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Undersea and Hyperbaric Medicine Section Newsletter - April 2007, Vol 14, #1

Undersea and Hyperbaric Medicine

circle_arrow Message From the Chair
circle_arrow Non-traditional Indications for HBOT

Newsletter Index

Hyperbaric Medicine Section


Message From the Chair

Sorabh Khandelwal, MDSorabh Khandelwal, MD

I think you will find this edition of our newsletter full of interesting and helpful information. Congratulations should go out to Robert L. Sherwin, MD, for his efforts.

As I thought about what thoughts I would like to share with our membership, many came to mind, but one stood out. I have been reflecting on the trend that we have seen with regard to our membership numbers. As the graph below demonstrates, it is concerning and needs to be addressed by our section.

HBO Section Membership

Data from the past 6 3\4 years demonstrates a peak membership of 171 and a subsequent decline to 116. Why the decrease in membership? While I understand that the hyperbaric community is small (and smaller if only ACEP members are included), I do not believe that our community is becoming smaller. I am constantly hearing of ED groups looking into starting HBO/wound care centers. Then why are people leaving our membership? Is the section not providing interesting and useful information? Are there other sections that ACEP members are joining at the expense of the Hyperbaric Section? Maybe my initial hypothesis is wrong and we indeed have fewer ACEP members interested in hyperbaric medicine. Kevin R. Hardy, MD, immediate past-chair of the section, put forth efforts at increasing our section numbers last year but his hard work unfortunately did not translate into increased membership. But the momentum he generated must continue. We need to maintain a minimum of 100 members to assure representation on the ACEP Council floor. Thus, I think a major effort from our section should be geared at maintaining section members and recruiting new section members. Obviously, the first step is to reach out to existing ACEP section members and ask for their opinions on how we can make the section more useful to them. At the same time I think we should be asking our members to share their ideas on recruitment. In my opinion, the section should continue publishing high quality newsletters, perhaps increasing the number from bi-yearly to quarterly. Enlisting material from the Undersea & Hyperbaric Medical Society (UHMS) and the American College of Hyperbaric Medicine (ACHM) may help provide a more robust newsletter. Suggestions to ACEP to have hyperbaric–related lectures as part of Scientific Assembly from experts within our discipline may be helpful. It appears that HBO in CO poisoning is the "hot" topic right now so maybe a debate at Scientific Assembly may be an attractive way to gain exposure for the field and for our section. I personally find the use of our section e-list very useful and engaging. Perhaps more use of the section e-list for promoting interesting discussion would be beneficial. I am asking all section members to try and recruit one colleague to our section. I know it sounds goofy but it may work. I will try (am going) to convince one faculty member from my institution to join our section before this newsletter arrives at your door. Any advice from our membership to help with our section numbers is tremendously appreciated.

Here is an update regarding our discussion on the CO clinical policy that ACEP is trying to write/approve. We were able to hold off an initial vote by the Board because of our great concerns about the wording of the clinical policy as it relates to HBO and CO. The next Board meeting will occur in mid-April to discuss the policy. Our section’s concerns, nicely summarized by Christopher J. Logue, MD, speaks to ACEP’s interpretation and grading of both Scheinkestel’s and Weaver’s studies addressing the effect of HBO on persistent and delayed neurologic sequelae. I will keep you informed of the Board’s decision when it is finalized. I think that we will have an opportunity for an editorial with the published clinical policy if we are still unhappy with the content.

I hope you enjoy the newsletter and if I can be of any assistance to section members, please do not hesitate to contact me. I look forward to hearing your comments and suggestions on ways to improve membership numbers and on ways to improve our section to meet your needs.





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Non-traditional Indications for HBOT

Robert L. Sherwin, MD

Reimbursable diagnoses for hyperbaric oxygen therapy (HBOT) vary between payers. Thorough reviews are available for these, however it is important not to dismiss indications that have less support or are considered experimental at this time. There exist a number of conditions for which some literature or at least case reports are available in the literature (Figure 1).

In this edition of the section newsletter, it was our goal to review a few of the many potential indications for which there is some body of evidence supporting its use. The topics selected below are viral diseases, acute myocardial infarction (AMI), acute stroke and sepsis. Though these are certainly the tip of the iceberg for an intervention once referred to as "a therapy in search of diseases," it represents a taste of possible future directions of hyperbaric medicine.

Following are four potential indications:

  • Hyperbaric Medicine and Viral Diseases
  • Hyperbaric Oxygen and Acute Myocardial Infarction
  • Hyperbaric Oxygen in Acute Ischemic Stroke
  • Treating Sepsis with Hyperbaric Oxygen
Non-traditional Indications for HBO (Abridged)
Acute myocardial infarction Brown recluse spider bites
Cerebral edema Cerebral palsy
Encephalitis & viral infections Headaches (ie, cluster, migraine)
Human immunodeficiency virus (HIV) Lyme disease
Lymphadema Malignant otitis externa
Multiple sclerosis Ophthalmologic conditions
Rheumatoid arthritis Sepsis
Sickle cell disease Soft tissue injury
Spinal cord injury Stroke
Thermal burns Tinnitus
Traumatic brain injury Venous stasis ulcers

Figure 1: Non-traditional indications for HBO, abridged

Hyperbaric Medicine and Viral Diseases

Stephen D. Gutherie, MD

The quest for an effective use of hyperbaric exposures in the treatment of viral diseases has been engendered by striking, albeit anecdotal, case reports.1,2 Investigators have been emboldened by basic science studies clearly indicating that lethal antiviral effects can occur when ambient pressures are increased and inhaled gas mixtures are altered.3,4 This brief review offers a few tantalizing examples of those anecdotes and summary statements identifying loci within the viral illness paradigm with demonstrable vulnerability to such interdictions.

Several elements of viral pathogenesis must be eliminated from this discussion as they rightly deserve their own examination. Subjects not addressed include the entire inflammatory cascade and the subject of hyperbaric exposure therapy in the reparative processes that follow the disease. Further, no distinction is made between the potential effects of hyperbaric exposures in acute viral illnesses or those in chronic infections. Mention is made of the distinct points within the viral pathological pathway where environmental manipulations imposed on the host could disrupt the morbid and mortal consequences the virus inflicts.

Chronologically, and geographically, the first site of our attack should be the first site of the viruses’ attack, the cell membrane. The fusion, or entry, of inhibitors is a distinct class of antiviral drugs designed to block entry of the virus through membranes, cellular, nuclear or mitochondrial.5 Perturbations of membranes, or disruption of receptor sites, have long been studied by anesthesiologists examining the mode of action of those agents.6 Membrane effects evoked by inert gases under hyperbaric conditions are referred to as "nitrogen membrane anesthetic effects." This membrane effect was speculated to be the antiviral locus through which hyperbaric chamber exposures had their positive effect in murine leukemia viral infections.7 This work led directly to the current Phase-IIA clinical trial in HIV/AIDS patients.8

Once past any membrane barriers, the viral genetic material is incorporated into the host’s DNA, commandeering that machinery to replicate, encapsulate and release a new generation of viruses. This multifaceted portion of viral pathogenesis is regulated by the viral infectivity factor (Viƒ) protein9 and potentially may be suppressed by the "silencing" ribonucleic acid interference (RNAi) systems.10 Several delicate steps in these intricate processes are sensitive to the oxidation/reduction reaction (redox) balance of the host cell.11 High levels of reactive oxygen species (ROS) develop following hyperbaric exposures rich in O2.11 Enveloped viruses are particularly ROS sensitive and the virucidal effects of HBO2 exposures likely explain the laudable effects seen in Hepatitis C infections12 and in influenza encephalitis.13

Restraining rapid viral mutation and augmenting innate immune capacity may be further positive consequences of manipulating the host’s ambient surroundings. These facets of viral pathogenesis are also susceptible to changes in redox balance. Nitrous oxide-induced oxidative stress accelerates mutation in herpes simplex virus (HSV) infected animal models.14 Further, several elements of the human immune armamentarium are increased following long-term, saturation diving exposures.15

A single example of dramatic clinical improvement in a severe viral infection following hyperbaric treatment ought to be enough to provoke intense investigation into this modality’s therapeutic potential. Medical literature is replete with such clinical examples and soon will be replete with reports of the resultant careful clinical studies.

Hyperbaric Oxygen and Acute Myocardial Infarction

Sorabh Khandelwal, MD
Ohio State University

HBOT for acute coronary syndrome (ACS) was first reported in a canine experiment model in 195816 and in a human subject in 1964.17 The theoretical arguments for HBO in the setting of ACS are improvement of hypoxia in marginally perfused tissue and modulation of tissue repair, specifically through increased expression of antioxidant enzymes, reduction of lipid peroxidation, and modification of ischemia-reperfusion injury.

The role of hyperbaric oxygen therapy in myocardial infarction is unsettled. Although several uncontrolled studies demonstrating positive results have been published, there have been only five randomized controlled trials (RCTs) dealing with this area.

Thurston18 in 1973 enrolled 221 patients and although there was a trend towards lower mortality, it was not statistically significant. Thurston did demonstrate a statistically significant reduction in significant dysrhythmias. Swift19 in 1992 enrolled 34 subjects with the purpose of looking at HBOT in AMI patients to identify myocardial segments capable of functional improvement. Swift demonstrated a non-significant improvement of left ventricular (LV) function in those receiving HBOT. The HOT MI trial20 published in 1998 demonstrated a statistically significant reduction in "time to pain resolution" with the HBOT arm but statistically non-significant effects (but favorable trending) for CPK levels, EFs and mortality. Sharifi21 in 2004 demonstrated a significant benefit of hyperbaric oxygen when added to percutaneous coronary intervention in reducing clinical re-stenosis.

The Cochrane Database of Systematic Reviews (which includes the 4 aforementioned RCTs) states the following in their conclusions: "[HBO] may reduce the time to pain relief and the chance of adverse heart events in people with heart attack and unstable angina, but it is not clear if the risk of dying is reduced…"22

The most recent randomized control trial involves a group of authors from Yugoslavia who demonstrated a favorable effect of HBOT after thrombolysis on LV systolic function and the remodeling process23 but at the same time demonstrated no effect on LV diastolic filling.24

As an interesting aside, there is some promising literature on the use of hyperbaric oxygen after cardiopulmonary bypass. In a study by Alex et al, pretreatment with hyperbaric oxygen reduced neuropsychometric dysfunction and also modulated the inflammatory response after cardiopulmonary bypass.25

Thus, hyperbaric oxygen therapy may indeed have an important role in acute MI but further research needs to be performed. I see the glass as half full rather than half empty.

Hyperbaric Oxygen in Acute Ischemic Stroke

Grant Orthmeyer, MD
Robert L. Sherwin, MD
Wayne State University

Stroke is the third leading cause of death and leading cause of disability in the US.26 As of yet there are few effective primary or adjunctive treatments. There have been numerous studies of the use of HBOT in both animals and humans in acute ischemic stroke27, yet no consensus on its efficacy.

The mechanism of cerebral injury is thought to be a result of an ischemic cascade of events that resulting in a reversible ischemic penumbra. The initial ischemic insult leads to depolarization and neuron failure with an influx of calcium. This initiates the release of multiple neurotransmitters that depolarize surrounding neurons which ultimately generates free radicals, arachidonic acid and nitric oxide (NO) and further neuronal damage. This process evolves into a production of various cytokines causing inflammation and microcirculatory compromise. Proponents believe that HBOT may mitigate this ischemic cascade possibly providing a neuroprotective benefit while giving time for primary intervention (thrombolysis).

The original rational for HBO in ischemic stroke was to provide increased levels of oxygen to hypoxic tissue, but it now appears that HBOT has a more indirect neuroprotective effect. In animal models it seems that HBO decreases neuronal shrinkage, edema, damage and apoptosis. It is believed that this is a result of decreased inflammation and excitotoxicity. Animal models have also shown a neuroprotective benefit when used within 4-6 hours of ischemic event with earlier intervention being of greater benefit. Treatment after 6 hours, however, generally showed no benefit and possible harm when compared to controls. Optimum HBO pressure seems to be around 2.5 atm. Human studies have shown less clear benefit than animal models.

In the last 40 years, hundreds of stroke patients have been treated in clinical trials. Earlier trials which showed some benefit were generally poorly controlled and executed. Three of the most recent studies have been double blinded, randomized, controlled trials. Anderson et al randomized 39 patients within 2 weeks of cerebral infarction to multiple treatments of either HBO at 1.5 atmosphere absolute (ATA) or hyperbaric air at similar pressure.28 At 4 months, no significant difference was seen on a graded neurologic exam and the trial was stopped early. Nighoghossian et al treated 34 patients presenting within 24 h of onset with multiple treatments at 1.5 ATA or sham treatment.29 There was no difference in the mean Rankin scores at 1 year, whereas the Orgogozo and Trouillas outcome scores were significantly higher in the treatment group. The most recent trial by Rusyniak et al randomized 33 patients presenting in less than 24 h to one treatment of HBO at 2.5 ATA or a sham of 100% O2 at 1.14 ATA.30 Analysis at 3 months showed a better outcome in the control group on the National Institutes of Health Stroke Scale (NIHSS) and Rankin scales, suggesting a potentially harmful effect of HBO, but intention-to-treat analysis showed no statistical difference between the groups.

The results of recent controlled studies showed little benefit from HBO in the context of acute ischemic stroke. However, as of yet, there has not been an adequately powered study of the efficacy of HBO in acute ischemic stroke. It seems fairly clear based on animal models that if any benefit is to be derived from HBO therapy it must be initiated shortly after onset of symptoms, ideally less than 3 hours. Recent studies have been unable to initiate intervention within that time period. It is also unclear whether HBO may be a beneficial adjunct in patients receiving thrombolysis. While there is limited evidence at this time to support the use of HBO for ischemic stroke, further investigation in this area is warranted and should be guided by lessons learned from animal models.

Treating Sepsis with Hyperbaric Oxygen

Robert L. Sherwin, MD

The pathophysiology of sepsis includes hypovolemia, vasodilation, myocardial suppression, a profound inflammatory response, endothelial dysfunction and coagulation/complement defects which all contribute to the development of multiorgan dysfunction. The treatment of infection and sepsis with hyperbaric oxygen is far from new, however. The adverse effect of prolonged hyperbaric oxygen exposure to organisms was initially reported by Paul Bert himself in 1878.31 A number of scientific reports are available from as early as the 1960’s concerning the benefits of HBOT in infection32-33

The antibiotic effect of HBOT has been widely described. G.H. Bornside reported in 1967 that HBOT at 3.0 significantly lowered the minimum inhibitory concentration (MIC) of several antibiotics. HBOT is completely bactericidal against certain bacteria and bacteriostatic to others.34,35 Multiple authors have reported significantly decreased bacterial dissemination following HBOT,36,37 yet the mechanism by which this occurs is yet undescribed. In humans, both the respiratory burst as well as phagocytic killing are enhanced through the application of HBOT.38

The immune effects of HBOT include cytokine modulation, signal transduction and anti-oxidant augmentation.39,40 Tumor necrosis factor alpha (TNF-a), nitrous oxide (NO) and interleukin-10 all have described roles in sepsis. Loungo et al showed in a rat model that TNF-a, and NO release were inhibited by HBOT therapy.41 Recently, Buras et al, using a murine cecal ligation and puncture (CLP) model, demonstrated improved 4 day survival following BID treatment at 2.5 ATA.36 The study by Buras et al further added to the general understanding of HBOT mediation of sepsis by showing that any mortality benefit of HBOT was limited to interleukin 10 (IL-10) +/+ animal strains and were absent in IL-10 -/- strains. This confirms previous data which strongly suggests an integral role of IL-10, an anti-inflammatory cytokine, in the positive effect of HBOT in sepsis.

Results from multiple different animal models support both a mortality benefit and a therapeutic window for HBOT use in sepsis. Thom et al reported a 100% mortality versus 8% in rats with fecal implantation for control and HBOT arms respectively (p<0.005).42 In a second model using polymicrobial injection, the same authors further reported that HBOT decreased the mortality from 79% to 23% (p< 0.005). In zymogan-shocked animals, Loungo et al reported that HBOT prevented all mortality.41 Holt et al using mice and a CLP and a dose finding protocol corroborated the notion of a therapeutic window for HBOT in sepsis.37 Though normobaric oxygen showed no improvement, only 65% of those mice treated at 2.5 ATA died compared to 79% of the control (p = 0.0003) and 100% treated at 3 ATA. Oter et al reported improved mortality with decreased bacterial loads in a CLP-rat model of sepsis treated at 2.5 ATA for 90 minutes BID compared to normobaric oxygen. The mortality dramatically worsened at 3 ATA versus 2.5 ATA, however. Interestingly, Buras et al also reported that no animal treated in the 3 ATA arm survived past 36 hours further corroborating a therapeutic window for HBOT in sepsis.36 A possible explanation was put forth by Oter et al who reported an increase in thiobarbituric acid (a marker of lipid peroxidation) dramatically increases in the lung and brain at 3.0 ATA.43

Though multiple well-established animal models of sepsis exist, they are not fully representative of the evolution or treatment of sepsis in humans. In conclusion, despite remaining questions concerning HBOT use in sepsis, a body of evidence is available supporting its value and safety which should not deter the pursuit of clinical trials in the near future.

The Future (…of Hyperbarics and the HBO Newsletter!)

Robert L. Sherwin, MD

Observed challenges to the indications discussed above include rising healthcare costs and the relative limited availability of HBOT. The astute reader may recognize symmetry between some of the selected indications and the current emphasis of federal research funding which focuses on neurologic and cardiovascular emergencies. Furthermore, a multidisciplinary (including hyperbaricists, neurologists, cardiologists and others) and multi-center approach will likely be mandatory to succeed in these endeavors.

I certainly appreciate the support and latitude conveyed to me in putting out this newsletter.  Traditional sections, such as Journal Watch, will be reinstituted in the next volume. In assuming this charge, my goal was to add significant and unique value for our constituents regarding the potential and future of hyperbaric medicine. I hope the information provided was as educational to read as it was to assemble. We have reviewed four topics in this newsletter and future editions will include a separate section committed to non-traditional indications such as these. Thank you, good diving.


  1. Choi J, Forman HJ, Ou JH, Lai MM, Seronello S, Nandipati A. Redox modulation of the hepatitis C virus replication complex is calcium dependent. Free Radic Biol Med. Nov 1 2006;41(9):1488-1498.
  2. Lui W, Zhau W, Li X, Zheng X, et al. Clinical Pathological Study of Treatment of Chronic Hepatitis with Hyperbaric Oxygen. Chin Med J. 2002;115(8):1153-1157.
  3. Ngondi JL, Oben J, Forkah DM, Etame LH, Mbanya D. The effect of different combination therapies on oxidative stress markers in HIV infected patients in cameroon. AIDS Res Ther. 2006;3:19.
  4. Choi J, Lee KJ, Zheng Y, Yamaga AK, Lai MM, Ou JH. Reactive oxygen species suppress hepatitis C virus RNA replication in human hepatoma cells. Hepatol. Jan 2004;39(1):81-89.
  5. Moore JP, Doms RW. The entry of entry inhibitors: a fusion of science and medicine. Proc Natl Acad Sci U S A. Sep 16 2003;100(19):10598-10602.
  6. Tu K, Tarek M, Klein ML, Scharf D. Effects of anesthetics on the structure of a phospholipid bilayer: molecular dynamics investigation of halothane in the hydrated liquid crystal phase of dipalmitoylphosphatidylcholine. Biophys J. Nov 1998;75(5):2123-2134.
  7. Pollock N, Harris M. Effect of Hyperbaric Exposures in a Murine Leukemia Virus Model. Undersea and Hyperbaric Medicine. 2002 (Abstract);22(5):136.
  8. Gutherie SD. Effect of Repeated Exposure to Compressed Air on Patients with AIDS. 2005;FDA No. Q050021.
  9. Harris RS, Bishop KN, Sheehy AM, et al. DNA deamination mediates innate immunity to retroviral infection. Cell. Jun 13 2003;113(6):803-809.
  10. Bagasra O. RNAi as an antiviral therapy. Expert Opin Biol Ther. Nov 2005;5(11):1463-1474.
  11. Baugh MA. HIV: reactive oxygen species, enveloped viruses and hyperbaric oxygen. Med Hypotheses. Sep 2000;55(3):232-238.
  12. Choi J, Wen L, Ou J-H, Pandalai SG. Structure and Function of Hepatitis C Virus Core Protein. Recent Research Dev Virol. 2001;3(1):105-120.
  13. Dohgomori H, Arikawa K, Kanmura Y. Hyperbaric oxygen therapy (HBOT) in a child with suspected influenza-associated encephalopathy. Can J Anaesth. Feb 2003;50(2):204.
  14. Akaike T, Maeda H. Nitric oxide and virus infection. Immunol. Nov 2000;101(3):300-308.
  15. Brenner I, Shephard RJ, Shek PN. Immune function in hyperbaric environments, diving, and decompression. Undersea Hyperb Med. Spring 1999;26(1):27-39.
  16. Smith G, Lawson D. Experimental coronary arterial occlusion: effects of administration of oxygen under pressure. Scott Med J. 1958;3:346-350.
  17. Moon AJ, Williams KG, Hopkinson WI. A Patient with Coronary Thrombosis Treated with Hyperbaric Oxygen. Lancet. Jan 4 1964;18:18-20.
  18. Thurston JG, Greenwood TW, Bending MR, Connor H, Curwen MP. A controlled investigation into the effects of hyperbaric oxygen on mortality following acute myocardial infarction. Q J Med. Oct 1973;42(168):751-770.
  19. Swift PC, Turner JH, Oxer HF, O'Shea JP, Lane GK, Woollard KV. Myocardial hibernation identified by hyperbaric oxygen treatment and echocardiography in postinfarction patients: comparison with exercise thallium scintigraphy. Am Heart J. Nov 1992;124(5):1151-1158.
  20. Stavitsky Y, Shandling AH, Ellestad MH, et al. Hyperbaric oxygen and thrombolysis in myocardial infarction: the 'HOT MI' randomized multicenter study. Cardiol. Oct 1998;90(2):131-136.
  21. Sharifi M, Fares W, Abdel-Karim I, Koch JM, Sopko J, Adler D. Usefulness of hyperbaric oxygen therapy to inhibit restenosis after percutaneous coronary intervention for acute myocardial infarction or unstable angina pectoris. Am J Cardiol. Jun 15 2004;93(12):1533-1535.
  22. Bennett M, Jepson N, Lehm J. Hyperbaric oxygen therapy for acute coronary syndrome. Cochrane Database Syst Rev. 2005(2):CD004818.
  23. Dekleva M, Neskovic A, Vlahovic A, Putnikovic B, Beleslin B, Ostojic M. Adjunctive effect of hyperbaric oxygen treatment after thrombolysis on left ventricular function in patients with acute myocardial infarction. Am Heart J. Oct 2004;148(4):E14.
  24. Vlahovic A, Neskovic AN, Dekleva M, et al. Hyperbaric oxygen treatment does not affect left ventricular chamber stiffness after myocardial infarction treated with thrombolysis. Am Heart J. Jul 2004;148(1):e1.
  25. Alex J, Laden G, Cale AR, et al. Pretreatment with hyperbaric oxygen and its effect on neuropsychometric dysfunction and systemic inflammatory response after cardiopulmonary bypass: a prospective randomized double-blind trial. J Thorac Cardiovasc Surg. Dec 2005;130(6):1623-1630.
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  28. Anderson DC, Bottini AG, Jagiella WM, et al. A pilot study of hyperbaric oxygen in the treatment of human stroke. Stroke. Sep 1991;22(9):1137-1142.
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  30. Rusyniak DE, Kirk MA, May JD, et al. Hyperbaric oxygen therapy in acute ischemic stroke: results of the Hyperbaric Oxygen in Acute Ischemic Stroke Trial Pilot Study. Stroke. Feb 2003;34(2):571-574.
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  33. Ross RM, McAllister TA. Protective Action of Hyperbaric Oxygen in Mice with Pneumococcal Septicaemia. Lancet. Mar 13 1965;191:579-581.
  34. Hill GB, Osterhout S. Experimental effects of hyperbaric oxgen on selected clostridial species. I. In-vitro studies. J Infect Dis. Jan 1972;125(1):17-25.
  35. Muhvich KH, Park MK, Myers RA, Marzella L. Hyperoxia and the antimicrobial susceptibility of Escherichia coli and Pseudomonas aeruginosa. Antimicrob Agents Chemother. Sep 1989;33(9):1526-1530
  36. Buras JA, Holt D, Orlow D, Belikoff B, Pavlides S, Reenstra WR. Hyperbaric oxygen protects from sepsis mortality via an interleukin-10-dependent mechanism. Crit Care Med. Oct 2006;34(10):2624-2629.
  37. Holt D, Pavlides S, Orlow D, Belikoff B, Reenstra W, Buras J. Hyperbaric Oxygen Protects from Sepsis Mortality and Reduces Splenic Bacterial Load (Abstract). Acad Emerg Med. 2005;12(5 Supp 1):63-64.
  38. Labrouche S, Javorschi S, Leroy D, Gbikpi-Benissan G, Freyburger G. Influence of hyperbaric oxygen on leukocyte functions and haemostasis in normal volunteer divers. Thromb Res. Nov 15 1999;96(4):309-315.
  39. Davidson JD, Mustoe TA. Oxygen in wound healing: more than a nutrient. Wound Repair Regen. May-Jun 2001;9(3):175-177.
  40. Buras J. Basic mechanisms of hyperbaric oxygen in the treatment of ischemia-reperfusion injury. Int Anesthesiol Clin. Winter 2000;38(1):91-109.
  41. Luongo C, Imperatore F, Cuzzocrea S, et al. Effects of hyperbaric oxygen exposure on a zymosan-induced shock model. Crit Care Med. Dec 1998;26(12):1972-1976.
  42. Thom SR, Lauermann MW, Hart GB. Intermittent hyperbaric oxygen therapy for reduction of mortality in experimental polymicrobial sepsis. J Infect Dis. Sep 1986;154(3):504-510.
  43. Oter S, Korkmaz A, Topal T, et al. Correlation between hyperbaric oxygen exposure pressures and oxidative parameters in rat lung, brain, and erythrocytes. Clin Biochem. Aug 2005;38(8):706-711.




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This publication is designed to promote communication among emergency physicians of a basic informational nature only. While ACEP provides the support necessary for these newsletters to be produced, the content is provided by volunteers and is in no way an official ACEP communication. ACEP makes no representations as to the content of this newsletter and does not necessarily endorse the specific content or positions contained therein. ACEP does not purport to provide medical, legal, business, or any other professional guidance in this publication. If expert assistance is needed, the services of a competent professional should be sought. ACEP expressly disclaims all liability in respect to the content, positions, or actions taken or not taken based on any or all the contents of this newsletter.

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