Ventilation with the noble gas argon in an in vivo model of idiopathic pulmonary arterial hypertension in rats

Giorgio, Daria De; Magliocca, Aurora; Fumagalli, Francesca; Novelli, Deborah; Olivari, Davide; Staszewsky, Lidia; Latini, Roberto; Ristagno, Giuseppe

doi:10.4103/2045-9912.314333

Cited by 3 publications

(1 citation statement)

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“…27,30 In a rat isolated lung model vasodilation was observed in animals with argon ventilation. 32,33 To assure constant brain perfusion, cerebral blood vessels are equipped with different regulatory mechanisms subsumed as auto-regulation. 34 An increase in blood pressure leads to vasoconstriction, a decrease in vessel diameter and a decrease in blood pressure leads to vasodilation.…”

Section: Discussionmentioning

confidence: 99%

Effects of argon in the acute phase of subarachnoid hemorrhage in an endovascular perforation model in rats

Krenzlin,

Wesp,

Korinek

et al. 2024

Preprint

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Objective: Subarachnoid hemorrhage (SAH) is a devastating disease with high morbidity and mortality. Neuroprotective effects of the noble gas Argon have been shown in animal models of ischemia. The aim of this study was to investigate the effects of Argon in the immediate early phase of SAH in a rat model. Methods: 19 male Wistar rats were randomly assigned to 3 treatment groups. SAH was induced using the endovascular filament perforation model. Cerebral blood flow (CBF), mean arterial blood pressure (MAP) and body temperature were measured continuously. Group A received 2 hours of ventilation by 50% Argon/50% O2 (n=7) immediately following SAH. Group B underwent a sham operation, and was also ventilated by Argon/O2 (n=6). Group C received a SAH but no further treatment (n=6). Pre- and postoperatively neurological and behavioral testing was performed. Histology and immunohistochemistry were used to evaluate the extent of brain injury and vasospasm. Results: The CBF dropped in both treatment groups after SAH induction (SAH: 63.0±11.6% of baseline; SAH + argon: 80.2±8.2 % of baseline). During SAH MAP increased (135.2±10.5%) compared to baseline (85.8±26.0mmHG) and normalized thereafter. MAP in both groups showed no significant differences (p=0.3123). Immunohistochemical staining for NeuN demonstrated a decrease of hippocampal immunoreactivity after SAH in the CA 1-3 region compared to baseline (p=0.0127). Animals in the argon ventilated group showed less neuronal loss compared to untreated SAH animals (p<0.0001). Iba-1 staining showed a decreased accumulation after SAH + argon (CA1: 2.57±2.35%; CA2: 1.89±1.89%; CA3: 2.19±1.99%; DG: 2.6±2.24%) compared to untreated SAH animals (CA1: 5.48±2.39%; CA2: 4.85±4.06%; CA3: 4.22±3.01%; DG: 3.82±3.23%). Less microglia accumulation indicated less activation in the argon ventilated group (p=0.0007). The Neuroscore assessment revealed no treatment benefit after SAH compared to baseline (p=0.385). Conclusion: In the present study neuroprotective effects of argon occurred early after SAH. As neurological deterioration was similar in the pre- and absence of Argon, it remains uncertain if neuroprotective effects translate in improved outcome over time.

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Section: Discussionmentioning

confidence: 99%

Effects of argon in the acute phase of subarachnoid hemorrhage in an endovascular perforation model in rats

Krenzlin,

Wesp,

Korinek

et al. 2024

Preprint

View full text Add to dashboard Cite

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Effects of Argon in the Acute Phase of Subarachnoid Hemorrhage in an Endovascular Perforation Model in Rats

Krenzlin,

Wesp,

Korinek

et al. 2024

Neurocrit Care

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Background Subarachnoid hemorrhage (SAH) is a devastating disease with high morbidity and mortality. Neuroprotective effects of the noble gas argon have been shown in animal models of ischemia. The aim of this study was to investigate the effects of argon in the immediate early phase of SAH in a rat model. Methods A total of 19 male Wistar rats were randomly assigned to three treatment groups. SAH was induced using a endovascular filament perforation model. Cerebral blood flow, mean arterial blood pressure (MAP), and body temperature were measured continuously. Group A received 2 h of ventilation by 50% argon/50% O2 (n = 7) immediately following SAH. Group B underwent a sham operation and was also ventilated by 50% argon/50% O2 (n = 6). Group C underwent SAH and 50% O2/50% N2 ventilation (n = 6). Preoperative and postoperative neurological and behavioral testing were performed. Histology and immunohistochemistry were used to evaluate the extent of brain injury and vasospasm. Results The cerebral blood flow dropped in both treatment groups after SAH induction (SAH, 63.0 ± 11.6% of baseline; SAH + argon, 80.2 ± 8.2% of baseline). During SAH, MAP increased (135.2 ± 10.5%) compared with baseline values (85.8 ± 26.0 mm Hg) and normalized thereafter. MAP in both groups showed no significant differences (p = 0.3123). Immunohistochemical staining for neuronal nuclear antigen demonstrated a decrease of hippocampal immunoreactivity after SAH in the cornu ammonis region (CA) 1–3 compared with baseline hippocampal immunoreactivity (p = 0.0127). Animals in the argon-ventilated group showed less neuronal loss compared with untreated SAH animals (p < 0.0001). Ionized calcium-binding adaptor molecule 1 staining showed a decreased accumulation after SAH + argon (CA1, 2.57 ± 2.35%; CA2, 1.89 ± 1.89%; CA3, 2.19 ± 1.99%; DG, 2.6 ± 2.24%) compared with untreated SAH animals (CA1, 5.48 ± 2.39%; CA2, 4.85 ± 4.06%; CA3, 4.22 ± 3.01%; dentate gyrus (DG), 3.82 ± 3.23%; p = 0.0007). The neuroscore assessment revealed no treatment benefit after SAH compared with baseline (p = 0.385). Conclusion In the present study, neuroprotective effects of argon occurred early after SAH. Because neurological deterioration was similar in the preadministration and absence of argon, it remains uncertain if neuroprotective effects translate in improved outcome over time.

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Organoprotective Properties of Argon (Review)

Boeva

Гребенчиков

2022

Obŝaâ reanimatologiâ

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The history of studying the organoprotective properties of argon (Ar) began in 1998 when a group of Russian researchers investigated the effect of hypoxic gas mixtures on mammalian organisms. Over several decades, evidence of the cardio-, neuro-, and nephroprotective effects of argon in various diseases and conditions in experimental models in vivo and in vitro have been accumulated. However, the lack of clinical studies to date has prompted us to carry out a systematic review analyzing the results of preclinical studies revealing organoprotective properties of argon, which could provide a rationale for its future clinical studies.The aim of this review is to describe the mechanisms of organoprotective properties of argon determined in preclinical studies.Material and methods. The search yielded 266 articles. The search algorithm was developed in accordance with the requirements and reporting guidelines for systematic reviews and meta-analysis (PRISMA) in the PubMed and Google Scholar databases. The methodology included using search queries, keywords (including MeSH), and logical operators. The keywords used for the search in the PubMed and Google Scholar databases were «argon», «ar», «protection», and «mechanism». The review included in vivo and in vitro studies.Results. The following mechanisms of argon action were identified: activation of N-terminal c-Jun kinase(JNK), p38(ERK1/2), and ERK1/2 in models of airway epithelial cells, neuronal and astroglial cell cultures, as well as in models of retinal ischemia and reperfusion injury in rats and a rabbit model of ischemia-reperfusion myocardium. Significant neuroprotective effects of argon and its influence on apoptosis were shown using small rodent models.Conclusion. The results of preclinical studies of argon have proved both its safety and organoprotective properties in in vitro and in vivo models. Analysis of the data provides a rationale for the initiation of clinical studies of argon, which could significantly improve outcomes in patients after cerebrovascular accidents, particularly post ischemic stroke.

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Ventilation with the noble gas argon in an in vivo model of idiopathic pulmonary arterial hypertension in rats

Cited by 3 publications

References 6 publications

Effects of argon in the acute phase of subarachnoid hemorrhage in an endovascular perforation model in rats

Effects of argon in the acute phase of subarachnoid hemorrhage in an endovascular perforation model in rats

Effects of Argon in the Acute Phase of Subarachnoid Hemorrhage in an Endovascular Perforation Model in Rats

Organoprotective Properties of Argon (Review)

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