Hyperbaric Oxygen Administration Research Articles

Negative Effect of Immediate Hyperbaric Oxygen Therapy in Acute Acoustic Trauma

Objective: The functional evaluation of the effect of the hyperbaric oxygen therapy (HBOT) onset time on cochlea by using distortion product otoacoustic emission. Study Design: Animal study. Methods: Twenty-four Wistar albino rats were divided into six groups and their right ears were directly exposed to a 110-dB sound pressure level (1-12 kHz) white noise for 25 minutes. The first group was considered the control group. HBOT was started at 1 hour postexposure for the second group, at 2 hours postexposure for the third group, at 6 hours postexposure for the fourth group, at 24 hours postexposure for the fifth group, and at 48 hours postexposure for the sixth group. Signal-to-noise ratios (SNRs) were recorded before the noise exposure; immediately after the noise exposure; and on the 3rd, 7th, and 10th day of postexposure. Results: SNRs at 6 to 8 kHz were significantly decreased after the acoustic trauma. The evaluation on the third day of postexposure showed that recovery begun in all groups except the group in which the HBOT was started at 1 hour postexposure. SNRs in the control group and HBOT groups were back to the preexposure levels at 10 days postexposure, except the 1- and 2-hour postexposure groups. However, in the group in which the HBOT was started at 1 hour postexposure, distortion product otoacoustic emissions were lost except at 4 kHz. The recovery of the SNRs in hyperbaric oxygen administration at 2 hours postexposure almost completed on the 10th day after noise exposure. Conclusion: Immediate HBOT in acoustic trauma treatment is not necessary; on the contrary, it has an adverse effect.

Preoperative and Postoperative Administration of Hyperbaric Oxygen Improves Biochemical and Mechanical Parameters on Ischemic and Normal Colonic Anastomoses

Colonic anastomotic leaks are a major postoperative complication, causing increased mortality and morbidity. Tissue ischemia is one of the most important factors that disrupt anastomotic healing. It is possible to reverse inadequate tissue oxygenation by using increased atmospheric pressure and hyperoxia, which are obtained from hyperbaric oxygen treatment (HBO). Our aim was to investigate the effects of preoperative and postoperative HBO treatment on normal and ischemic colonic anastomoses in rats. Eighty male Wistar Albino rats, weighing between 180 and 240 g, were divided into 8 equal groups. A 1-cm segment of left colon was resected 3 cm proximal to the peritoneal reflection in all groups and colonic anastomosis was performed. In groups 2, 4, 6 and 8, colonic ischemia was established by ligating 2 cm of mesocolon on either side of the anastomosis. Control groups (1 and 2) received no HBO. HBO treatment was given preoperatively in groups 3 and 4, postoperatively in groups 5 and 6, and both preoperatively and postoperatively in groups 7 and 8. HBO treatment was applied for 2 days in the preoperative period and 4 days in the postoperative period. Relaparotomy was performed on postoperative day 5 and a perianastomotic colon segment 2 cm in length was excised for detection of biochemical and mechanical parameters of anastomotic healing and histopathological evaluation. HBO treatment increased tissue hydroxyproline levels in all groups, and this difference was significant in normal anastomosis groups receiving preoperative HBO compared to controls (p =. 013 for group 1 vs. group 3; p =. 023 for group 1 vs. group 5). This improvement was more evident in ischemic and normal groups treated by administration of combined pre- and postoperative HBO (p =. 021 and p =. 013). HBO treatment also increased the mean bursting pressure values in all groups, and again, a statistically significant increase was noted in the ischemic groups compared to controls (p =. 002 for group 2 vs. group 6; p =. 001 for group 2 vs. group 8). Histopathological evaluation of anastomotic line fibrosis was not found to show significant differences between the groups. Adequate tissue oxygenation is the main factor in wound and anastomosis healing. HBO treatment has a positive effect on biochemical and mechanical parameters of ischemic and normal colon anastomoses in rats. It is possible to see this effect more clearly with combined HBO treatment applied before and after ischemic anastomosis.

Protective effects of exogenously administered or endogenously produced melatonin on hyperbaric oxygen‐induced oxidative stress in the rat brain

1. Hyperbaric oxygen (HBO) is a widely used treatment modality in many diseases. A known side-effect of HBO is the production of reactive oxygen species (ROS). Many anti-oxidants, such as vitamins C and E, riboflavin and selenium, have been used successfully to scavenge the ROS produced by HBO administration. 2. The aim of the present study was to determine whether melatonin, a newly discovered anti-oxidant, has a protective effect against the overproduction of ROS produced by HBO in rat brain tissue. 3. Seventy male Sprague-Dawley rats were divided into seven groups as follows: 1, daytime control; 2, daytime HBO; 3, melatonin; 4, daytime HBO plus melatonin; 5, night-time control; 6, night-time HBO; and 7, night-time HBO under light exposure. 4. Hyperbaric oxygen was administered at 303 kPa for 120 min. Melatonin was injected at a dose of 10 mg/kg, i.p. Brain malondialdehyde (MDA), superoxide dismutase (SOD) and glutathione peroxidase (GPx) levels were measured to elucidate oxidant status. 4. The MDA and SOD levels of groups 2 and 7 increased significantly. Exogenous (group 4) and endogenous (group 6) melatonin protected against HBO-induced lipid peroxidation. Exogenously administered melatonin (groups 3 and 4) had increased levels of the anti-oxidant enzymes SOD and GPx. 5. In conclusion, HBO caused oxidative stress and melatonin exhibited protective effects. Both endogenously produced and exogenously administered melatonin were found to be effective.

Hyperbaric oxygen reduces blood-brain barrier damage and edema after transient focal cerebral ischemia

Hyperbaric oxygen (HBO) has been shown to protect the brain parenchyma against transient focal cerebral ischemia but its effects on the ischemic microcirculation are largely unknown. We examined the potential of HBO to reduce postischemic blood-brain barrier (BBB) damage using repetitive MR-imaging and Na-Fluorescein uptake during 72 h of reperfusion and measured the effect of HBO on postischemic edema. Wistar rats and C57/Bl6 mice underwent focal ischemia for 2 h induced by filament occlusion of the middle cerebral artery (MCAO). Forty minutes after filament introduction, animals were placed in a HBO chamber and breathed either 100% O2 at 3.0 atmospheres absolute (ata; HBO group) or at 1.0 ata (control) for 1 h. In rats, MR-images were obtained 15 min after MCAO, and after 15 min, 3, 6, 24, 72 h of reperfusion. Volume of T1w postcontrast enhancement and an interhemispheric quotient of mean gray values (MGV) in T1w images were calculated for estimation of BBB damage. In ischemic mice, BBB permeability for Na-Fluorescein was measured fluoroscopically after 24 h of reperfusion. Physiological parameters and ischemic MR-perfusion did not differ between groups. Increased postischemic BBB permeability on postcontrast T1w images had a biphasic pattern and was located within the hyperintense areas on DWI and T2w images, respectively. HBO reduced volume of early and delayed BBB damage on postcontrast T1w images. Mean abnormal enhancing volumes at the various time points were at 15 min of reperfusion: 297 mm3 (control) vs. 196 mm3 (HBO); at 3 h: 3811 mm3 vs. 287 mm3; at 6 h: 4916 mm3 vs. 318 mm3; at 24 h: 5114 mm3 vs. 358 mm3; at 72 h: 9728 mm3 vs. 6817 mm3 (p<0.05 for 6, 24, 72 h). The quotient of MGV was significantly lower in the HBO treated animals at all time points: at 15 min of reperfusion: 1.730.11 (control) vs. 1.570.07 (HBO); at 3 h: 1.740.07 vs. 1.600.06; at 6 h: 1.770.07 vs. 1.620.06; at 24 h: 1.790.10 vs. 1.600.05; at 72 h: 1.810.10 vs. 1.620.07. Reduction of postischemic BBB damage by HBO was confirmed in mice. After 24 h of reperfusion, mean interhemispheric quotient (ischemic/nonischemic) of relative fluorescence units was significantly larger in control (1.560.50) than in HBO (1.110.16) treated mice. Effect of HBO on ischemic focal brain edema was estimated by two ways. First, volume of hyperintensity on T2w images, which represent both parenchymal damage and brain edema in the ischemic hemisphere, was significantly larger in control than in HBO treated animals at 72 h after MCAO. Second, on histological sections, volume attributable to focal edema was 7229 mm3 in the control and 4114 mm3 in the HBO group (p<0,05). In conclusion, early administration of HBO reduces rapid and delayed BBB damage and brain edema after transient focal cerebral ischemia. The molecular and cellular targets of this HBO effect and its potential implications for reduction of secondary microvascular complications are currently under investigation.

Effects of the hyperbaric oxygen treatment on the Na +,K +-ATPase and superoxide dismutase activities in the optic nerves of global cerebral ischemia-exposed rats

The effects of hyperbaric oxygen (HBO) treatment on the Na +,K +-ATPase and superoxide dismutase (SOD) activities were examined in the optic nerves of the rats exposed to global cerebral ischemia. Animals were exposed to global cerebral ischemia of 20-min duration and were either sacrificed or exposed to the first HBO treatment immediately, 0.5, 1, 2, 6, 24, 48, 72 or 168 h after ischemic procedure (for Na +,K +-ATPase activities measurement) or 2, 24, 48 or 168 h after ischemia (for SOD activities measurement). HBO procedure was repeated for 7 consecutive days. It was found that global cerebral ischemia induced a statistically significant decrease in the Na +,K +-ATPase activity of the optic nerves, starting from 0.5 to 168 h of reperfusion. Maximal enzymatic inhibition was registered 24 h after the ischemic damage. The decline in the Na +,K +-ATPase activity was prevented in the animals exposed to HBO treatment within the first 6 h of reperfusion. The results of the presented experiments demonstrated also a statistically significant increase in the SOD activity after 24, 48 and 168 h of reperfusion in the optic nerves of non-HBO-treated ischemic animals as well as in the ischemic animals treated with HBO. Our results indicate that global cerebral ischemia induced a significant alterations in the Na +,K +-ATPase and SOD activities in the optic nerves during different periods of reperfusion. HBO treatment, started within the first 6 h of reperfusion, prevented ischemia-induced changes in the Na +,K +-ATPase activity, while the level of the SOD activity in the ischemic animals was not changed after HBO administration.

Effect of hyperbaric oxygen on the ligament healing process in rats.

Animal experiments were done to investigate whether administration of hyperbaric oxygen promotes scar tissue formation, increases expression of the Type I procollagen gene, and improves the tensile properties of healing ligament. In 76 Sprague-Dawley rats, a 2-mm segment of the medial collateral ligament was removed. Thirty-eight rats were exposed to hyperbaric oxygen at 2.5 atmospheres absolute for 2 hours 5 days per week (Group H), whereas the remaining rats were exposed to room air (Group C). The animals were sacrificed at 3, 7, 14, and 28 days postoperatively. In situ hybridization histochemistry was done to examine the Type I procollagen gene expression in healing ligaments in 40 rats, whereas a tensile failure test was done in the remaining rats. The amount of scar tissue was greater in Group H than in Group C. Type I procollagen gene expression at 7 or 14 days was significantly greater in Group H than in Group C. The ultimate load and stiffness in Group H were significantly greater than in Group C at 14 days. Administration of hyperbaric oxygen promotes scar tissue formation and increases Type I procollagen gene expression in healing ligaments. These effects are associated with the improvement of their tensile properties.

Exogenously administered and endogenously produced melatonin reduce hyperbaric oxygen-induced oxidative stress in rat lung

Hyperbaric oxygen (HBO) is a widely used treatment modality in many diseases. A known side effect of HBO is the production of reactive oxygen species. Many antioxidants such as vitamins C and E, riboflavin and selenium have been used successfully to scavenge the reactive oxygen species caused by HBO administration. In this study, we aimed to see if melatonin, a newly discovered antioxidant, has a protective effect against the overproduction of reactive oxygen species produced by HBO in rat lung tissue. Sixty male Sprague-Dawley rats were divided into 5 groups as follows: control, daytime HBO (3 ATA, 120 min), daytime HBO plus melatonin (10 mg/kg), nighttime HBO and nighttime HBO (under light exposure). The MDA, SOD and CAT levels of daytime and nighttime HBO (under light exposure) increased significantly. This significance was not found in the daytime HBO plus melatonin and nighttime HBO groups when compared with the control. In this study, HBO caused oxidant stress, and melatonin decreased the levels of MDA, SOD and CAT. Moreover, endogenous melatonin was found to be a more effective antioxidant than exogenous 10 mg/kg melatonin.

Hyperbaric oxygen enhances the expression of prion protein and heat shock protein 70 in a mouse neuroblastoma cell line.

1. Cellular prion protein, PrP(C), is a ubiquitous glycoprotein strongly expressed in neurons with an as yet unknown biological function. In previous studies, we demonstrated that PrP(C) could be regulated by heat shock stress, implying that it might be a stress-responsive protein. Hyperbaric oxygen (HBO) administration is a well-defined model for the study of oxidative stress. 2. This study investigated the effect of HBO on PrP(C) and Hsp 70 expression in mouse neuroblastoma cell lines (N18), assessing the expression of PrP(C) and Hsp 70 using RT-PCR and Western blotting. HBO administration resulted in a time- and dose-dependent increase in PrP(C) and Hsp70 expression in N18 cells at both mRNA and protein levels, with a concomitant upregulation of c-Jun N-terminal kinase (JNK). 3. Under HBO treatment, luciferase reporter constructs of the rat PrP(C) promoter, containing the heat shock element (HSE) also present in Hsp70, expressed higher luciferase activity (3- to 10-fold) than those constructs without HSE. 4. In summary, these data suggest that PrP(C) and Hsp 70 may be regulated by HBO, through the activation of JNK. Thus, the activated heat shock transcriptional factor 1, phosphorylated by JNK interacted with HSE in the promoter of PrP(C) resulted in increased gene expression. These findings are vital for future therapeutic approaches in transmissible spongiform encephalopathies and the understanding of the function of the PrP(C).

Evaluation and management of decompression illness—an intensivist’s perspective

Decompression illness (DCI) is becoming more prevalent as more people engage in activities involving extreme pressure environments such as recreational scuba-diving. Rapid diagnosis and treatment offer these patients the best chance of survival with minimal sequelae. It is thus important that critical care physicians are able to evaluate and diagnose the signs and symptoms of DCI. The cornerstones of current treatment include the administration of hyperbaric oxygen and adjunctive therapies such as hydration and medications. However, managing patients in a hyperbaric environment does present additional challenges with respect to the particular demands of critical care medicine in an altered pressure environment. This article reviews the underlying pathophysiology, clinical presentation and therapeutic options available to treat DCI, from the intensivist's perspective.

Hyperbaric oxygen modulates antioxidant enzyme activity in rat skeletal muscles.

In skeletal muscle the activity of the enzymatic antioxidants superoxide dismutase (SOD), glutathione peroxidase (GPx) and catalase (CAT) is regulated in response to generation of reactive oxygen species (ROS). Increased activity of these enzymes is observed after repeated bouts of aerobic exercise, a potent stimulus for intracellular ROS production. Hyperbaric oxygen (HBO) inhalation also stimulates intracellular ROS production although the effects of HBO on skeletal muscle SOD, GPx and CAT activity have not been studied. We tested the hypothesis that SOD, GPx and CAT activity is modulated in skeletal muscles in response to acute and repeated HBO administration. In adult male rats acute HBO inhalation (60 mm at 3 atmospheres absolute) reduced catalase activity by approximately 51% in slow-twitch soleus muscles. Additionally, repeated HBO inhalation (twice daily for 28 days) increased Mn2+-superoxide dismutase activity by approximately 241% in fast-twitch extensor digitorum longus muscles. We conclude that both acute and repeated HBO inhalation can alter enzymatic antioxidant activity in skeletal muscles.

Hyperbaric oxygen reduces infarct volume in rats by increasing oxygen supply to the ischemic periphery

Hyperbaric oxygen (HBO) increases oxygen supply to anoxic areas. To examine the therapeutic effect of HBO on ischemic stroke, we measured infarct volume as well as cerebral blood flow (CBF), oxygen supply, and lipid peroxidation in the ischemic periphery. Prospective experimental study in rats. Experimental laboratory in a university teaching hospital. Thirty-eight adult rats. The rats were anesthetized (1% halothane) and intubated. Focal ischemia was induced by ligating the right middle cerebral and right common carotid arteries. Nineteen animals were exposed to 2 hrs of HBO (100% oxygen, 3 atmospheres absolute), initiated 10 mins after the onset of ischemia. The remaining animals were kept at ambient pressure and used as controls. At the initiation of ischemia, CBF measured by a laser-Doppler flow probe placed in the ischemic periphery was reduced to 47%+/-11% and 51%+/-15% of normal levels in animals exposed or not to HBO, respectively. These altered values were not affected further by administration of HBO and remained stable throughout a 2-hr observation period. Arterial oxygen pressure and content were significantly increased to 1571+/-130 torr (209.41+/-17.32 kPa; p < .0001) and 1.03+/-0.04 mmol/dL (p < 0.0001), respectively, in HBO-treated animals compared with nontreated animals (139+/-14 torr [18.53+/-1.87 kPa] and 0.86+/-0.04 mmol/dL, respectively). The calculated increase in the oxygen supply to the ischemic periphery was 20%. The infarct volume of HBO-treated animals measured 24 hrs after the onset of focal cerebral ischemia was significantly reduced by 18% (HBO-treated, 132+/-13 mm3 vs. nontreated, 161+/-29 mm3; p = .02). Lipid peroxidation was unchanged after 120 mins of HBO administration in the cerebral cortex where the laser-Doppler flow probe was placed. HBO at 3 atmospheres absolute reduced infarct volume by increasing oxygen supply to the ischemic periphery without aggravating lipid peroxidation, suggesting that HBO can be useful in treating stroke victims.

EFFECT OF HYPERBARIC OXYGEN THERAPY ON TESTICULAR ISCHEMIA-REPERFUSION INJURY

Purpose Testicular torsion is a urologic emergency representing a form of ischemia-reperfusion (IR) injury that requires prompt care to achieve tissue salvage and a reduction in post-torsion morbidity. Hyperbaric oxygen (HBO) has shown benefits in previous musculoskeletal models of IR. We evaluated the efficacy of HBO treatment in a rat testicular torsion model. Materials and Methods Four groups of male Wistar rats were included in this study: 1) Sham (n = 16), spermatic cord exposed but not occluded; 2) Control (n = 16), 4 hours of bilateral spermatic cord occlusion; 3) HBO during ischemia (n = 18), 4 hours of occlusion and administration of HBO during the last 90 minutes of ischemia; and 4) HBO on reperfusion (n = 8), HBO administered immediately upon reperfusion of the testes. The animals were sacrificed at two weeks and architecture and germinal epithelial cell thickness were determined by histological examination on each testicle. Average thickness (in cell layers) of each group was compared with control using Student's t test. Results Control testicles showed a significant reduction in germinal cell thickness compared with sham (1.7 versus 6.3, p <0.05). The animals treated with HBO during ischemia showed a significant increase in epithelial cell thickness compared with control (2.8 versus 1.7, p <0.05). Hyperbaric oxygen treatment during reperfusion had the greatest beneficial effect compared with control (5.1 versus 1.7, p <0.05). Conclusions Adjunctive HBO therapy administered during ischemia or reperfusion significantly reduced injury to the testicle in this animal model. These results suggest a potential benefit of HBO treatment in clinical situations of testicular torsion.

Effect of hyperbaric oxygen on neutrophil concentration and pulmonary sequestration in reperfusion injury.

To evaluate the effect of hyperbaric oxygen (HBO) on muscle flap arterial neutrophil concentration and pulmonary neutrophil sequestration following ischemia-reperfusion injury in a rat gracilis muscle microcirculation model. Prospective randomized experimental trials. Laboratory. Male Wistar rats weighing 150 to 300 g. Gracilis muscle flaps were raised on isolated vascular pedicles. Three groups were evaluated: (1) sham (flap raised, 4-hour observation, no ischemia, no HBO), (2) ischemia control (4-hour flap is ischemia, no HBO); and (3) ischemia (4-hour flap is ischemia) plus HBO (last 90 minutes of ischemia, 100% oxygen, 2.5 atm absolute). Flap pedicle arterial leukocyte and neutrophil concentrations were assessed at 5 and 90 minutes of reperfusion in the 3 groups. Pulmonary neutrophil sequestration was measured in a blinded fashion, using histologic examination and myeloperoxidase assay in the 3 groups at 5 and 90 minutes of reperfusion. Ischemia produced an increase in pedicle arterial leukocyte and neutrophil concentrations in blood flowing to the gracilis muscle flap; administration of HBO significantly reduced concentration to sham levels (P < .05). There were no significant differences in pulmonary neutrophil sequestration among the experimental groups. In this rat gracilis muscle microcirculation model, the increase in pedicle arterial leukocyte and neutrophil concentrations following ischemia-reperfusion injury was significantly reduced to sham levels by HBO treatment. This observed reduction was not attributable to HBO-induced pulmonary sequestration, which did not significantly change with HBO administration. Further investigation is required to elucidate the mechanisms of action of HBO in ameliorating ischemia-reperfusion injury in this model.

Peroneal motor nerve crush injury and hyperbaric oxygen effect

The potential therapeutic effect of hyperbaric oxygen (HBO) after rat peroneal nerve crush was evaluated. Animals were given 100% oxygen at 2.5 atmosphere absolute for 90 minutes twice daily for 1 week and then once daily for 1 week. Edema increased in crushed nerves compared with control nerves, but no effect was associated with the administration of HBO. Gait analysis demonstrated injury at 1, 7, and 14 days after nerve crush, but no difference was found at 22 and 28 days after injury (analysis of variance: P < .001, 10 animals per group). Eight weeks after injury, nerve stimulation and muscle force measurements were 114 g for the injured group and 146 g for the control group (P < .001). There were no HBO-associated changes in gait parameter or nerve/muscle force measurements. This study demonstrated that rat peroneal nerve crush injury causes acute intraneural edema and temporary decrement of gait parameters. Elicited nerve stimulation demonstrated persistent loss of force 4 weeks after normalization of gait, but no HBO effect.

Treatment of Burned Mice With Hyperbaric Oxygen Reduces Mesenteric Bacteria but Not Pulmonary Neutrophil Deposition

I read with interest the article by Tenenhaus et al 1 in the December 1994 issue of theArchivesabout the effects of hyperbaric oxygen (HBO) administration on bacterial translocation in a murine burn model. Their results appear to focus on bacterial translocation only, ignoring the effects of increased oxygen administration on survival. The effects of increased oxygen delivery on specific tissues is interesting for its ability to provide insight into the mechanisms of bacterial spread after a major burn. However, the results of such a manipulation must be evaluated in the context of the overall mortality rate. These results (as shown in Table 1 of their article 1 ) suggest an additional conclusion from this study. Animals that underwent administration of HBO had a significant mortality rate. In contrast, none of the non–HBO-treated animals died. These results are similar to those found in a different murine model of serious trauma,

Hydroxyl radical production in the brain after CO hypoxia in rats

Reactive oxygen species (ROS) have been implicated in the pathogenesis of neuronal injury after carbon monoxide (CO) poisoning. Severe CO poisoning is treated with hyperbaric oxygen (HBO), which eliminates CO quickly from hemoglobin and body tissue stores, but has a potential to increase ROS generation. In this study, the effects of HBO on generation of highly reactive hydroxyl radical (HO ·) in the brain after CO poisoning in rats was investigated using nonenzymatic hydroxylation of salicylic acid to 2,3 dihydroxybenzoic acid (2,3-DHBA) as a probe. In control studies, the concentrations of 2,3-DHBA after HBO in brain mitochondria and postmitochondrial supematant (cytosol) were similar to air-exposed animals. After CO poisoning, 2,3-DHBA concentration increased in brain mitochondria but not in the cytosol. After CO exposure and HBO administration at 1.5 atmospheres absolute (ATA), a decrease in 2,3-DHBA production was detected in brain mitochondria. After CO and HBO at 2.5 ATA, 2,3-DHBA concentration increased in both mitochondria and cytosol. The oxidant scavenger dimethylthiourea (DMTU) and the monoamine oxidase (MAO) inhibitor pargyline, administered to CO poisoned rats after HBO at 2.5 ATA, diminished 2,3-DHBA production in both subcellular compartments. These findings indicate that brain HO ḃ production can be either diminished or accelerated after severe CO poisoning depending on the oxygen partial pressure employed during therapy.

Carbon monoxide poisoning. An occult epidemic.

Carbon monoxide poisoning is a significant health threat in the United States. Smoke inhalation from fires is the most common source. History of carbon monoxide exposure and elevated carboxyhemoglobin levels should alert physicians to the diagnosis of acute poisoning. When there is no history of exposure, carbon monoxide poisoning must be considered when two or more patients are similarly or simultaneously sick. The diagnosis must be excluded by a directed history and physical examination. If suspicion remains, carboxyhemoglobin levels should be determined and oxygen therapy should be started empirically while laboratory results are pending. Prompt administration of hyperbaric oxygen may reduce the risk of death. If carbon monoxide poisoning is confirmed, the source must be identified and recommendations for correction or avoidance should be made.

Effects of Hyperbaric Oxygen Preservation on Rat Limb Replantation: A Preliminary Report

The effect of hyperbaric oxygen, administered during storage, on the survival of replanted limbs was evaluated in rats. The right hindlimbs of male Sprague-Dawley rats were severed and were replanted by microvascular anastomoses after storage in either room air or hyperbaric oxygen (100% oxygen at 2.9 atm absolute) at 23 degrees C for 5 hours. The administration of hyperbaric oxygen during storage improved limb survival from 50% in the room-air, control rats to 100% (p less than 0.05). The gastrocnemius muscle of limbs treated with hyperbaric oxygen demonstrated a higher level of energy reserves (creatine phosphate, adenosine triphosphate, glycogen, and glucose) than the same muscle in room-air, control rats. The mechanisms of the beneficial effect of hyperbaric oxygen on limb survival appears to be related to preservation of high-energy phosphates and glycogen.

Survival time of rats exposed to different high oxygen pressures after administration of perfluorochemicals.

Hyperbaric oxygen administration is considered useful in the treatment of anaerobic infections (Cline and Turnbull, 1985) as well as in tumour radiation therapy (Fischer, Rockwell and Martin, 1986) where very high tissue partial pressures of oxygen are needed. The most commonly used oxygen pressure of 300 kPa (3 ATA) may not be sufficient to reach this goal. There must be sufficient oxygen capacity in the blood to maintain an elevated partial pressure even at the venous end of capillaries when oxygen is consumed. More effective treatment could be accomplished if haemoglobin were to remain in the oxygenated form. The administration of perfluorochemicals (PFC) which increase the oxygen capacity under elevated oxygen partial pressure can help in attaining this goal. However, as judged from previous results obtained by Geyer (1983), hyperbaric oxygen treatment combined with PFC administration can be expected to augment oxygen toxicity considerably. To test this supposition hyperbaric oxygen was applied and survival times were measured in rats as an index of the overall tolerance of the organism at various oxygen pressures. Survival time was found to give a more precise endpoint than the determination of the onset of convulsions. It was the goal of this study to establish the relationship between oxygen tension and lethal duration of exposure in both control and PFC-treated animals.

Hyperbaric oxygen therapy for pyoderma gangrenosum.

Hyperbaric oxygen administered systemically has been advocated in the treatment of pyoderma gangrenosum. Owing to the serious potential risks of oxygen toxicity with systemic administration, we have devised a simplified technique for the administration of hyperbaric oxygen topically, and have used this method successfully to treat two patients with pyoderma gangrenosum, in whom the underlying etiology was not apparent, and specific therapy, therefore, not possible. The abundant formation of granulation tissue and the ability of the hyperbaric oxygen to arrest further extension of the ulceration suggests that this form of therapy might become the treatment of choice for all ulcers of the pyoderma gangrenosum type.