Dexmedetomidine (DEX) can prolong duration of anesthesia and shorten onset of sensory and motor block relative to clonidine. This study attempted to compare the efficacy of intravenous DEX and clonidine for hemodynamic changes and block after spinal anesthesia with ropivacaine in lower limb orthopedic surgery. In a double-blind randomized clinical trial, 120 patients undergoing spinal anesthesia in lower limb orthopedic surgery were recruited and divided into three groups using balanced block randomization: DEX group (n = 40; intravenous DEX 0.2 µg/kg), clonidine group (n = 40; intravenous clonidine 0.4 µg/kg), and placebo group (n = 40; intravenous normal saline 10 mL) in which pain scores were assessed using visual analogue scales (at recovery, and 2, 4, 6, and 12 hours after surgery) and time to achieve and onset of sensory and motor block. Statistically significant differences were found in mean arterial pressure among the groups at all times except baseline (P = 0.001), with a less mean arterial pressure and a prolonged duration of sensory and motor block (P = 0.001) in the DEX group where pain relieved in patients immediately after surgery and at above mentioned time points (P = 0.001). Simultaneous administration of intravenous DEX with ropivacaine for spinal anesthesia prolongs the duration of sensory and motor block and relieves postoperative pain, and however, can decrease blood pressure. Although intravenous DEX as an adjuvant can be helpful during spinal anesthesia with ropivacaine, it should be taken with caution owing to a lowering of mean arterial pressure in patients especially in the older adults. This study was approved by Ethical Committee of Arak University of Medical Sciences (No. IR.Arakmu.Rec.1395.450) in March, 2017, and the trial was registered and approved by the Iranian Registry of Clinical Trials (IRCT No. IRCT2017092020258N60) in 2017.

Persistent postconcussion syndrome (PPCS) after mild traumatic brain injury (mTBI) is a significant public health and military problem for which there is limited treatment evidence. The aim of this study was to determine whether forty 150 kPa hyperbaric oxygen therapies (HBOTs) can improve symptoms and cognitive function in subjects with the PPCS of mTBI, using a randomized controlled crossover design with 2-month follow-up. Sixty-three civilian and military subjects with mTBI/PPCS were randomized to either 40 HBOTs at 150 kPa/60 minutes, once daily, 5 days per week in 8 weeks or an equivalent no-treatment control period. The Control Group was then crossed over to HBOT. Subjects underwent symptom, neuropsychological, and psychological testing, before and after treatment or control with retesting 2 months after the 40^th HBOT. Fifty subjects completed the protocol with primary outcome testing. HBOT subjects experienced significant improvements in Neurobehavioral Symptom Inventory, Memory Index, Automated Neuropsychological Assessment Metrics, Hamilton Depression Scale, Hamilton Anxiety Scale, Post-Traumatic Stress Disorder Checklist, Pittsburgh Sleep Quality Index, and Quality Of Life after Brain Injury compared to the Control Group. After crossing over to HBOT the Control Group experienced near-identical significant improvements. Further improvements were experienced by both groups during the 2-month follow-up period. These data indicate that 40 HBOTs at 150 kPa/60 minutes demonstrated statistically significant improvements in postconcussion and Post-Traumatic Stress Disorder symptoms, memory, cognitive functions, depression, anxiety, sleep, and quality of life in civilian and military subjects with mTBI/PPCS compared to controls. Improvements persisted at least 2 months after the 40^th HBOT. The study was registered on ClinicalTrials.gov (NCT02089594) on March 18, 2014 and with the U.S. Food and Drug Administration under Investigational New Drug #113823. The Institutional Review Boards of the United States Army Medical Research and Materiel Command Office of Research Protections Human Research Protection Office and the Louisiana State University School of Medicine (approval No. 7381) approved the study on May 13, 2014 and December 20, 2013, respectively.

Repeated sprint exercise can interfere with intramuscular redox balance and cause systemic oxidative stress and muscle damage. There is growing evidence that molecular hydrogen counteracts oxidative and/or inflammatory responses. Therefore, we investigated the effects of molecular hydrogen-rich water (HW) on muscle performance and oxidative stress markers induced by strenuous exercise. A single-blind, crossover, randomized controlled trial has been designed. Eight male volunteers completed two 3-day consecutive exercise tests under two conditions: HW and placebo water (PW). The exercise test included a countermovement jump, maximal voluntary isometric contraction of knee extensors, and sprint cycling. The sprint cycling exercise was comprised three repetitions of 10-second maximal pedaling against a resistance of 7.5% body mass and 110-second active rest (no-load pedaling). Before and after the exercise test, participants drank the 500 mL of HW (5.14 ± 0.03 ppm in H₂ concentration) or PW (0.00 ± 0.00 ppm). At 7 hours before the first exercise test (Day 1), as baseline, and 16 hours after the exercise test on each day, blood samples were obtained. Exercise performances in both conditions were not significantly different over 3 consecutive days. In PW trial, relative changes in biological antioxidant potential/diacron-reactive oxygen metabolites, as an index of systemic antioxidant potential, from baseline gradually decreased as the day passed. However, HW suppressed the reduction in biological antioxidant potential/diacron-reactive oxygen metabolites observed in PW. Drinking HW contributed to the maintenance of the redox status during consecutive days of strenuous exercise and might help prevent accumulative muscular fatigue. The study was approved by the Human Research Ethics Committee of the University of Yamanashi, Japan (approval No. H26-008) on December 17, 2014.

In intensive care medicine heat moisture exchangers are standard tools to warm and humidify ventilation gases in order to prevent temperature loss of patients or airway epithelia damage. Despite being at risk of hypothermia especially after trauma, intubated emergency medicine patients are often ventilated with dry and in winter probably cold ventilation gases. We tried to assess the amount of temperature-loss due to ventilation with cold, dry medical oxygen in comparison to ventilation with warm and humidified oxygen. We ventilated a 50-kg water-dummy representing the calorimetric capacity of a 60-kg patient over a period of 2 hours (tidal volume 6.6 mL/kg = 400 mL; respiratory rate 13/min). Our formal null-hypothesis was that there would be no differences in temperature loss in a 50 kg water-dummy between ventilation with dry oxygen at 10°C vs. ventilation with humidified oxygen at 43°C. After 2 hours the temperature in the water-dummy using cold and dry oxygen was 29.7 ± 0.1°C compared to 30.4 ± 0.1°C using warm and humidified oxygen. This difference in cooling rates between both ventilation attempts of 0.7 ± 0.1°C after 2 hours represents an increased cooling rate of ~0.35°C per hour. Ventilation with cool, dry oxygen using an automated transport ventilator resulted in a 0.35°C faster cooling rate per hour than ventilation with warm humidified oxygen in a bench model simulating calorimetric features of a 60-kg human body.

Carbon monoxide (CO) has been the leading cause of poisoning mortality in many countries and hyperbaric oxygen (HBO) is a widely accepted treatment for CO poisoning. However, some patients with CO poisoning will still develop neurocognitive sequelae regardless of HBO therapy, which can persist since CO poisoning or be present days to weeks after a recovery from CO poisoning. HBO has been used in the prevention and treatment of neurocognitive sequelae after CO poisoning, and some mechanisms are also proposed for the potential neuroprotective effects of HBO on the neurocognitive impairment after CO poisoning, but there is still controversy on the effectiveness of HBO on neurocognitive sequelae after CO poisoning. In this paper, we briefly introduce the neurocognitive sequelae after CO poisoning, summarize the potential predictive factors of neurocognitive sequelae, and discuss the use of HBO in the treatment and prevention of neurocognitive sequelae after CO poisoning.

Nitric oxide, studied to evaluate its role in cardiovascular physiology, has cardioprotective and therapeutic effects in cellular signaling, mitochondrial function, and in regulating inflammatory processes. Heme oxygenase (major role in catabolism of heme into biliverdin, carbon monoxide (CO), and iron) has similar effects as well. CO has been suggested as the molecule that is responsible for many of the above mentioned cytoprotective and therapeutic pathways as CO is a signaling molecule in the control of physiological functions. This is counterintuitive as toxic effects are related to its binding to hemoglobin. However, CO is normally produced in the body. Experimental evidence indicates that this toxic gas, CO, exerts cytoprotective properties related to cellular stress including the heart and is being assessed for its cytoprotective and cytotherapeutic properties. While survival of adult cardiomyocytes depends on oxidative phosphorylation (survival and resulting cardiac function is impaired by mitochondrial damage), mitochondrial biogenesis is modified by the heme oxygenase-1/CO system and can result in promotion of mitochondrial biogenesis by associating mitochondrial redox status to the redox-active transcription factors. It has been suggested that the heme oxygenase-1/CO system is important in differentiation of embryonic stem cells and maturation of cardiomyocytes which is thought to mitigate progression of degenerative cardiovascular diseases. Effects on other cardiac cells are being studied. Acute exposure to air pollution (and, therefore, CO) is associated with cardiovascular mortality, myocardial infarction, and heart failure, but changes in the endogenous heme oxygenase-1 system (and, thereby, CO) positively affect cardiovascular health. We will review the effect of CO on heart health and function in this article.

It has been revealed that the cause of senescence and diseases is associated with the reactive oxygen species “hydroxyl radicals” (·OH). Senescence and diseases may be overcome as long as we can scavenge •OH mostly produced in mitochondria. It is one and only one “molecular hydrogen” (H₂) that can both penetrate into the mitochondria and scavenge the •OH. The H₂ in the body can function in disease prevention and recovery. H₂ gas is explosive so that a safe hydrogen inhaler has to be developed for home use. We would like to advocate the great use of H₂.

Glioma is one of the most frequent primary brain tumors. Currently, the most common therapeutic strategy for patients with glioma is surgical resection combined with radiotherapy or/and adjuvant chemotherapy. However, due to the metastatic and invasive nature of glioma cells, the recurrence rate is high, resulting in poor prognosis. In recent years, gas therapy has become an emerging treatment. Studies have shown that the proliferation, metastasis and invasiveness of glioma cells exposed to anesthetic gases are obviously inhibited. Therefore, anesthetic gas may play a special therapeutic role in gliomas. In this review, we aim to collect existing research and summarize the rules of using anesthetic gases on glioma, providing potential strategies for further clinical treatment.

Acute or chronic inflammatory reactions aim to control lesions, resist to pathogens attack and repair damaged tissue. The therapeutic administration of ozone known as ozone therapy appears as a possible treatment for tissue repair, as it promotes the healing of wounds. It has bactericidal, antiviral and antifungal properties and has been used as a therapeutic resource to treat inflammation. The objective was to carry out an integrative review regarding the use of ozonated oil in acute and chronic inflammations. The keywords “ozone therapy,” “inflammation” and “ozone” were used in the Portuguese, Spanish and English languages. The paper selection was based on inclusion and exclusion criteria. In total, 28 articles were selected. It has been seen that ozonated oil is effective in healing cutaneous wounds. The beneficial effects are due to the healing of wounds, due to the reduction of microbial infection, debridement effect, modulation of the inflammatory phase, stimulation to angiogenesis as well as biological and enzymatic reactions that favor the oxygen metabolism, improving the wound cicatrization. In addition to promoting healing, ozonated oil reduces symptoms related to skin burns, prevents post-lesion hyperpigmentation, and reduces the pain of aphthous ulcers. Therefore, ozonated oil represents an effective and inexpensive therapeutic alternative that must be implanted in the public health system.