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Twenty-nine patients with necrotizing fasciitis were treated from 1980 to 1988. This study evaluates how the addition of hyperbaric oxygen (HBO) therapy to surgical treatment has affected mortality and the number of debridements required to achieve wound control in these patients. Two groups of patients were viewed: group 1 (n = 12) received surgical debridement and antibiotics only; group 2 (n = 17) received HBO (90 minutes at 2.5 atm, average 7.4 treatments) in addition to surgery and antibiotics. Both groups were similar in age, race, sex, wound bacteriology, and antimicrobial therapy. Body surface area affected was similar, however, perineal involvement was more common in group 2 (53%) than in group 1 (12%). The admitting conditions of patients in group 1 (non-HBO) were diabetic, 33%; white blood cell count more than 12,000, 50%; and shock, 8%. The admitting conditions of patients in group 2 (HBO) were diabetic, 47%; white blood cell count more than 12,000, 59%; and shock, 29%. Although group 2 patients receiving HBO were more seriously ill on admission, mortality was significantly lower (23%) compared to group 1 (66%) (p less than 0.02). In addition, only 1.2 debridements per group 2 patient were required to achieve wound control versus 3.3 debridements per group 1 patient (p less than 0.03). The addition of HBO therapy to the surgical and antimicrobial treatment of necrotizing fasciitis significantly reduced mortality and wound morbidity (number of debridements) in this study, especially among nonclostridial infections. We conclude that HBO should be used routinely in the treatment of necrotizing fasciitis.

BACKGROUND: Despite ongoing controversy, hyperbaric oxygen (HBO) therapy is frequently administered in various clinical situations. Probably because of the unique atmospheric conditions to which the patient is exposed, there are concerns about the safety aspects of this therapy. Possible complications during HBO therapy include barotraumatic lesions (middle ear, nasal sinuses, inner ear, lung, teeth), oxygen toxicity (central nervous system, lung), confinement anxiety, and ocular effects (myopia, cataract growth). METHODS: To analyze the medical safety of HBO therapy, this report reviewed complications and side effects of 782 patients treated for various indications with a total of 11,376 HBO therapy sessions within a multiplace chamber. The absolute treatment pressure was 240 or 250 kPa 114 or 15 msw). The compression was performed in a linear manner with 14 to 15 kPa (1.4 to 1.5 msw) x min(-1). All data were gathered prospectively within a special database. RESULTS: More than 17% of all patients experienced ear pain or discomfort as an expression of problems in equalizing the middle ear pressure. Most episodes were not related to a persistent eustachian tube dysfunction since they only occurred once. Barotraumatic lesions on visual otological examinations (ear microscopy) were verified in 3.8% of all patients. Patients with sensory deficits involving the ear region need special attention, because they seem to be at risk for rupture of the tympanic membrane (three cases documented). A barotrauma of the nasal sinuses occurred rarely and no barotraumatic lesions of the inner ear, lung, or teeth were noted. Oxygen toxicity of the CNS manifested by generalized seizures affected four patients without any recognizable risk factors or prodromes. None of the patients suffered recurrences or sequelae. Regular checks of the blood glucose in diabetics failed to reveal episodes of hypoglycemia as a cause for seizures. Lung function tests of patients undergoing prolonged treatment (average 52.8 sessions) did not deteriorate. CONCLUSION: Patients scheduled for HBO therapy need a careful pre-examination and monitoring. If safety guidelines are strictly followed, HBO therapy is a modality with an acceptable rate of complications. The predominant complication is represented by pressure equalization problems within the middle ear. Serious complications rarely occur.

Hyperbaric oxygen therapy (HBO) is increasingly used in a number of areas of medical practice. It is a unique intervention whose method of action is not well understood. Clinicians may request its use for their patients, but often will not fully understand its mechanisms. It is hoped that this review and discussion of HBO and the literature surrounding its use may be useful to clinicians who are unsure whether their patients will benefit from this exciting intervention. Hyperbaric oxygen therapy is defined by the Undersea and Hyperbaric Medical Society (UHMS) as a treatment in which a patient intermittently breathes 100% oxygen while the treatment chamber is pressurized to a pressure greater than sea level (1 atmosphere absolute, ATA).1 The pressure increase must be systemic, and may be applied in monoplace (single person) or multiplace chambers. Multiplace chambers are pressurized with air, with oxygen given via face-mask, hood tent or endotracheal tube; while monoplace chambers are pressurized with oxygen. We began by obtaining the most recent UHMS committee report,1 and performed Medline searches (1966 to present), with the search terms ‘hyperbaric’ and ‘oxygen’, combining this basic search with searches for each of the thirteen indications recommended by the UHMS. Using information from these papers, and the resulting references, this paper outlines the history, physiology, current indications for and effects of hyperbaric oxygen therapy. Hyperbaric therapy was first documented in 1662, when Henshaw built the first hyperbaric chamber, or ‘domicilium’.2 Since this time, reports of beneficial effects from increased pressure have increased, and by 1877, chambers were used widely for many conditions, though there was little scientific rationale or evidence. In 1879, the surgical application of hyperbaric therapy in prolonging safe anaesthesia was realized and explored.3 In 1927, Cunningham4 reported improvement in circulatory disorders at sea level … Address correspondence to Dr C.N.A. Bell, Division of Oral & Maxillo-Facial Surgery, Bristol Dental Hospital, Lower Maudlin Street, Bristol BS1 2LY. e-mail: chris.bell{at}bristol.ac.uk

The morphologic events in the microcirculation that lead to reperfusion injury of ischemic skeletal muscle remain incompletely understood. The purpose of this experiment was to evaluate leukocyte endothelial adherence characteristics and dynamic changes in microvessel caliber during reperfusion of an in vivo skeletal muscle ischemia preparation. In addition, the effect of hyperbaric oxygen treatment on these microcirculatory changes also was studied. An intravital microscopy preparation of a transilluminated gracilis muscle in 27 rats was used to observe a total of 101 arterioles and 63 venules (13 to 73 microns diameter). Baseline hemodynamics were videotaped for 30 minutes following muscle isolation. The animals were divided into six groups: (1) sham, no ischemia, (2) 4 hours of global ischemia only, (3) no ischemia plus hyperbaric oxygen (one 2.5 ATA/1 hour of treatment with 100% oxygen), (4) 4 hours of ischemia plus hyperbaric oxygen during ischemia, (5) 4 hours of ischemia plus hyperbaric oxygen immediately on reperfusion, and (6) 4 hours of ischemia plus hyperbaric oxygen 1 hour after reperfusion. Changes in arteriolar and venular diameters at specific times during 3 hours of reperfusion were recorded, and the number of adherent and slow-rolling leukocytes in 100-microns venular segments were counted and compared with baseline measurements. The proximity of arterioles to venules was classified as adjacent (< 15 microns) or distant (> 15 microns). No significant changes in leukocyte endothelial adherence or arteriolar diameter were noted in group 1 sham or group 3 nonischemic hyperbaric oxygen-treated rats when compared with baseline measurements. A significant increase in adherent leukocytes was observed in group 2 ischemic venules (+14.9 +/- 2.5) within 5 minutes of reperfusion, which was maintained for 3 hours. Reperfusion measurements of arteriolar diameter in group 2 ischemic muscle preparations demonstrated an initial vasodilation that was followed at 1 hour by a progressive and severe vasoconstriction (-46.9 +/- 11.3 percent at 3 hours) in arterioles adjacent to venules that was not seen in distant arterioles. The increase in adherent leukocytes seen in group 2 ischemic venules was significantly reduced by hyperbaric oxygen treatment given during ischemia (group 4) or up to 1 hour during reperfusion (groups 5 and 6). In addition, the progressive ischemic arteriolar vasoconstriction was inhibited in all groups (4, 5, and 6) treated with hyperbaric oxygen.(ABSTRACT TRUNCATED AT 400 WORDS)

Over the past 40 years hyperbaric oxygen therapy has been recommended and used in a wide variety of medical conditions, often without adequate scientific validation of efficacy or safety. Consequently a high degree of medical scepticism has developed regarding its use. The Undersea and Hyperbaric Medical Society approves use of hyperbaric oxygen for a few conditions for which there is thought to be reasonable scientific evidence or well validated clinical experience. In these conditions early referral is essential. #### Therapeutic uses of hyperbaric oxygen ##### Strong scientific evidence ##### Suggestive scientific evidence Hyperbaric oxygen has been shown ineffective in diseases such as multiple sclerosis and dementia, but it continues to be used despite the risks of the treatment. For conditions where its use remains unproved—for example, rheumatoid arthritis, cirrhosis, and gastroduodenal ulcer—hyperbaric oxygen should be used only in the context of well controlled clinical trials. At sea level the plasma oxygen concentration is 3 ml/l. Tissues at rest require about 60 ml of oxygen per litre of blood flow (assuming normal perfusion) to maintain normal cellular metabolism, although requirements vary between tissues. At a pressure of 3 atmospheres (304 kPa) dissolved oxygen approaches 60 ml/l of plasma, which is almost sufficient to supply the resting total oxygen requirement of many tissues without a contribution from oxygen bound to haemoglobin. This has advantages in situations such as carbon monoxide poisoning or in severe anaemia where difficult crossmatching or religious belief prevents blood transfusion. #### Cellular and biochemical benefits of hyperbaric oxygen

The therapy of rhinocerebral mucormycosis includes aggressive surgical debridement, administration of high-dose amphotericin B, and control of underlying predisposing conditions, especially diabetes and immunosuppression or immunodeficiency. Hyperbaric oxygen suppresses fungal growth in vitro and has theoretical value in treating mucormycosis because it reduces the tissue hypoxia and acidosis that accompany vascular invasion by the fungus. In a retrospective review of patients at Duke University Medical Center with rhinocerebral mucormycosis, six patients were treated with hyperbaric oxygen and seven cases (involving six patients) were treated without hyperbaric oxygen. All patients received surgical debridement and amphotericin B. Two of six patients receiving hyperbaric oxygen therapy died, and four of seven patients not receiving hyperbaric oxygen therapy died. Adverse effects from hyperbaric oxygen were minimal. Because mucormycosis occurs infrequently, this retrospective review involved a small number of patients. Despite this limitation, adjunctive hyperbaric oxygen appears to be a promising clinical modality for the treatment of rhinocerebral mucormycosis and warrants further investigation.

PURPOSE: We review the use of hyperbaric oxygen therapy in urology, and present the mechanisms of hyperoxia action in whole body hyperbaric chamber treatments, patient outcomes and patient selection criteria. MATERIALS AND METHODS: The literature on hyperbaric oxygen use in urology was reviewed. RESULTS: Hyperbaric oxygen is a treatment alternative for patients with an underlying ischemic process unresponsive to conventional therapy. Specific factors which may influence patient selection of hyperbaric oxygen include cancer and absolute contraindications of active viral disease, intercurrent pneumothorax and treatment with doxorubicin or cisplatin. This technique is particularly useful in the treatment of intractable hemorrhagic cystitis secondary to pelvic radiation therapy. Further investigation of the efficacy of hyperbaric oxygen is warranted for patients with necrotizing fasciitis (Fournier's gangrene), posttraumatic ischemic injury and/or impaired wound healing. CONCLUSIONS: Hyperbaric oxygen is a therapeutic alternative which complements the surgical and medical options for select patients.

Hyperbaric oxygen — 100 percent oxygen at two to three times the atmospheric pressure at sea level — can result in arterial oxygen tension in excess of 2000 mm Hg1 and oxygen tension in tissue of almost 400 mm Hg.2,3 Such doses of oxygen have a number of beneficial biochemical, cellular, and physiologic effects, and today there are 259 hyperbaric facilities in the United States with 344 single-occupant (“monoplace”) hyperbaric-oxygen chambers.4 In this article, we review the mechanisms of action, evidence of clinical efficacy, and risks of therapy with hyperbaric oxygen.Physiologic EffectsFor hyperbaric oxygen, pressure is expressed . . .

BACKGROUND: Patients with acute carbon monoxide poisoning commonly have cognitive sequelae. We conducted a double-blind, randomized trial to evaluate the effect of hyperbaric-oxygen treatment on such cognitive sequelae. METHODS: We randomly assigned patients with symptomatic acute carbon monoxide poisoning in equal proportions to three chamber sessions within a 24-hour period, consisting of either three hyperbaric-oxygen treatments or one normobaric-oxygen treatment plus two sessions of exposure to normobaric room air. Oxygen treatments were administered from a high-flow reservoir through a face mask that prevented rebreathing or by endotracheal tube. Neuropsychological tests were administered immediately after chamber sessions 1 and 3, and 2 weeks, 6 weeks, 6 months, and 12 months after enrollment. The primary outcome was cognitive sequelae six weeks after carbon monoxide poisoning. RESULTS: The trial was stopped after the third of four scheduled interim analyses, at which point there were 76 patients in each group. Cognitive sequelae at six weeks were less frequent in the hyperbaric-oxygen group (19 of 76 [25.0 percent]) than in the normobaric-oxygen group (35 of 76 [46.1 percent], P=0.007), even after adjustment for cerebellar dysfunction and for stratification variables (adjusted odds ratio, 0.45 [95 percent confidence interval, 0.22 to 0.92]; P=0.03). The presence of cerebellar dysfunction before treatment was associated with the occurrence of cognitive sequelae (odds ratio, 5.71 [95 percent confidence interval, 1.69 to 19.31]; P=0.005) and was more frequent in the normobaric-oxygen group (15 percent vs. 4 percent, P=0.03). Cognitive sequelae were less frequent in the hyperbaric-oxygen group at 12 months, according to the intention-to-treat analysis (P=0.04). CONCLUSIONS: Three hyperbaric-oxygen treatments within a 24-hour period appeared to reduce the risk of cognitive sequelae 6 weeks and 12 months after acute carbon monoxide poisoning.

OBJECTIVE: To assess neurological sequelae in patients with all grades of carbon monoxide (CO) poisoning after treatment with hyperbaric oxygen (HBO) and normobaric oxygen (NBO). DESIGN: Randomised controlled double-blind trial, including an extended series of neuropsychological tests and sham treatments in a multiplace hyperbaric chamber for patients treated with NBO. SETTING: The multiplace hyperbaric chamber at the Alfred Hospital, a university-attached quarternary referral centre in Melbourne providing the only hyperbaric service in the State of Victoria. PATIENTS: All patients referred with CO poisoning between 1 September 1993 and 30 December 1995, irrespective of severity of poisoning. Pregnant women, children, burns victims and those refusing consent were excluded. INTERVENTION: Daily 100-minute treatments with 100% oxygen in a hyperbaric chamber--60 minutes at 2.8 atmospheres absolute for the HBO group and at 1.0 atmosphere absolute for the NBO group--for three days (or for six days for patients who were clinically abnormal or had poor neuropsychological outcome after three treatments). Both groups received continuous high flow oxygen between treatments. MAIN OUTCOME MEASURES: Neuropsychological performance at completion of treatment, and at one month where possible. RESULTS: More patients in the HBO group required additional treatments (28% v. 15%, P = 0.01 for all patients; 35% v. 13%, P = 0.001 for severely poisoned patients). HBO patients had a worse outcome in the learning test at completion of treatment (P = 0.01 for all patients; P = 0.005 for severely poisoned patients) and a greater number of abnormal test results at completion of treatment (P = 0.02 for all patients; P = 0.008 for severely poisoned patients). A greater percentage of severely poisoned patients in the HBO group had a poor outcome at completion of treatment (P = 0.03). Delayed neurological sequelae were restricted to HBO patients (P = 0.03). No outcome measure was worse in the NBO group. CONCLUSION: In this trial, in which both groups received high doses of oxygen, HBO therapy did not benefit, and may have worsened, the outcome. We cannot recommend its use in CO poisoning.

BACKGROUND: This article outlines therapeutic mechanisms of hyperbaric oxygen therapy and reviews data on its efficacy for clinical problems seen by plastic and reconstructive surgeons. METHODS: The information in this review was obtained from the peer-reviewed medical literature. RESULTS: Principal mechanisms of hyperbaric oxygen are based on intracellular generation of reactive species of oxygen and nitrogen. Reactive species are recognized to play a central role in cell signal transduction cascades, and the discussion will focus on these pathways. Systematic reviews and randomized clinical trials support clinical use of hyperbaric oxygen for refractory diabetic wound-healing and radiation injuries; treatment of compromised flaps and grafts and ischemia-reperfusion disorders is supported by animal studies and a small number of clinical trials, but further studies are warranted. CONCLUSIONS: Clinical and mechanistic data support use of hyperbaric oxygen for a variety of disorders. Further work is needed to clarify clinical utility for some disorders and to hone patient selection criteria to improve cost efficacy.

OBJECTIVE: Chronic diabetic foot ulcers are a source of major concern for both patients and health care systems. The aim of this study was to evaluate the effect of hyperbaric oxygen therapy (HBOT) in the management of chronic diabetic foot ulcers. RESEARCH DESIGN AND METHODS: The Hyperbaric Oxygen Therapy in Diabetics with Chronic Foot Ulcers (HODFU) study was a randomized, single-center, double-blinded, placebo-controlled clinical trial. The outcomes for the group receiving HBOT were compared with those of the group receiving treatment with hyperbaric air. Treatments were given in a multi-place hyperbaric chamber for 85-min daily (session duration 95 min), five days a week for eight weeks (40 treatment sessions). The study was performed in an ambulatory setting. RESULTS: Ninety-four patients with Wagner grade 2, 3, or 4 ulcers, which had been present for >3 months, were studied. In the intention-to-treat analysis, complete healing of the index ulcer was achieved in 37 patients at 1-year of follow-up: 25/48 (52%) in the HBOT group and 12/42 (29%) in the placebo group (P = 0.03). In a sub-analysis of those patients completing >35 HBOT sessions, healing of the index ulcer occurred in 23/38 (61%) in the HBOT group and 10/37 (27%) in the placebo group (P = 0.009). The frequency of adverse events was low. CONCLUSIONS: The HODFU study showed that adjunctive treatment with HBOT facilitates healing of chronic foot ulcers in selected patients with diabetes.

In recent years, reports have shown positive effects of hyperbaric oxygen (HBO) treatment in posttraumatic circulatory insufficiency of the extremities. A tourniquet model for temporary ischemia was used to examine such treatment in rats. The circulation of the rat hindlimb was interrupted for 3 hours, while the contralateral uninjured leg served as control. There was a significant (p less than 0.001) postischemic edema in the tourniquet leg up to 48 hours after restoration of circulation. One group of animals received treatment with hyperbaric oxygen at 2.5 atmospheres absolute (ATA) for 45 minutes after release of the tourniquet. This significantly reduced (p less than 0.001) the postischemic edema, and the reduction persisted for 40 hours after the last treatment. It is concluded that hyperbaric oxygen reduces postischemic edema. Hyperbaric oxygen may therefore be useful as an adjuvant in the treatment of acute ischemic conditions when surgical repair alone fails or is not sufficient to reverse the ischemic process.

BACKGROUND AND PURPOSE: The effects of hyperbaric oxygen (HBO) therapy on humans are uncertain. Our study aims first to outline the practical aspects and the safety of HBO treatment and then to evaluate the effect of HBO on long-term disability. METHODS: Patients who experienced middle cerebral artery occlusion and were seen within 24 hours of onset were randomized to receive either active (HBO) or sham (air) treatment. The HBO patients were exposed daily to 40 minutes at 1.5 atmospheres absolute for a total of 10 dives. We used the Orgogozo scale to establish a pretreatment functional level. Changes in the Orgogozo scale score at 6 months and 1 year after therapy were used to assess the therapeutic efficacy of HBO. In addition, we used the Rankin scale and our own 10-point scale to assess long term-disability at 6 months and 1 year. Two sample t tests and 95% confidence intervals were used to compare the mean differences between the two treatment groups. Student's two-tailed test was used to compare the differences between pretherapeutic and posttherapeutic scores at 6 months and 1 year in the two treatment groups. RESULTS: Over the 3 years of study enrollment, 34 patients were randomized, 17 to hyperbaric treatment with air and 17 to hyperbaric treatment with 100% oxygen. There was no significant difference at inclusion between groups regarding age, time from stroke onset to randomization, and Orgogozo scale scores. Neurological deterioration occurred during the first week in 4 patients in the sham group, 3 of whom died; this worsening was clearly related to the ischemic damage. Treatment was also discontinued for 3 patients in the HBO group who experienced myocardial infarction, a worsening related to the ischemic process, and claustrophobia. Therefore, 27 patients (13 in the sham group and 14 in the HBO group) completed a full course of therapy. The mean score of the HBO group was significantly better on the Orgogozo scale at 1 year (P < .02). However, the difference at 1 year between pretherapeutic and posttherapeutic scores was not significantly different in the two groups (P < .16). Moreover, no statistically significant improvement was observed in the HBO group at 6 months and 1 year according to Rankin score (P < .78) and our own 10-point scale (P < .50). CONCLUSIONS: Although the small number of patients in each group precludes any conclusion regarding the potential deleterious effect of HBO, we did not observe the major side effects usually related to HBO. Accordingly, it can be assumed that hyperbaric oxygen might be safe. We hypothesize that HBO might improve outcome after stroke, as we detected an outcome trend favoring HBO therapy. A large randomized trial might be required to address the efficacy of this therapy.

The goal of this review is to outline advances addressing the role that reactive species of oxygen and nitrogen play in therapeutic mechanisms of hyperbaric oxygen. The review will be organized around major categories of problems or processes where controlled clinical trials have demonstrated clinical efficacy for hyperbaric oxygen therapy. Reactive species are now recognized to play a major role in cell signal transduction cascades, and the discussion will focus on how hyperbaric oxygen acts through these pathways to mediate wound healing and ameliorate postischemic and inflammatory injuries.

The effect on the human lens of prolonged hyperbaric oxygen therapy is reported. Eye examinations were given to 25 patients before, during, and after a series of 150 or more exposures to hyperbaric oxygen. All patients changed refraction in the direction of myopia during treatment. Fifteen of the patients had clear lens nuclei before treatment. Seven of these developed a nuclear cataract with reduced visual acuity during treatment. Reversible lens myopia has previously been noticed as a side effect of exposure to hyperbaric oxygen, but the cataractogenic effect in man has not been reported by other workers. This report strongly supports the theory of an oxidative damage to the lens proteins as a cause of nuclear cataract.

The tenth European Consensus Conference on Hyperbaric Medicine took place in April 2016, attended by a large delegation of experts from Europe and elsewhere. The focus of the meeting was the revision of the European Committee on Hyperbaric Medicine (ECHM) list of accepted indications for hyperbaric oxygen treatment (HBOT), based on a thorough review of the best available research and evidence-based medicine (EBM). For this scope, the modified GRADE system for evidence analysis, together with the DELPHI system for consensus evaluation, were adopted. The indications for HBOT, including those promulgated by the ECHM previously, were analysed by selected experts, based on an extensive review of the literature and of the available EBM studies. The indications were divided as follows: Type 1, where HBOT is strongly indicated as a primary treatment method, as it is supported by sufficiently strong evidence; Type 2, where HBOT is suggested as it is supported by acceptable levels of evidence; Type 3, where HBOT can be considered as a possible/optional measure, but it is not yet supported by sufficiently strong evidence. For each type, three levels of evidence were considered: A, when the number of randomised controlled trials (RCTs) is considered sufficient; B, when there are some RCTs in favour of the indication and there is ample expert consensus; C, when the conditions do not allow for proper RCTs but there is ample and international expert consensus. For the first time, the conference also issued 'negative' recommendations for those conditions where there is Type 1 evidence that HBOT is not indicated. The conference also gave consensus-agreed recommendations for the standard of practice of HBOT.

Further analyses of the material contained in trials of the hyperbaric oxygen chamber in the radiotherapy of carcinoma of the cervix have shown that patients who were severely anaemic prior to radiotherapy, and who required blood transfusion, showed very poor local tumour control when conventionally treated after transfusion, but very good local tumour control when treated in hyperbaric oxygen. The finding of a special sub-group where hypoxia would seem to be an important cause of radiation failure, and where hyperbaric oxygen was successful in overcoming it, may have importance in the evaluation of other methods for overcoming the hypoxia, including the use of chemical sensitising agents.

1. Pigeon heart mitochondria produce H(2)O(2) at a maximal rate of about 20nmol/min per mg of protein. 2. Succinate-glutamate and malate-glutamate are substrates which are able to support maximal H(2)O(2) production rates. With malate-glutamate, H(2)O(2) formation is sensitive to rotenone. Endogenous substrate, octanoate, stearoyl-CoA and palmitoyl-carnitine are by far less efficient substrates. 3. Antimycin A exerts a very pronounced effect in enhancing H(2)O(2) production in pigeon heart mitochondria; 0.26nmol of antimycin A/mg of protein and the addition of an uncoupler are required for maximal H(2)O(2) formation. 4. In the presence of endogenous substrate and of antimycin A, ATP decreases and uncoupler restores the rates of H(2)O(2) formation. 5. Reincorporation of ubiquinone-10 and ubiquinone-3 to ubiquinone-depleted pigeon heart mitochondria gives a system in which H(2)O(2) production is linearly related to the incorporated ubiquinone. 6. The generation of H(2)O(2) by pigeon heart mitochondria in the presence of succinate-glutamate and in metabolic state 4 has an optimum pH value of 7.5. In states 1 and 3u, and in the presence of antimycin A and uncoupler, the optimum pH value is shifted towards more alkaline values. 7. With increase of the partial pressure of O(2) to the hyperbaric region the formation of H(2)O(2) is markedly increased in pigeon heart mitochondria and in rat liver mitochondria. With rat liver mitochondria and succinate as substrate in state 4, an increase in the pO(2) up to 1.97MPa (19.5atm) increases H(2)O(2) formation 10-15-fold. Similar pO(2) profiles were observed when rat liver mitochondria were supplemented either with antimycin A or with antimycin A and uncoupler. No saturation of the system with O(2) was observed up to 1.97MPa (19.5atm). By increasing the pO(2) to 1.97MPa (19.5atm), H(2)O(2) formation in pigeon heart mitochondria with succinate as substrate increased fourfold in metabolic state 4, with antimycin A added the increase was threefold and with antimycin A and uncoupler it was 2.5-fold. In the last two saturation of the system with oxygen was observed, with an apparent K(m) of about 71kPa (0.7-0.8atm) and a V(max.) of 12 and 20nmol of H(2)O(2)/min per mg of protein. 8. It is postulated that in addition to the well-known flavin reaction, formation of H(2)O(2) may be due to interaction with an energy-dependent component of the respiratory chain at the cytochrome b level.