Medical Gas Research最新文献

Necrotizing enterocolitis is the most common gastrointestinal emergency in newborns. Its etiology involves bacterial colonization, enteral formula feeding, and hypoxic-ischemic injury. The pathology of necrotizing enterocolitis is characterized by coagulation necrosis and bacterial overgrowth, with limited preventative methods available. In addition to affecting the intestine, this disease has long-term neurological consequences for survivors. Hyperbaric oxygen therapy, a well-established treatment for soft tissue infections and injuries caused by hypoperfusion, may serve as an alternative approach for necrotizing enterocolitis. In this study, a necrotizing enterocolitis model was developed in newborn Sprague-Dawley rat pups through the administration of a hyperosmolar formula, combined with exposure to hypothermia and hypoxia. The rat pups received hyperbaric oxygen therapy sessions at 3 absolute atmospheres for 2 hours each, which were administered over 1 or 2 days. The results demonstrated that hyperbaric oxygen therapy significantly reduced mortality in rats with necrotizing enterocolitis and preserved the number of brain cells in the hippocampus. Additionally, hyperbaric oxygen therapy increased the expression of nitric oxide synthase, intestinal fatty acid-binding protein, and superoxide dismutase 3 in the intestine, and elevated superoxide dismutase 3 levels in the hippocampus. These findings suggest that hyperbaric oxygen therapy not only reduces mortality but also mitigates the severity of intestinal and brain lesions in experimental necrotizing enterocolitis, preserving intestinal cell integrity and enhancing antioxidant mechanisms.

Heart failure (HF) is a leading cause of mortality among patients with cardiovascular disease and is often associated with myocardial apoptosis and endoplasmic reticulum stress (ERS). While hydrogen has demonstrated potential in reducing oxidative stress and ERS, recent evidence suggests that magnesium may aid in hydrogen release within the body, further enhancing these protective effects. This study aimed to investigate the cardioprotective effects of magnesium in reducing apoptosis and ERS through hydrogen release in a rat model of isoproterenol (ISO)-induced HF. Magnesium was administered orally to ISO-induced HF rats, which improved cardiac function, reduced myocardial fibrosis and cardiac hypertrophy, and lowered the plasma levels of creatine kinase-MB, cardiac troponin-I, and N-terminal B-type natriuretic peptide precursor in ISO-induced HF rats. It also inhibited cardiomyocyte apoptosis by upregulating B-cell lymphoma-2, downregulating Bcl-2-associated X protein, and suppressing ERS markers (glucose-related protein 78, activating transcription factor 4, and C/EBP-homologous protein). Magnesium also elevated hydrogen levels in blood, plasma, and cardiac tissue, as well as in artificial gastric juice and pure water, where hydrogen release lasted for at least four hours. Additionally, complementary in vitro experiments were conducted using H9C2 cardiomyocyte injury models, with hydrogen-rich culture medium as the intervention. Hydrogen-rich culture medium improved the survival and proliferation of ISO-treated H9C2 cells, reduced the cell surface area, inhibited apoptosis, and downregulated ERS pathway proteins. However, the protective effects of hydrogen were negated by tunicamycin (an inducer of ERS) in H9C2 cells. In conclusion, magnesium exerts significant cardioprotection by mitigating ERS and apoptosis through hydrogen release effects in ISO-induced HF.

In recent years, medical gas therapy has emerged as a promising approach for treating neuropathic pain. This review article aimed to investigate the therapeutic effects of medical gas therapy on neuropathic pain and its underlying mechanisms, thereby providing a theoretical foundation for clinical practice. A literature search was conducted using the Web of Science Core Collection database. Co-occurrence analysis of keywords revealed that terms including "neuropathic pain," "nitric oxide," "nitric oxide synthase," "pain," and "ozone" frequently appeared. Cluster analysis grouped these keywords into four primary categories: intervertebral disc disease and gas therapy, mechanisms of neuropathic pain and gas interventions, the role of nitric oxide in modulating neuropathic pain and gas therapy, and the effects of gas therapy on mental disorders in the context of neuropathic pain treatment. The analysis of highly cited literature in the field of medical gas therapy for neuropathic pain emphasizes the crucial roles of nitric oxide and nitric oxide synthase in nerve injury and pain. Various types of gas therapy, including oxygen-ozone therapy and nitric oxide-related therapies, show promise in treating pain following peripheral nerve injury. Oxidative stress and nitric oxide are crucial regulatory factors in the pain signaling associated with trigeminal neuralgia. Ozone therapy alleviates trigeminal pain by inhibiting inflammatory responses, reducing oxidative stress, and modulating neurotransmitter release. Novel nanomaterials, such as manganese oxide nanoparticles, have also demonstrated potential in scavenging free radicals and alleviating sciatic nerve pain. Ozone therapy has shown good clinical efficacy in treating lumbar disc herniation and sciatica, whereas both ozone therapy and hyperbaric oxygen therapy have demonstrated effectiveness and safety in managing postherpetic neuralgia. In conclusion, medical gas therapy for neuropathic pain primarily includes oxygen-ozone therapy, nitric oxide-related therapies, hydrogen sulfide-related therapies, and hyperbaric oxygen therapy. While these therapies exhibit efficacy in managing neuropathic pain, further research is necessary to elucidate their mechanisms of action and safety profiles. Although hyperbaric oxygen therapy and ozone therapy have already been implemented in clinical research, other types of gas therapy are still in the animal testing phase. Therefore, future studies should focus on conducting more multicenter, large-sample randomized controlled trials to accelerate clinical translation and provide more effective treatment options for patients suffering from neuropathic pain.

Metformin is the first-line treatment for type 2 diabetes mellitus. Type 2 diabetes mellitus is associated with decreased nitric oxide bioavailability, which has significant metabolic implications, including enhanced insulin secretion and peripheral glucose utilization. Similar to metformin, nitric oxide also inhibits hepatic glucose production, mainly by suppressing gluconeogenesis. This review explores the combined effects of metformin and nitric oxide on hepatic gluconeogenesis and proposes the potential of a hybrid metformin-nitric oxide drug for managing type 2 diabetes mellitus. Both metformin and nitric oxide inhibit gluconeogenesis through overlapping and distinct mechanisms. In hepatic gluconeogenesis, mitochondrial oxaloacetate is exported to the cytoplasm via various pathways, including the malate, direct, aspartate, and fumarate pathways. The effects of nitric oxide and metformin on the exportation of oxaloacetate are complementary; nitric oxide primarily inhibits the malate pathway, while metformin strongly inhibits the fumarate and aspartate pathways. Furthermore, metformin effectively blocks gluconeogenesis from lactate, glycerol, and glutamine, whereas nitric oxide mainly inhibits alanine-induced gluconeogenesis. Additionally, nitric oxide contributes to the adenosine monophosphate-activated protein kinase-dependent inhibition of gluconeogenesis induced by metformin. The combined use of metformin and nitric oxide offers the potential to mitigate common side effects. For example, lactic acidosis, a known side effect of metformin, is linked to nitric oxide deficiency, while the oxidative and nitrosative stress caused by nitric oxide could be counterbalanced by metformin's enhancement of glutathione. Metformin also amplifies nitric oxide -induced activation of adenosine monophosphate-activated protein kinase. In conclusion, a metformin-nitric oxide hybrid drug can benefit patients with type 2 diabetes mellitus by enhancing the inhibition of hepatic gluconeogenesis, decreasing the required dose of metformin for maintaining optimal glycemia, and lowering the incidence of metformin-associated lactic acidosis.

JOURNAL/mgres/04.03/01612956-990000000-00064/figure1/v/2025-10-02T154314Z/r/image-tiff Video-assisted thoracoscopic surgery during one-lung ventilation may impair cerebral oxygen balance and increase the risk of postoperative cognitive impairment. This perspective study aimed to analyze the effect of non-intubated anesthesia with preserved spontaneous breathing on cerebral oxygen saturation and postoperative cognitive dysfunction in elderly patients with lung cancer during video-assisted thoracoscopic surgery. A total of 104 elderly patients with lung cancer who underwent video-assisted thoracoscopic surgery in Jinhua Municipal Central Hospital from January 2023 to October 2024 were selected, and they were randomly divided into non-intubated group (n = 52) and intubated group (n = 52). The cerebral oxygen saturation, postoperative cognitive dysfunction incidence and laboratory indicators were compared between the two groups. At last, the influencing factors to postoperative cognitive dysfunction were analyzed by multivariate Logistic regression. The cerebral oxygen saturation was higher at 15, 30 and 60 minutes after operation than at the beginning of anesthesia, and moreover, it in the non-intubation group were significantly higher than that in the intubated group (P < 0.05). At 72 hours after operation, the levels of tumor necrosis factor-α, interleukin-6 and S100β in serum were lower than those before operation, and the levels in the non-intubated group were significantly lower than those in the intubated group; the levels of epinephrine, atrial natriuretic peptide and cortisol in serum were higher than those before operation, and they in the non-intubated group were significantly more than those in the intubated group (P < 0.05). The total incidence of postoperative cognitive dysfunction in intubation group was higher than that in the non-intubated group within 2 months after operation (P < 0.05). Multivariate Logistic regression analysis showed that age (odds ratio = 1.729), cerebral oxygen saturation at 30 minutes after operation (odds ratio = 0.727) and cerebral oxygen saturation at 60 minutes after operation (odds ratio = 0.734) were independent influencing factors for postoperative cognitive dysfunction (all P < 0.05). Non-tracheal intubation anesthesia with preserved spontaneous breathing can increase cerebral oxygen saturation, reduce systemic inflammatory response and stress response, and decrease the incidence of postoperative cognitive dysfunction in elderly patients with lung cancer undergoing video-assisted thoracoscopic surgery, which is conducive to promoting postoperative recovery in such patients.

Oxygen supplementation is widely used to enhance oxygen delivery and to treat or prevent hypoxia; however, it requires careful management to avoid the harmful effects of excessive oxygen exposure. Both hyperoxia (inspiratory oxygen fraction exceeding 0.21) and hyperoxemia (arterial oxygen tension oxygen partial pressure [PaO2] > 100 mmHg) can contribute to lung injury, promote systemic vasoconstriction, and increase the production of reactive oxygen species, which can impair macromolecular and cellular functions. Conversely, in certain situations, hyperoxemia may provide benefits, such as hemodynamic stabilization in hyperdynamic shock, immunomodulation, and bactericidal effects. The literature presents conflicting evidence regarding the impact of different oxygen targets (i.e., PaO2 and/or peripheral saturation of oxygen [SpO2]) on both short- and long-term outcomes in patients with acute critical conditions, such as acute respiratory distress syndrome, sepsis, cardiac arrest, and acute central nervous system injuries. These discrepancies may stem from the small differences between the oxygenation targets used in randomized trials, the physiological limitations of PaO2 and SpO2 targets, which reflect blood oxygen content rather than oxygen delivery, the lack of measurements of microvascular function or oxygen delivery, and the heterogeneity in treatment response. Furthermore, advanced analytical methods (e.g., machine learning) are emerging as promising tools to implement population enrichment strategies. By refining patient sub-group identification, these approaches can significantly optimize precision medicine, enabling more personalized oxygen therapy tailored to individual patient characteristics.