Narcotic Nitrogen Effects Persist after a Simulated Deep Dive.

Background and Objectives: Scuba divers often experience persistent inert gas narcosis (IGN) even after surfacing. This study aimed to test the hypothesis that breathing oxygen (O2) before surfacing can reduce postdive IGN. Materials and Methods: A group of 58 experienced divers underwent a 5 min dive at a depth of 50 m in a multi-place hyperbaric chamber. They were decompressed using air (air group). Another group of 28 divers (O2 group) breathed 100% O2 during the end of decompression. Prior to and after the dive, all participants performed the Sharpened Romberg test (SRT) and a modified tweezers test. Results: In the air group, the number of positive SRT results increased postdive (47% vs. 67%), indicating a greater impairment in the vestibular system (Cohen's d = 0.41). In the O2 group, the percentage of positive SRT results remained constant at 68% both before and after the dive. In terms of the modified tweezers test, the air group showed no significant change in the number of picked beads (40 ± 9 vs. 39 ± 7), while the O2 group demonstrated an increase (36 ± 7 vs. 44 ± 10) (Cohen's d = 0.34). Conclusion: The results reveal that the SRT revealed a negative effect of nitrogen (N2) on the vestibular system in the air group. The increased number of beads picked in the O2 group can be attributed to the learning effect, which was hindered in the air group. Consistent with our hypothesis, breathing O2 during decompression appears to reduce postdive IGN.

The topical use of non-thermal dielectric barrier discharge (DBD): nitric oxide related effects on human skin.

Dielectric barrier discharge (DBD) devices generate air plasma above the skin containing active and reactive species including nitric oxide (NO). Since NO plays an essential role in skin physiology, a topical application of NO by plasma may be useful in the treatment of skin infections, impaired microcirculation and wound healing. Thus, after safety assessments of plasma treatment using human skin specimen and substitutes, NO-penetration through the epidermis, the loading of skin tissue with NO-derivates in vitro and the effects on human skin in vivo were determined. After the plasma treatment (0-60 min) of skin specimen or reconstructed epidermis no damaging effects were found (TUNEL/MTT). By Franz diffusion cell experiments plasma-induced NO penetration through epidermis and dermal enrichment with NO related species (nitrite 6-fold, nitrate 7-fold, nitrosothiols 30-fold) were observed. Furthermore, skin surface was acidified (~pH 2.7) by plasma treatment (90 s). Plasma application on the forearms of volunteers increased microcirculation fourfold in 1-2 mm and twofold in 6-8 mm depth in the treated skin areas. Regarding the NO-loading effects, skin acidification and increase in dermal microcirculation, plasma devices represent promising tools against chronic/infected wounds. However, efficacy of plasma treatment needs to be quantified in further studies and clinical trials.

Hyperoxia and the cardiovascular system: experiences with hyperbaric oxygen therapy.

Hyperoxia has been described to induce bradycardia by direct stimulation of the parasympathetic nervous system. Also, hyperoxia has been found to increase blood pressure by an elevation of vascular resistance. However, the latter effect itself would induce bradycardia by baroreceptor stimulation. This single-arm monocentric retrospective study aims to evaluate the correlation between these effects by investigating the relation between oxygen (O2) administration and heart rate over time. Data were collected from 23 patients without cardiovascular problems undergoing hyperbaric oxygen therapy (2.4 bar) retrospectively. During single oxygen bouts, transcutaneously measured partial pressure of O2 was increased. During this surge of oxygen pressure, the arterial blood pressure was increased while the heart rate was decreased. Respiration rate was maintained independently from breathing 100% O2 or air. During single oxygen bouts, the half-life of transcutaneously measured partial pressure of O2 was 5.4 ± 2.1 mmHg/s, and the half-life of heart rate was 0.45 ± 0.19 beats/min. It has been shown that hyperbaric oxygen therapy increases the transcutaneously measured partial pressure of O2. This increase was rather fast, followed by a rather slow decrease in HR. This finding does not support direct vagal activation. Heart rate is not decreased due to a direct vagal activation during hyperbaric oxygen therapy. Our single-arm, retrospective study has additionally confirmed that oxidative stress injures the endothelium, and the reduced endothelial-derived vasodilators cause vasoconstriction. As a consequence, blood pressure increases, and heart rate is then further decreased via the baroreceptor reflex.

Plate-associated localized osteitis in mini-pig by biofilm-forming Methicillin-resistant Staphylococcus aureus (MRSA): establishment of a novel experimental model.

PURPOSE: The increasing number of implant-associated infections during trauma and orthopedic surgery caused by biofilm-forming Staphylococcus aureus in combination with an increasing resistance of conventional antibiotics requires new therapeutic strategies. One possibility could be testing for different therapeutic strategies with differently coated plates. Therefore, a clinically realistic model is required. The pig offers the best comparability to the human situation, thus it was chosen for this model. The present study characterizes a novel model of a standardized low-grade acute osteitis with bone defect in the femur in mini-pigs, which is stabilized by a titanium locking plate to enable further studies with various coatings. METHODS: A bone defect was performed on the femur of 7 Aachen mini-pigs and infected with Methicillin-resistant S. aureus (MRSA ATCC 33592). The defect zone was stabilized with a titanium plate. After 14 days, a plate change, wound debridement and lavage were performed. Finally, after 42 days, the animals were lavaged and debrided again, followed by euthanasia. The fracture healing was evaluated radiologically and histologically. RESULTS: A local osteitis with radiologically visible lysis of the bone could be established. The unchanged high Colony-forming Units (CFU) in lavage, the significant differences in Interleukin (IL)-6 in blood compared to lavage and the lack of increase in Alkaline Phosphates (ALP) in serum over the entire observation period show the constant local infection. CONCLUSION: The study shows the successful induction of local osteitis with lysis of the bone and the lack of enzymatic activity to mineralize the bone. Therefore, this standardized mini-pig model can be used in further clinical studies, to investigate various coated implants, bone healing, biofilm formation and immune response in implant-associated osteitis.

Non-Thermal Dielectric Barrier Discharge (DBD) Effects on Proliferation and Differentiation of Human Fibroblasts Are Primary Mediated by Hydrogen Peroxide.

The proliferation of fibroblasts and myofibroblast differentiation are crucial in wound healing and wound closure. Impaired wound healing is often correlated with chronic bacterial contamination of the wound area. A new promising approach to overcome wound contamination, particularly infection with antibiotic-resistant pathogens, is the topical treatment with non-thermal "cold" atmospheric plasma (CAP). Dielectric barrier discharge (DBD) devices generate CAP containing active and reactive species, which have antibacterial effects but also may affect treated tissue/cells. Moreover, DBD treatment acidifies wound fluids and leads to an accumulation of hydrogen peroxide (H2O2) and nitric oxide products, such as nitrite and nitrate, in the wound. Thus, in this paper, we addressed the question of whether DBD-induced chemical changes may interfere with wound healing-relevant cell parameters such as viability, proliferation and myofibroblast differentiation of primary human fibroblasts. DBD treatment of 250 µl buffered saline (PBS) led to a treatment time-dependent acidification (pH 6.7; 300 s) and coincidently accumulation of nitrite (~300 µM), nitrate (~1 mM) and H2O2 (~200 µM). Fibroblast viability was reduced by single DBD treatments (60-300 s; ~77-66%) or exposure to freshly DBD-treated PBS (60-300 s; ~75-55%), accompanied by prolonged proliferation inhibition of the remaining cells. In addition, the total number of myofibroblasts was reduced, whereas in contrast, the myofibroblast frequency was significantly increased 12 days after DBD treatment or exposure to DBD-treated PBS. Control experiments mimicking DBD treatment indicate that plasma-generated H2O2 was mainly responsible for the decreased proliferation and differentiation, but not for DBD-induced toxicity. In conclusion, apart from antibacterial effects, DBD/CAP may mediate biological processes, for example, wound healing by accumulation of H2O2. Therefore, a clinical DBD treatment must be well-balanced in order to avoid possible unwanted side effects such as a delayed healing process.