Medical Gas Research最新文献

JOURNAL/mgres/04.03/01612956-202609000-00005/figure1/v/2026-01-06T135433Z/r/image-tiff Sevoflurane is a new type of halogen inhalation anesthetic gas with a rapid induction and emergence. It is widely used for general anesthesia. Previous studies have demonstrated that sevoflurane postconditioning alleviates cerebral ischemia-reperfusion injury and enhances the tolerance of the brain to ischemia and hypoxia. However, whether sevoflurane postconditioning can reduce cerebral ischemia-reperfusion injury caused by hemorrhagic shock and resuscitation and the underlying mechanism are unclear. The present study established cerebral ischemia-reperfusion injury models through an in vivo hemorrhagic shock and resuscitation method in C57BL/6 mice and an in vitro oxygen-glucose deprivation/reoxygenation method in HT22 cells. After hemorrhagic shock and resuscitation treatment, the mice developed significant spatial learning and memory impairments accompanied by aggravated cerebral infarction, whereas sevoflurane postconditioning significantly improved these effects. After in vitro oxygen-glucose deprivation/reoxygenation, the survival rate of HT22 cells was decreased, the apoptosis rate was increased, the expression of silent information regulatory factor 1 was decreased, and the expressions of hypoxia-inducible factor 1α, NOD-like receptor protein 3, gasdermin D, caspase-1, and interleukin-1β were increased. Sevoflurane postconditioning inhibited oxygen-glucose deprivation/reoxygenation-induced changes. Following silent information regulatory factor 1 knockdown by small interfering RNA, the cytoprotective effects of sevoflurane postconditioning were significantly attenuated. These findings suggest that the anesthetic gas sevoflurane postconditioning ameliorates hemorrhagic shock and resuscitation-induced cognitive impairment. This may be mediated by the silent information regulatory factor 1/hypoxia-inducible factor 1α/NOD-like receptor protein 3 pathway.

JOURNAL/mgres/04.03/01612956-202609000-00001/figure1/v/2026-01-06T135433Z/r/image-tiff Delayed neurocognitive recovery is an important cause of morbidity and disability after surgery. This perspective randomized clinical study mainly explored the effects of different fractions of inspired oxygen (FiO2) on Delayed neurocognitive recovery in patients with one-lung ventilation. Between December 2021 and July 2022, 88 patients aged 30-70 years who underwent thoracoscopic pulmonary lobectomy with one-lung ventilation at the First Affiliated Hospital of Sun Yat-sen University, China, were divided into two groups. One group received 70% FiO2 (70% FiO2 group), while the other received 100% FiO2 (100% FiO2 group) during one-lung ventilation. The outcomes were the incidence of delayed neurocognitive recovery on postoperative days 1 and 3, the incidence of cerebral oxygen desaturation during surgery, and the perioperative level of blood gas, inflammatory response, and oxidative stress. The incidence rates of cerebral oxygen desaturation and delayed neurocognitive recovery on postoperative days 1 and 3 were similar between the two groups. Compared with the 70% FiO2 group, in the 100% FiO2 group, the oxygenation index was significantly higher at 30 minutes after one-lung ventilation and 60 minutes after one-lung ventilation, and the arterial partial pressure of carbon dioxide was significantly lower at 15, 30 and 60 minutes after one-lung ventilation, while that of superoxide dismutase was significantly lower at 15 minutes after one-lung ventilation. Compared with 70% FiO2, 100% FiO2 did not increase the incidence of delayed neurocognitive recovery on days 1 and 3 post-operatively in patients with one-lung ventilation.

JOURNAL/mgres/04.03/01612956-202609000-00003/figure1/v/2026-01-06T135433Z/r/image-tiff Lumbar disc herniation complicated by lumbar spinal stenosis is a common degenerative condition in spinal surgery, particularly among middle-aged and elderly individuals. Conservative treatments or open surgery are commonly used but often have limited efficacy or significant risks, especially in older patients. Oxygen-ozone therapy, known for its mechanical decompression, anti-inflammatory, analgesic, and neuroprotective effects, is gaining attention as a minimally invasive treatment for lumbar disc herniation, offering an alternative to traditional treatments. Therefore, this study aimed to evaluate the clinical therapeutic effect of computed tomography-guided percutaneous oxygen-ozone injection on lumbar disc herniation complicated by lumbar spinal stenosis. This retrospective study analyzed the clinical outcomes of 47 patients with lumbar disc herniation complicated by lumbar spinal stenosis who were treated between September 2023 and February 2024. Patients were divided into two groups: the ozone group received computed tomography-guided percutaneous oxygen-ozone injection ( n = 25), and the caudal epidural steroid injection group underwent ultrasound-guided ( n = 22). Pain relief and functional outcomes were assessed preoperatively and at 1 day, 1 month, 3 months, and 6 months postoperatively using the visual analog scale, and Oswestry Disability Index and modified MacNab criteria. Both groups showed significant reduction in visual analog scale and Oswestry Disability Index at 1 day and 1 month postoperatively compared with preoperatively ( P < 0.05), with the ozone group demonstrating more pronounced improvements than the caudal epidural steroid injection group. At 3 months, although further improvement was observed in both groups, the differences in visual analog scale and Oswestry Disability Index between the two groups were not statistically significant ( P > 0.05). By 6 months, the ozone group showed significantly greater improvements than the caudal epidural steroid injection group ( P < 0.05). The total effective rate based on modified MacNab criteria increased over time in both groups. Although the ozone group exhibited a slightly higher rate, the difference was not statistically significant ( P > 0.05). Computed tomography-guided oxygen-ozone injection provides sustained pain relief and functional recovery in lumbar disc herniation with lumbar spinal stenosis, demonstrating superior long-term efficacy to epidural steroids.

Ischemia-reperfusion injury, a critical pathophysiological phenomenon in multiple organ systems, remains a formidable therapeutic challenge in clinical practice. As the third endogenously produced gaseous signaling molecule, hydrogen sulfide (H2S) has emerged as a pivotal regulator of diverse physiological processes and pathological cascades. Accumulating evidence indicates that H2S exerts cytoprotective effects against cerebral, cardiac, hepatic, renal, and pulmonary ischemia-reperfusion injuries through multifaceted mechanisms involving mitigation of inflammatory responses, suppression of oxidative stress, modulation of autophagic processes, and inhibition of apoptotic pathways. This comprehensive review systematically examines the endogenous biosynthesis and metabolic regulation of H2S, while elucidating the molecular mechanisms underlying its organ protective effects during ischemia-reperfusion injury. Particular emphasis is placed on the therapeutic potential of H2S synthase isoforms and bioactive metabolites in ischemic pathophysiology. Notably, recent advances in H2S pharmacology have catalyzed the development of novel H2S donors and slow-releasing compounds, including HSDF-NH2, S-allyl cysteine, S-propargyl cysteine, and S-(4-fluorobenzyl)-N-(3,4,5-trimethoxybenzoyl)-L-cysteine. These pharmacological innovations demonstrate enhanced tissue specificity and controlled release kinetics, paving the way for clinical translation of H2S-based therapeutics in ischemia-reperfusion injury management. Future research directions should focus on optimizing drug delivery systems and elucidating the spatiotemporal dynamics of H2S signaling in organ-specific ischemia-reperfusion pathologies.

Facts Hydrogen sulfide (H 2 S) is a key endogenous signaling molecule involved in cardiovascular, neurological, respiratory, and cancer-related pathophysiology. Dynamic monitoring of trace H 2 S levels provides critical insight into disease initiation, progression, and therapeutic response. Emerging spectroscopic techniques, particularly quartz-enhanced photoacoustic spectroscopy (QEPAS), offer unprecedented sensitivity and selectivity for H 2 S detection in biological samples. Breath and skin gas analysis represent promising non-invasive approaches for translating H 2 S sensing from bench to bedside. Open questions What are the precise physiological thresholds of H 2 S concentration that differentiate healthy and pathological states across diverse organ systems? How can QEPAS and other spectroscopic methods be miniaturized and standardized for reliable, real-time clinical use? Can H 2 S modulation be safely targeted in therapy without disturbing other gasotransmitter pathways (nitric oxide and carbon monoxide)? What regulatory and validation frameworks are required to translate H 2 S-based diagnostics into routine clinical practice? Hydrogen sulfide, as a critical endogenous gasotransmitter, plays a significant role in the pathophysiology of various diseases, including cardiovascular diseases, neurodegenerative disorders, respiratory dysfunctions, and cancer. The dynamic fluctuations in hydrogen sulfide concentration are closely associated with the onset and progression of these conditions. The precise monitoring of trace amounts of hydrogen sulfide in biological samples holds substantial value for elucidating disease mechanisms, developing diagnostic biomarkers, and enabling targeted therapies. This review provides a comprehensive overview of the current advancements in hydrogen sulfide detection technologies in medical applications, with a particular focus on the groundbreaking potential of novel spectroscopic techniques in medical diagnostics. This paper through an integrated research approach that bridges hydrogen sulfide biology, sensing technology, and clinical applications-particularly by utilizing breath and skin gas analysis as windows into metabolic and disease states. A core innovation presented in this work is the proposed optimization of the hydrogen sulfide-quartz-enhanced photoacoustic spectroscopy technique for medical settings, which provides a transformative tool for non-invasive disease screening, precise detection, and targeted therapeutic research. The ultimate goal is to bridge the gap between basic research, sensor technology, and clinical needs, driving innovative applications of hydrogen sulfide in precision medicine.

Long-term oxygen therapy is used to treat of chronic respiratory diseases with chronic hypoxia. To date, long-term oxygen therapy has significantly contributed to the relief of dyspnea in the daily life of patients with chronic respiratory disease and chronic hypoxemia. Chronic hypoxia is a possible cause of cognitive impairment, and patients with chronic respiratory disease using long-term oxygen therapy with severe chronic hypoxia may be at a higher risk of cognitive impairment than patients using non-long-term oxygen therapy. Cognitive impairment in patients with chronic respiratory disease can lead to a decline in treatment adherence, including medication usage, health care check-ups, and smoking cessation efforts, which contribute to disease progression. In addition, patients using long-term oxygen therapy require oxygen delivery equipment. Operating oxygen delivery equipment is difficult for patients with cognitive impairment, and the inability to use long-term oxygen therapy properly is a serious challenge that can affect their life expectancy. Patients with chronic respiratory disease who use long-term oxygen therapy may be more affected by cognitive impairment than non-long-term oxygen therapy patients. Several review articles have addressed cognitive impairment in patients with chronic respiratory disease; however, none specifically focus on patients with chronic respiratory disease using long-term oxygen therapy. This narrative review describes the current knowledge and future issues regarding cognitive impairment in patients with chronic respiratory disease using the long-term oxygen therapy.