresponding time points after HBO therapy, and brain tissue and blood were harvested immediately. Hematoxylin and eosin (H&E) staining was used to investigate the pathological changes in the rat brain. Immunohistochemistry (IHC), real-time polymerase chain reaction (PCR), and Western blotting were used to detect the expression of Nestin mRNA and protein in the subventricular zone (SVZ) of the brain. The levels of coagulation function (prothrombin time, activated partial thromboplastin time [APTT], and fibrinogen) and oxidation/antioxidation index (malondialdehyde [MDA] and superoxide dismutase [SOD]) were analyzed. Data were analyzed using one-way analysis of variance.Results:The brain tissue from rats in the poison model was observed for pathological changes using H&E staining. Tissues showed edema, decreased cell number, and disordered arrangement in the SVZ in the snake venom group. The antivenom − HBO intervention significantly alleviated these observations and was more prominent in the antivenom + HBO group. The serum levels of SOD and MDA in the snake venom group were increased and the antivenom − HBO intervention further increased the SOD levels but significantly decreased the MDA levels; however, this was enhanced within 1 h after HBO administration (MDA: F = 5.540, P = 0.008, SOD: F = 7.361, P = 0.000). Activated partial thromboplastin time (APTT) was significantly abnormal after venom administration but improved after antivenom and was even more significant in the antivenom + HBO group 5 h after envenomation (F = 25.430, P = 0.000). Only a few nestin-positive cells were observed in the envenomation model. The expression levels were significant in the antivenom and antivenom + HBO groups within 1 and 5 h after envenomation and were more significant in the antivenom + HBO group as determined by IHC, real-time PCR, and Western blotting (P < 0.05). D. acutus envenomation has neurotoxic effects in the brain of rats.Conclusions:Antivenin and HBO, respectively, induced a neuroprotective effect after D. acutus envenomation by attenuating brain edema, upregulating nestin expression in SVZ, and improving coagulopathy and oxidative stress. The intervention efficacy of antivenom with HBO was maximum within 5 h after envenomation and was more efficacious than antivenom alone.