Medical Gas Research最新文献

Traumatic central nervous system injuries encompass brain and spinal cord injuries. Recent studies have identified hydrogen sulfide (H₂S) as a potent endogenous gasotransmitter with multifaceted roles in neuroprotection and central nervous system repair. In this systematic review, we explore the mechanisms and therapeutic potential of H₂S in traumatic central nervous system injuries, emphasizing its anti-inflammatory, antioxidant, and anti-apoptotic properties. H₂S suppresses inflammation by modulating the nuclear factor-kappa B pathway, shifting microglial polarization to a reparative phenotype. Further, it mitigates oxidative stress by activating the nuclear factor erythroid 2-related factor 2 and mechanistic target of the rapamycin pathway, and inhibiting glutamate-mediated damage. Additionally, H₂S regulates cell death by inhibiting apoptosis, ferroptosis, pyroptosis, and autophagy while promoting axonal growth and microvascular integrity. Emerging H₂S delivery strategies, including slow-releasing donors such as GYY4137 and advanced hydrogel-based systems, address challenges in achieving sustained and targeted therapeutic effects. Although preclinical evidence has demonstrated the promise of H₂S-based therapies, further research is required to optimize delivery methods, investigate concentration-dependent effects, and validate clinical efficacy. This review provides a comprehensive foundation for advancing H₂S as a therapeutic agent in traumatic central nervous system injuries.

JOURNAL/mgres/04.03/01612956-202606000-00001/figure1/v/2025-08-18T154854Z/r/image-tiff Pulmonary hypertension can lead to hemodynamic instability and worsen the outcome after the repair of cyanotic congenital heart disease with decreased pulmonary blood flow. However, the safety and effectiveness of targeted therapy, such as inhaled nitric oxide, remain controversial. This retrospective cohort study included patients who underwent corrective repair for tetralogy of Fallot, double outlet right ventricle, or pulmonary atresia with ventricular septal defect with hypoplastic pulmonary vasculature at Fuwai Hospital between 2014 and 2021. Patients were divided into a regular treatment group and a combined treatment group depending on whether inhaled nitric oxide was prescribed. The improvement in low cardiac output syndrome within 24 hours after surgery and the main clinical outcomes during hospitalization were compared between the two groups after 1:1 propensity score matching. Compared with those in the regular treatment group, both the incidence of low cardiac output syndrome and the rate of renal replacement therapy were lower in the combined treatment group. Inhaled nitric oxide therapy is effective in the treatment of patients with pulmonary hypertension after corrective repair of cyanotic congenital heart disease.

Although hyperbaric oxygen therapy (HBOT) is promising for the alleviation of limb trauma or crush muscle injuries, critical examination of the state of related science is lacking. We conducted a scoping review and evaluation of HBOT on muscle injury in preclinical models. A search of PubMed and Web of Science databases yielded 157 reports published from the start of the databases until November 7, 2024, which narrowed to 19 after removing duplicates, non-muscle studies, and dissertations/reviews. The studies involved mice or rats treated with tourniquets or exposed to a myotoxic agent (bupivacaine and cardiotoxin) or crush to induce muscle injury. HBOT counteracted metabolic effects and had differential effects on oxidative stress in the tourniquet model. Overall, HBOT promoted or quickened muscle regeneration initiated by myotoxic agents and crush. These findings also indicate that HBOT benefits may persist, and early initiation of HBOT is important. However, more sessions do not always yield better outcomes. The evaluation of the state of the science revealed that the inclusion of females in these studies is limited, and milder pressure levels have been undertested, which may be important for fewer adverse effects and access. Future research in these and other areas may lead to increased use and acceptability of HBOT for the treatment of limb trauma or crush muscle injuries.

JOURNAL/mgres/04.03/01612956-202606000-00005/figure1/v/2025-08-18T154854Z/r/image-tiff Low-flow anesthesia aims to minimize anesthetic gas consumption while maintaining adequate anesthesia. To examine the effects of minimal-flow anesthesia on perioperative lung dynamics and postoperative pulmonary function tests, a prospective, randomized controlled study was conducted between October 2023 and March 2024 at Atatürk University. A total of 66 patients (15 males, 45 females) with confirmed American Society of Anesthesiologists (ASA) grade I-II, aged 18-65 years, and scheduled for elective laparoscopic cholecystectomy were included in the study. Patients were randomized into two groups: MeFA (medium flow anesthesia, 2 L/min fresh gas flow) and MiFA (minimal flow anesthesia, 0.5 L/min fresh gas flow). In both groups, dynamic compliance values, peak inspiratory pressure (PIP) values, total inhalation anesthetic drug consumption, total remifentanil drug consumption, duration of anesthesia, duration of surgery, and spirometry test results were recorded. Respiratory measurements were recorded at the 5th minute after intubation (T1), 5th (T2), 10th (T3), 30th (T4), and 60th (T5) minutes after surgical incision and immediately after the surgical suturing (T6) pulse. There was no significant difference in compliance or PIP values between the groups from T1 to T5 (P > 0.05). However, at T6, the MeFA group exhibited a significant decrease in compliance and an increase in PIP compared with the MiFA group (P < 0.05). Additionally, significant differences in compliance and PIP values were found across all time intervals compared with those at T1, except for the T5-6 compliance values in the MiFA group (P < 0.001). No significant difference in respiratory function test values was noted between the groups (P > 0.05). The MiFA group exhibited a relatively milder reduction in compliance values and a lesser elevation in PIP values. Compared with medium-flow anesthesia, minimal-flow anesthesia may help mitigate perioperative lung function deterioration. These findings suggest potential benefits in preserving lung mechanics, warranting further research. This trial was registered at clinicaltrials.gov (identifier No. NCT06055335, registered March 25, 2023).

Hyperbaric oxygen therapy, as a unique non-drug treatment method, is gradually gaining wide recognition by clinicians. In the field of neurosurgery, there is conclusive evidence that hyperbaric oxygen has significant positive effects on the treatment of craniocerebral trauma, cerebrovascular diseases, intracranial infections and intracranial tumors. This review focuses on the mechanism and application of hyperbaric oxygen therapy in neurosurgery.

Given that chronic hyperglycemia in type 2 diabetes induces functional cellular hypoxia by constraining the release of oxygen from hemoglobin, a hypothesis of glycohypoxia was proposed. This hypothesis positions glucose as a novel regulator of respiratory dynamics beyond its metabolic functions. This narrative review aims to unravel the molecular framework of glycohypoxia, reinterpret diabetic complications from a hypoxia-centric perspective, highlight underrecognized hypoxic interconnections, and advocate for innovative hypoxia-targeted therapeutic strategies to transform diabetes management. The glycohypoxia hypothesis illuminates type 2 diabetes as a disorder of impaired oxygen delivery. According to this hypothesis, non-enzymatic glycation of hemoglobin may yield glycated hemoglobin via covalent binding to β-chain N-terminal valine, potentially locking hemoglobin in a high-affinity state, shifting the oxyhemoglobin dissociation curve leftward (the partial pressure of oxygen at which hemoglobin is 50% saturated, P50≍23 mmHg vs. 26.8 mmHg), and restricting oxygen unloading, possibly undermining Bohr and Haldane effects. Hyperglycemia may exacerbate this process by driving osmotic stress through glucose transporter-mediated influx, aquaporin-1/3 activation, and sodium-potassium adenosine triphosphatase engagement, resulting in cellular swelling. The polyol pathway, catalyzed by aldose reductase, may convert glucose into sorbitol. This process depletes nicotinamide adenine dinucleotide phosphate and generates reactive oxygen species via nicotinamide adenine dinucleotide phosphate oxidase, thereby impairing glycocalyx integrity and mitochondrial function. Insulin resistance may further compromise glucose transporter type 4 translocation, perpetuating hyperglycemia and limiting adenosine triphosphate synthesis. Overall, these cascades may activate hypoxia-inducible factor-1α, elevate vascular endothelial growth factor and transforming growth factor-β, and promote fibrosis and angiogenesis, contributing to complications, such as retinopathy, neuropathy, nephropathy, cardiomyopathy, and potentially cancer, via Warburg-like metabolic shifts. Therefore, anti-glycation agents (e.g., aminoguanidine), polyol inhibitors (e.g., epalrestat), glucose transporter type 4 agonists (e.g., fisetin), and 2,3-bisphosphoglycerate enhancers can restore oxygen unloading function, improve hyperglycemia, and treat diabetes.

In clinical studies, the partial pressure of oxygen (PaO2) and oxygen pulse saturation are the main variables used to assess blood oxygenation and define the threshold of hypoxia/hyperoxia and hypoxemia/hyperoxemia. Determination of the optimal oxygenation target has generated a lot of interest in recent years, mainly because of the potential risk of worse outcomes associated with hyperoxia, whereas the risk associated with hypoxia has been already well known. In this short narrative review, we recall some fundamental elements of physiology regarding the meaning of PaO2, the diffusion of oxygen to cells, the definitions of hyperoxemia and hyperoxia and the mechanisms of oxygen toxicity to provide a better understanding of these concepts, to which intensive care clinicians are frequently confronted. PaO2 provides only limited information about oxygen concentration carried by blood and does not allow to determine whether cells are exposed to hyperoxia. This should be considered for the design of future studies that aim to determine optimal oxygenation target and by clinicians for their daily practice.