Therapeutic Actions Hyperbaric Treatment

NCBI pubmed

Impact of gas emboli and hyperbaric treatment on respiratory function of loggerhead sea turtles (Caretta caretta).

Related Articles Impact of gas emboli and hyperbaric treatment on respiratory function of loggerhead sea turtles (Caretta caretta). Conserv Physiol. 2018;6(1):cox074 Authors: Portugues C, Crespo-Picazo JL, García-Párraga D, Altimiras J, Lorenzo T, Borque-Espinosa A, Fahlman A Abstract Fisheries interactions are the most serious threats for sea turtle populations. Despite the existence of some rescue centres providing post-traumatic care and rehabilitation, adequate treatment is hampered by the lack of understanding of the problems incurred while turtles remain entrapped in fishing gears. Recently it was shown that bycaught loggerhead sea turtles (Caretta caretta) could experience formation of gas emboli (GE) and develop decompression sickness (DCS) after trawl and gillnet interaction. This condition could be reversed by hyperbaric O2 treatment (HBOT). The goal of this study was to assess how GE alters respiratory function in bycaught turtles before recompression therapy and measure the improvement after this treatment. Specifically, we assessed the effect of DCS on breath duration, expiratory and inspiratory flow and tidal volume (VT), and the effectiveness of HBOT to improve these parameters. HBOT significantly increased respiratory flows by 32-45% while VT increased by 33-35% immediately after HBOT. Repeated lung function testing indicated a temporal increase in both respiratory flow and VT for all bycaught turtles, but the changes were smaller than those seen immediately following HBOT. The current study suggests that respiratory function is significantly compromised in bycaught turtles with GE and that HBOT effectively restores lung function. Lung function testing may provide a novel means to help diagnose the presence of GE, be used to assess treatment efficacy, and contribute to sea turtle conservation efforts. PMID: 29340152 [PubMed]

Hyperbaric oxygen protects against myocardial reperfusion injury via the inhibition of inflammation and the modulation of autophagy.

Related Articles Hyperbaric oxygen protects against myocardial reperfusion injury via the inhibition of inflammation and the modulation of autophagy. Oncotarget. 2017 Dec 19;8(67):111522-111534 Authors: Chen C, Chen W, Li Y, Dong Y, Teng X, Nong Z, Pan X, Lv L, Gao Y, Wu G Abstract Our previous study demonstrated that hyperbaric oxygen (HBO) preconditioning protected against myocardial ischemia reperfusion injury (MIRI) and improved myocardial infarction. However, HBO's effect on MIRI-induced inflammation and autophagy remains unclear. In this study, we investigate the potential impact and underlying mechanism of HBO preconditioning on an MIRI-induced inflammatory response and autophagy using a ligation of the left anterior descending (LAD) coronary artery rat model. Our results showed that HBO restored myocardial enzyme levels and decreased the apoptosis of cardiomyocytes, which were induced by MIRI. Moreover, HBO significantly suppressed MIRI-induced inflammatory cytokines. This effect was associated with the inhibition of the TLR4-nuclear factor kappa-B (NF-κB) pathway. Interestingly, lower expression levels of microtubule-associated protein 1 light chain 3B (LC3B) and Beclin-1 were observed in the HBO-treatment group. Furthermore, we observed that HBO reduced excessive autophagy by activating the mammalian target of the rapamycin (mTOR) pathway, as evidenced by higher expression levels of threonine protein kinase (Akt) and phosphorylated-mTOR. In conclusion, HBO protected cardiomocytes during MIRI by attenuating inflammation and autophagy. Our results provide a new mechanistic insight into the cardioprotective role of HBO against MIRI. PMID: 29340072 [PubMed]

Human Umbilical Cord Mesenchymal Stem Cells Preserve Adult Newborn Neurons and Reduce Neurological Injury after Cerebral Ischemia by Reducing the Number of Hypertrophic Microglia/Macrophages.

Related Articles Human Umbilical Cord Mesenchymal Stem Cells Preserve Adult Newborn Neurons and Reduce Neurological Injury after Cerebral Ischemia by Reducing the Number of Hypertrophic Microglia/Macrophages. Cell Transplant. 2017 Nov;26(11):1798-1810 Authors: Lin W, Hsuan YC, Lin MT, Kuo TW, Lin CH, Su YC, Niu KC, Chang CP, Lin HJ Abstract Microglia are the first source of a neuroinflammatory cascade, which seems to be involved in every phase of stroke-related neuronal damage. Two weeks after transient middle cerebral artery occlusion (MCAO), vehicle-treated rats displayed higher numbers of total ionized calcium-binding adaptor molecule 1 (Iba-1)-positive cells, greater cell body areas of Iba-1-positive cells, and higher numbers of hypertrophic Iba-1-positive cells (with a cell body area over 80 μm2) in the ipsilateral ischemic brain regions including the frontal cortex, striatum, and parietal cortex. In addition, MCAO decreased the number of migrating neuroblasts (or DCX- and 5-ethynyl-2'-deoxyuridine-positive cells) in the cortex, subventricular zone, and hippocampus of the ischemic brain, followed by neurological injury (including brain infarct and neurological deficits). Intravenous administration of human umbilical cord-derived mesenchymal stem cells (hUC-MSCs; 1 × 106 or 4 × 106) at 24 h after MCAO reduced neurological injury, decreased the number of hypertrophic microglia/macrophages, and increased the number of newborn neurons in rat brains. Thus, the accumulation of hypertrophic microglia/macrophages seems to be detrimental to neurogenesis after stroke. Treatment with hUC-MSCs preserved adult newborn neurons and reduced functional impairment after transient cerebral ischemia by reducing the number of hypertrophic microglia/macrophages. PMID: 29338384 [PubMed - in process]

Efficacy of hyperbaric oxygen therapy in bacterial biofilm eradication.

Related Articles Efficacy of hyperbaric oxygen therapy in bacterial biofilm eradication. J Wound Care. 2018 Jan 01;27(Sup1):S20-S28 Authors: Sanford NE, Wilkinson JE, Nguyen H, Diaz G, Wolcott R Abstract OBJECTIVE: Chronic wounds typically require several concurrent therapies, such as debridement, pressure offloading, and systemic and/or topical antibiotics. The aim of this study was to examine the efficacy of hyperbaric oxygen therapy (HBOT) towards reducing or eliminating bacterial biofilms in vitro and in vivo. METHOD: Efficacy was determined using in vitro grown biofilms subjected directly to HBOT for 30, 60 and 90 minutes, followed by cell viability determination using propidium monoazide-polymerase chain reaction (PMA-PCR). The efficacy of HBOT in vivo was studied by searching our chronic patient wound database and comparing time-to-healing between patients who did and did not receive HBOT as part of their treatment. RESULTS: In vitro data showed small but significant decreases in cell viability at the 30- and 90-minute time points in the HBOT group. The in vivo data showed reductions in bacterial load for patients who underwent HBOT, and ~1 week shorter treatment durations. Additionally, in patients' chronic wounds there was a considerable emergence of anaerobic bacteria and fungi between intermittent HBOT treatments. CONCLUSION: The data demonstrate that HBOT does possess a certain degree of biofilm killing capability. Moreover, as an adjuvant to standard treatment, more favourable patient outcomes are achieved through a quicker time-to-healing which reduces the chance of complications. Furthermore, the data provided insights into biofilm adaptations to challenges presented by this treatment strategy which should be kept in mind when treating chronic wounds. Further studies will be necessary to evaluate the benefits and mechanisms of HBOT, not only for patients with chronic wounds but other chronic infections caused by bacterial biofilms. PMID: 29334015 [PubMed - in process]

Efficacy of Combined XingZhi-YiNao Granules and Hyperbaric Oxygen Therapy for Cognition and Motor Dysfunction in Patients with Delayed Encephalopathy after Acute Carbon Monoxide Poisoning.

Related Articles Efficacy of Combined XingZhi-YiNao Granules and Hyperbaric Oxygen Therapy for Cognition and Motor Dysfunction in Patients with Delayed Encephalopathy after Acute Carbon Monoxide Poisoning. Evid Based Complement Alternat Med. 2017;2017:1323297 Authors: Qin L, Meihua C, Dadong G, Li W, Jinglin W, Xiaoyu D, Mingjun B, Yong Z Abstract Purpose: To investigate the efficacy of XingZhi-YiNao (XZYN) granules and hyperbaric oxygenation (HBO) for cognition and motor dysfunction in patients with delayed encephalopathy after acute carbon monoxide poisoning (DEACMP). Methods: Eighty-nine patients with DEACMP were randomly divided into control group (n = 19), HBO group (n = 32), and XZYN group (n = 38). All patients received conventional treatment. HBO group received HBO therapy once daily. XZYN group received extra XZYN granules plus HBO treatment. The related indexes including activity of daily living (ADL) scale, Montreal cognitive assessment (MoCA) scale, and mini mental state examination (MMSE) scale were measured. Cerebral white matter injury, age related white matter changes (ARWMC) scale, and the amplitude and latency of P300 were assessed. Results: Compared with control group, the neurological function scores of ADL, MoCA, and MMSE in HBO and XZYN groups were significantly improved, the impairment degree of brain white matter and cognition function were obviously alleviated, the latencies of P300 were significantly shortened, and the amplitudes of P300 were evidently increased (P < 0.05). Treatment efficacy of XZYN group was superior to that of HBO group (P < 0.05). Conclusion: Combined XZYN granules and HBO can significantly improve cognition and motor functions in patients with DEACMP. PMID: 29333178 [PubMed]

Association between augmented renal clearance and clinical outcomes in patients receiving β-lactam antibiotic therapy by continuous or intermittent infusion: a nested cohort study of the BLING-II randomised, placebo-controlled, clinical trial.

Related Articles Association between augmented renal clearance and clinical outcomes in patients receiving β-lactam antibiotic therapy by continuous or intermittent infusion: a nested cohort study of the BLING-II randomised, placebo-controlled, clinical trial. Int J Antimicrob Agents. 2017 May;49(5):624-630 Authors: Udy AA, Dulhunty JM, Roberts JA, Davis JS, Webb SAR, Bellomo R, Gomersall C, Shirwadkar C, Eastwood GM, Myburgh J, Paterson DL, Starr T, Paul SK, Lipman J, BLING-II Investigators, ANZICS Clinical Trials Group Abstract Augmented renal clearance (ARC) is known to influence β-lactam antibiotic pharmacokinetics. This substudy of the BLING-II trial aimed to explore the association between ARC and patient outcomes in a large randomised clinical trial. BLING-II enrolled 432 participants with severe sepsis randomised to receive β-lactam therapy by continuous or intermittent infusion. An 8-h creatinine clearance (CLCr) measured on Day 1 was used to identify ARC, defined as CLCr ≥ 130 mL/min. Patients receiving any form of renal replacement therapy were excluded. Primary outcome was alive ICU-free days at Day 28. Secondary outcomes included 90-day mortality and clinical cure at 14 days following antibiotic cessation. A total of 254 patients were included, among which 45 (17.7%) manifested ARC [median (IQR) CLCr 165 (144-198) mL/min]. ARC patients were younger (P <0.001), more commonly male (P = 0.04) and had less organ dysfunction (P <0.001). There was no difference in ICU-free days at Day 28 [ARC, 21 (12-24) days; no ARC, 21 (11-25) days; P = 0.89], although clinical cure was significantly greater in the unadjusted analysis in those manifesting ARC [33/45 (73.3%) vs. 115/209 (55.0%) P = 0.02]. This was attenuated in the multivariable analysis. No difference was noted in 90-day mortality. There were no statistically significant differences in clinical outcomes in ARC patients according to the dosing strategy employed. In this substudy of a large clinical trial of β-lactam antibiotics in severe sepsis, ARC was not associated with any differences in outcomes, regardless of dosing strategy. PMID: 28286115 [PubMed - indexed for MEDLINE]

Molecular mechanisms underlying hyperoxia acute lung injury.

Related Articles Molecular mechanisms underlying hyperoxia acute lung injury. Respir Med. 2016 Oct;119:23-28 Authors: Dias-Freitas F, Metelo-Coimbra C, Roncon-Albuquerque R Abstract The management of acute hypoxemic respiratory failure frequently includes the use of supraphysiological fractions of inspired oxygen (FiO2), which can be beneficial in the short-term but not without risks in the long-term, causing acute lung injury (ALI). Over the last few years, much attention has been devoted to the intracellular signaling transduction pathways that lead to hyperoxia-induced cell damage, particularly MAP kinase cascades. Identification of involved signaling molecules and understanding of the regulation of the main signal transduction pathways might provide the basis for improving the outcome of patients under high FiO2 exposure through more effective therapeutic interventions. This review, which includes studies published from 1987 to 2015, presents an overview on recent progresses in the hyperoxia ALI field with special emphasis on potential therapeutic targets and clinical approaches based on the molecular mechanisms underlying hyperoxia-induced inflammation. Further studies are needed to gain deeper insight into controversial molecular mechanisms underlying hyperoxia-induced cell death, which may play a critical role in future pharmacological interventions, as well as into hyperoxia-induced cell damage, that could monitor and therefore prevent hyperoxia ALI. PMID: 27692143 [PubMed - indexed for MEDLINE]