Medical Gas Research最新文献

Cardiovascular diseases remain the leading cause of death worldwide, underscoring the urgent need for additional therapeutic strategies to reduce their mortality rates. This review systematically outlines the historical development and recent advances of hyperbaric oxygen therapy in cardiovascular diseases, with a focus on its therapeutic mechanisms and clinical outcomes. Hyperbaric oxygen therapy enhances oxygen delivery to ischemic and reperfused tissues, promotes angiogenesis, and significantly suppresses oxidative stress, inflammatory cascades, and cardiomyocyte apoptosis, demonstrating multifaceted therapeutic potential in cardiovascular conditions. Specifically, hyperbaric oxygen therapy combined with reperfusion strategies has been shown to markedly improve left ventricular ejection fraction in acute myocardial infarction. In heart failure, it facilitates myocardial repair and enhances cardiac function. For arrhythmias, hyperbaric oxygen therapy effectively reduces the frequency and duration of premature ventricular contractions and paroxysmal tachycardia, while mitigating the risk of neurological complications following atrial fibrillation ablation. Furthermore, hyperbaric oxygen therapy preconditioning in cardiac surgery has demonstrated improvements in left ventricular stroke work, reductions in postoperative myocardial injury, and a decrease in related complications. Despite its promising applications, the widespread adoption of hyperbaric oxygen therapy remains hindered by the lack of standardized treatment protocols and high-quality evidence from rigorous clinical trials. In conclusion, this review underscores the potential value of hyperbaric oxygen therapy in the cardiovascular domain while highlighting the need for further optimization of therapeutic parameters and exploration of its synergistic effects with conventional therapies to provide clearer guidance for clinical implementation.

A substantial body of evidence indicates a positive correlation between dyslipidemia and an elevated risk of chronic kidney disease, with renal interstitial fibrosis frequently serving as a common pathway in the advanced stages of chronic kidney disease progression. Hydrogen has anti-inflammatory and antioxidant properties, and magnesium hydride nanoparticle is a material with high hydrogen storage capacity. Magnesium hydride -fortified feed is capable of releasing hydrogen gas steadily and continuously within the digestive tract. A 12-week high-fat diet significantly elevated the serum urea and creatinine levels in mice. In contrast, dietary addition of magnesium hydride demonstrated a notable protective effect against pathological conditions. Additionally, magnesium hydride -fortified feed was found to reduce renal fibrosis and thereby improve renal function. In support of these findings, an in vitro study utilizing human kidney cortical proximal tubule epithelial cells (HK-2 cells) exposed to palmitic acid under conditions mimicking a high-fat diet confirmed the renoprotective effects of magnesium hydride. Furthermore, the primary target phosphatase and tensin homologue deleted on chromosome 10 and the molecular mechanisms underlying the effects of magnesium hydride, specifically its ability to inhibit the transforming growth factor-beta -Smad family member 2 and 3 (Smad2/3) axis through downregulating the expression of phosphatase and tensin homologue deleted on chromosome 10, were elucidated. Additionally, overexpression of Hes family BHLH transcription factor 1 can negate the beneficial effects of magnesium hydride, suggesting that Hes family BHLH transcription factor 1 may serve as an upstream regulatory target in the context of the effects of magnesium hydride. In conclusion, this study demonstrated that magnesium hydride functions as a safe and effective hydrogen source capable of inhibiting the activation of the transforming growth factor-beta/Smad2/3 and protein kinase B/mechanistic target of rapamycin pathways by increasing the expression of phosphatase and tensin homologue deleted on chromosome 10. This mechanism counteracts the progression of high-fat diet-induced chronic renal damage.

Using medical gas detectors offers a promising and non-invasive approach for the early identification of diseases. This technique provides a less painful and more accessible alternative to traditional diagnostic methods. In the development of these new detection methods, the use of nanomaterials as gas sensors has proven advantageous due to their large surface areas, which enhance reactivity and sensitivity in identifying volatile compounds. To evaluate the behavior of nanomaterials when in contact with medical gases, ab initio computational simulations based on density functional theory have shown to be effective. This literature review presents studies that have applied density functional theory to investigate intermolecular interactions between specific nanosystems and gases, such as toluene, hydrogen sulfide, ammonia, and nitric oxide. These studies have yielded promising results related to adsorption and dissociation energies, electronic properties, energy gaps, bond lengths, and charge transfer, suggesting the potential of nanomaterials as effective sensors for medical gas detection.

The present study aimed to assess the mechanisms of flow-induced dilation (FID) altered by acute/intermittent hyperbaric oxygenation (HBO 2 ) in isolated middle cerebral arteries of healthy male Sprague‒Dawley rats ( n = 96) and randomized to the Ac-HBO 2 group (exposed to a single HBO 2 session, 120 minutes of 100% O 2 at 2.0 bars), the 4Dys-HBO 2 group (4 consecutive days of single HBO 2 sessions, analyzed on the fifth day), and the CTRL (untreated) group. Results demonstrated increased vascular oxidative stress and decreased vascular nitric oxide bioavailability, as measured by direct fluorescence microscopy, leading to attenuated FID in the Ac-HBO 2 group compared with the CTRL and 4Dys-HBO 2 groups. Superoxide scavenging restored FID. Moreover, the increased expression of antioxidative enzymes in the cerebral vasculature in the 4Dys-HBO 2 group indicates the ability of intermittent HBO 2 to activate antioxidative mechanisms. Importantly, the results suggest a switch or at least activation of the compensatory mechanism of FID after HBO 2 from nitric oxide-dependent to epoxygenase metabolite-mediated via TRPV4 (transient receptor potential cation channel subfamily V member 4) and potassium channels, as demonstrated by increased protein expression of KCNMB1 (potassium calcium-activated channel subfamily M regulatory beta subunit 1), TRPV4, and Kir2 (a component of the inward rectifier-type potassium channel Kir2) in the vasculature. Overall, acute HBO 2 modulates FID in cerebral vessels by increasing oxidative stress and altering the subsequent mechanisms of FID, which are mainly mediated by nitric oxide, while suppressing potassium and TRPV4 channel function/expression due to increased oxidative stress. Moreover, intermittent HBO 2 activates antioxidative mechanisms and the compensatory mechanism of FID from nitric oxide-dependent to epoxygenase metabolite-mediated mechanisms via TRPV4, KCNMB1 and Kir2.1.

Sevoflurane is a widely used inhalation anesthetic during the perioperative period. Recent studies have suggested that sevoflurane has an enteroprotective effect, but its mechanism is unclear. To explore the mechanism of sevoflurane in intestinal ischemia‒reperfusion injury, an intestinal ischemia‒reperfusion injury mouse model was established. First, intestinal ischemia‒reperfusion injury was compared between aged and young mice. The results showed that intestinal ischemia‒reperfusion injury caused pathological intestinal injury and disrupted the intestinal mucosal barrier. The aged mice had more severe intestinal ischemia‒reperfusion injury than the young mice and therefore had a lower survival rate. The aged mice subsequently received sevoflurane via inhalation. Sevoflurane alleviated the pathological injury to the intestinal mucosa and repaired the function of the intestinal mucosal barrier in aged mice, thus increasing the level of intestinal mucosal hypoxia-inducible factor-1α and improving the survival rate of aged mice. However, preoperative administration of the hypoxia-inducible factor-1α inhibitor BAY87-2243 could counteract the enteroprotective effect of sevoflurane and lower the expression level of heme oxygenase-1, a downstream antioxidant enzyme of hypoxia-inducible factor-1α. Our findings suggest that sevoflurane alleviates intestinal ischemia‒reperfusion injury in aged mice by repairing the intestinal mucosal barrier through the activation of hypoxia-inducible factor-1α/heme oxygenase-1, providing a new target for the treatment of intestinal ischemia‒reperfusion injury in aged mice.

Initially, molecular hydrogen was considered a physiologically inert and non-functional gas. However, experimental and clinical studies have shown that molecular hydrogen has anti-inflammatory, anti-apoptotic, and strong selective antioxidant effects. This study aimed to evaluate the effects of 60 minutes of molecular hydrogen inhalation on respiratory gas analysis parameters using a randomized, double-blind, placebo-controlled, crossover design. The study was conducted at Faculty of Physical Culture, Palacký University Olomouc from September 2022 to March 2023. Twenty, physically active female participants aged 22.1 ± 1.6 years who inhaled either molecular hydrogen or ambient air through a nasal cannula (300 mL/min) for 60 minutes while resting were included in this study. Metabolic response was measured using indirect calorimetry. Breath-by-breath data were averaged over four 15-minute intervals. Compared with placebo (ambient air), molecular hydrogen inhalation significantly decreased respiratory exchange ratio and ventilation across all intervals. Furthermore, the change in respiratory exchange ratio was negatively correlated with body fat percentage from 30 minutes onwards. In conclusion, 60 minutes of resting molecular hydrogen inhalation significantly increased resting fat oxidation, as evidenced by decreased respiratory exchange ratio, particularly in individuals with higher body fat percentages.

Many patients experience long-term cognitive dysfunction after subarachnoid hemorrhage (SAH), and effective treatments are currently lacking. Carbon dioxide (CO 2 ), an inexpensive and easily produced gas, forms carbonic acid when dissolved in water. Studies have suggested that hypercapnia may have neuroprotective effects. However, the optimal concentration of CO 2 for therapeutic inhalation is still unclear. This study aimed to investigate the effects of various CO 2 concentrations on cognitive function in SAH rats and to explore the potential molecular mechanisms involved. In this study, we established a rat model of SAH by endovascular perforation of the internal carotid artery. The rat models inhaled CO 2 at concentrations of 10%, 20%, or 30%, for 1 hour after modeling. The results showed that inhalation of 10% CO 2 improved cortical blood flow following SAH, while higher concentrations of CO 2 (20% and 30%) worsened cortical hypoperfusion. The partial pressure of CO 2 did not change 1 hour after SAH, but it significantly increased with the inhalation of 10% CO 2 . Additionally, 10% CO 2 effectively inhibited neuronal apoptosis, enhanced locomotor activity, and improved memory and learning abilities in SAH rats. Moreover, 10% CO 2 upregulated the phosphorylation of phosphatidylinositol 3 kinase) and protein kinase B, increased the expression of Bcl-2, and decreased the expression of Bax. In conclusion, inhaling 10% CO 2 restores cerebral perfusion, inhibits neuronal apoptosis, and improves cognitive function in SAH rats. In contrast, higher concentrations of CO 2 led to worsened hypoperfusion. The neuroprotective effect of 10% CO 2 may occur through the activation of the phosphatidylinositol 3-kinase/protein kinase B signaling pathway.