In vivo studies of the therapeutic effects of argon in traumatic brain injury (TBI) are limited, and their results are contradictory. The aim of this study was to evaluate the effect of a three-hour inhalation of argon (70%Ar/30%O₂) after an open TBI on the severity of the neurological deficit and the degree of brain damage in rats. The experiments were performed on male Wistar rats (n = 35). The TBI was simulated by the dosed open brain contusion injury. The animals were divided into three groups: sham-operated (SO, n = 7); TBI + 70%N2/30%O₂ (TBI, n = 14); TBI + 70%Ar/30%O₂ (TBI + iAr, n = 14). The Neurological status was assessed over a 14-day period (using the limb-placing and cylinder tests). Magnetic resonance imaging (MRI) scans and a histological examination of the brain with an assessment of the volume of the lesions were performed 14 days after the injury. At each of the time points (days 1, 7, and 14), the limb-placing test score was lower in the TBI and TBI + iAr groups than in the SO group, while there were no significant differences between the TBI and TBI + iAr groups. Additionally, no differences were found between these groups in the cylinder test scores (day 13). The volume of brain damage (tissue loss) according to both the MRI and histological findings did not differ between the TBI and TBI + iAr groups. A three-hour inhalation of argon (70%Ar/30%O₂) after a TBI had no neuroprotective effect.

The thromboembolic ischemia model is one of the most applicable for studying ischemic stroke in humans. The aim of this study was to develop a novel thromboembolic stroke model, allowing, by affordable tools, to reproduce cerebral infarction in rats. In the experimental group, the left common carotid artery, external carotid artery, and pterygopalatine branch of maxillary artery were ligated. A blood clot that was previously formed (during a 20 min period, in a catheter and syringe, by mixing with a thromboplastin solution and CaCl₂) was injected into the left internal carotid artery. After 10 min, the catheter was removed, and the incision was sutured. The neurological status of the animals was evaluated using a 20-point scale. Histological examination of brain tissue was performed 6, 24, 72 h, and 6 days post-stroke. All groups showed motor and behavioral disturbances 24 h after surgery, which persisted throughout the study period. A histological examination revealed necrotic foci of varying severity in the cortex and subcortical regions of the ipsilateral hemisphere, for all experimental groups. A decrease in the density of hippocampal pyramidal neurons was revealed. Compared with existing models, the proposed ischemic stroke model significantly reduces surgical time, does not require an expensive operating microscope, and consistently reproduces brain infarction in the area of the middle cerebral artery supply.

The noble gas argon is one of the most promising neuroprotective agents for hypoxic-reperfusion injuries of the brain. However, its effect on traumatic injuries has been insufficiently studied. The aim of this study was to analyze the effect of the triple inhalation of the argon-oxygen mixture Ar 70%/O₂ 30% on physical and neurological recovery and the degree of brain damage after traumatic brain injury and to investigate the possible molecular mechanisms of the neuroprotective effect. The experiments were performed in male Wistar rats. A controlled brain injury model was used to investigate the effects of argon treatment and the underlying molecular mechanisms. The results of the study showed that animals with craniocerebral injuries that were treated with argon inhalation exhibited better physical recovery rates, better neurological status, and less brain damage. Argon treatment significantly reduced the expression of the proinflammatory markers TNFα and CD68 caused by TBI, increased the expression of phosphorylated protein kinase B (pAKT), and promoted the expression of the transcription factor Nrf2 in intact animals. Treatment with an argon-oxygen breathing mixture after traumatic brain injury has a neuroprotective effect by suppressing the inflammatory response and activating the antioxidant and anti-ischemic system.

Cardiac arrest remains one of the leading causes of death worldwide. Even with successful resuscitation, patient outcomes are often poor due to post-resuscitation syndrome, which includes cerebral hypoxia, myocardial dysfunction, microcirculatory disorders, coagulation abnormalities, and systemic inflammation. Argon, an inert noble gas, has neuroprotective and cardioprotective properties, making it a promising candidate for early post-resuscitation therapy. The aim of the study was to evaluate the organoprotective properties of an argon-oxygen mixture when inhaled in the early post-resuscitation period for 2 hours after asphyxial circulatory arrest in rats. Materials and methods. A prospective randomized controlled experimental study was conducted on male Wistar rats ( n = 43) using an asphyxial circulatory arrest model. The animals were divided into three groups: sham-operated (SO, n = 12), circulatory arrest with resuscitation (CAR, n = 13), and circulatory arrest with resuscitation and two-hour inhalation of a 70%/30% argon-oxygen mixture in the post-resuscitation period (CAR + iAr, n = 18). Hemodynamics, microcirculation, blood gas composition, coagulation (low-frequency piezothromboelastography), neurological status, and biomarkers of organ damage were evaluated. Beclin-1 and caspase-3 expression was analyzed immunohistochemically. Results. Argon inhalation did not have a significant effect on systemic hemodynamics, but it was accompanied by improved tissue oxygenation and metabolism: a decrease in blood lactate ( p = 0.043), an increase in the p/F oxygenation index ( p = 0.001), and stabilization of microcirculation variability (Kv, σ). Statistically significantly increased expression of the Beclin-1 protein in the lungs, myocardium, and hippocampus reflected activation of autophagy. In the CAR + iAr group, there was an improvement in neurological status compared to CAR ( p = 0.02), a decrease in serum neuron-specific enolase ( p = 0.011), and a decrease in the number of caspase-3-positive cells ( p = 0.011), indicating a reduction in apoptosis and damage to the nervous tissue. Argon had a moderate anticoagulant and antiplatelet effect (coagulation drive intensity — CDI, and maximum clot firmness-MCF reduction), while maintaining normal processes of clot retraction and lysis. The electrophysiological parameters of the heart (QRS, QTc) varied within the physiological range, indicating the absence of pro-arrhythmic effects in argon. Conclusion. Early inhalation of argon-oxygen mixture after circulatory arrest has a multisystem protective effect: improves oxygenation and microcirculation, promotes activation of autophagy mechanisms in vital organs, reduces the severity of neuronal damage, and modulates blood clotting in some measure. Argon can be considered a promising therapeutic agent for post-resuscitation syndrome. Further clarification is needed to assess argon’s molecular mechanisms of action and long-term outcomes after its use.