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Showing 7 results for Hyperoxia

Mohammad Reza Bigdeli, Sohrab Hajizadeh, Mehdi Frouzandeh, Ali Khoshbaten,
Volume 11, Issue 3 (12-2007)
Abstract

Introduction: Prolonged and intermittent oxygen pre-exposure is associated with protection against ischemic reperfusion (IR) injury. In the current study, attempts were made to investigate the relationship between exposure to prolonged and intermittent normobaric hyperoxia (NBHO) and expression of excitatory amino acids transporters (EAATs) and TNF-α level. Method: Rats were divided into four main experimental groups, each of 21 animals. The first two were exposed to 95% inspired NBHO 4 h/day for 6 consecutive days (intermittent NBHO) or for 24 continuous hours (prolonged NBHO). The second two groups considered as controls and were exposed to 21% oxygen in the same chamber (normobaric normoxia, NBNO). Each main group was subdivided to MCAO (middle cerebral artery occlusion), sham-operated (without MCAO) and intact (without any surgery) subgroups. After 24h, MCAO subgroups were subjected to 60 min of right MCAO. After 24 h reperfusion, neurologic deficit scores (NDS) were assessed in MCAO-operated subgroups. Immediately and 48 h after pretreatment, blood sampling were done for assessing level of serum TNF-α. The effect of intermittent and prolonged NBHO on EAATs expression level was also measured using western blotting. Result: Preconditioning with prolonged and intermittent NBHO decreased NDS and up-regulated EAAT1, EAAT2, and EAAT3, significantly. Also, oxygen exposure of prolonged and intermittent NBHO increased the level of serum TNF-α. Conclusion: Although further studies are needed to clarify the protective mechanisms OF hyperoxia, the intermittent and prolonged NBHO seems to partly exert their effects via increasing the serum level of TNF-α and upregulation of glutamate transporters. However, the intermittent NBHO seems to have appropriate effects with low toxicity.
Khalil Pourkhalili, Sohrab Hajizadeh, Ali Khoshbaten, Taki Tiraihi,
Volume 12, Issue 2 (8-2008)
Abstract

Abstract Introduction: Resent studies have been shown beneficial effects of hyperoxia pretreatment against ischemia-reperfusion injury in different organs. The aim of the present study was to investigate early and late effects of normobaric hyperoxia (≥95% O2) pretreatment on ischemia-reperfusion injuries in isolated rat hearts. Methods: Following 60 and 180 minutes of hyperoxia, rat hearts were isolated immediately (H60 and H180) or 24 hours later (H60/24 and H180/24), and subjected to 30 minutes of regional ischemia followed by 120 minutes of reperfusion. Incidence and severity of ventricular arrhythmias, mechanical function of the heart and coronary flow were assessed during 120 min of reperfusion. LDH and CK release and infarct size were also assessed. Results: Incidence and severity of reperfusion arrhythmias significantly reduced by hyperoxia pretreatment, especially in the early phase of treanment. H180 reduced the incidence of ventricular fibrillation (VF) to 0% vs. 50% of normoxic control, p<0.05). VF duration decreased in H180 group (0 vs. 50±31s in the NC group, p<0.05) and duration of VT decreased in H60 and H180 groups compared to normoxic control group (NC) (1.5±0.7 s and 7.5±2.5 s vs. 17.7±3.3 s respectively, p<0.05). Hyperoxia improves mycardial contractile function and improves coronary flow during reperfusion. Infarct size and enzymes release were also significantly decreased in early and late phase of hyperoxia pretreatment. Conclusions: These results indicate that hyperoxia pretreatment before induction of regional heart ischemia reduces cardiac infarct size and attenuates reperfusion induced arrhythmias in isolated rat heart. Keywords: Hyperoxia, Ischemia-reperfusion injury, Heart protection, Arrhythmias
Mohammad Reza Bigdeli, ,
Volume 13, Issue 1 (4-2009)
Abstract

Introduction: resent studies have been shown that normobaric hyperoxia (HO) can induce excitotoxicity and stress oxidative tolerance (ETT) in variety of organs such as brain. In this study, we examined the intermittent dose of normobaric hyperoxia (HO) on neurologic deficit, and superoxide dismutase activity in brain tissue of Huntington animal model. Method: The rats were divided to three groups. First group were exposed with HO intermittently (4h×6days HO) and second two main group acted as controls, and were exposed to 21% oxygen in the same chamber (room air, RA) discontinuously (4h×6days InRA). Immediately, HO and RA groups were subjected to Huntington animal model (20mg/kg of 3-nitropropionic acid for 6 days), Because Huntington disease is a neurodegenerative disorder. Then, ETT induced by HO were measured by neurologic deficits such as string, limb withdrawal, inclined plane, beam balance test, and assessment of superoxide dismutase activity. Result: Our findings indicated that HO is involved in the induction of ETT. Pretreatment with HO improved neurologic deficits including string, limb withdrawal, inclined plane, beam balance test significantly. Preconditioning with HO increased superoxide dismutase activity significantly. Conclusion: Although further studies are needed to clarify the mechanisms of excitotoxicity tolerance, pretreatment with HO seem to partly exert their effects via increase cell viability and superoxide dismutase activity.
Firoozeh Alavian, Sohrab Hajizadeh, Mohammad Reza Bigdeli, Gholam Reza Bayat, Mohammad Javan,
Volume 16, Issue 1 (4-2012)
Abstract

Introduction: ischemic preconditioning is one of the most important mechanisms, responsible for the increased brain resistance after stroke. One of the most important candidates to ischemia preconditioning is intermittent normobaric hyperoxia. In this study, the effect of intermittent normobaric hyperoxia on the expression of UCP2 was investigated in a stroke model. Methods: Rats were divided into 4 groups (normoxia – sham, hyperoxia – sham, normoxia – stroke and hyperoxia – stroke). Hyperoxia groups were exposed to 95% inspired O2, for 4 h/day and 6 consecutive days. Oxygen level in the control groups was %21 (normoxia). After 24 h, stroke groups were subjected to 60 min of right middle cerebral artery occlusion. After 24 h reperfusion neurological deficit scores were assessed. The brain UCP2 levels were analyzed by western blot. Results: The results of this study showed that following brain ischemia-reperfusion, UCP2 levels significantly increased in the stroke groups compared with the sham group while there was no significant difference in hyperoxia groups compared with normoxia. Also hyperoxia decreased neurological deficit scores. Conclusion: Following ischemia, oxidative stress caused by increase of ROS, leads to increased UCP2 levels in stroke groups. In this study, the neuroprotective effect of hyperoxia is independent of UCP2 expression.
Mohammad Hossein Esmaeili, Tahereh Dargahi, Hashem Haghdoost-Yazdi,
Volume 19, Issue 2 (5-2015)
Abstract

Introduction: A large body of evidence points to oxidative stress as prime candidate mediating the behavioral impairments and memory deficits in Alzheimer's disease (AD). It has been demonstrated that hyperoxia preconditioning activates complex endogenous neuroprotective mechanisms including an increase in capacity of antioxidant defence mechanisms. The aim of this study was to investigate the beneficial effects of normobaric hyperoxia preconditioning in streptozotocin (STZ)- induced memory impairment in rats. Materials and Methods: Male Wistar rats were first exposed to air with high oxygen concentration (>90%) or atmospheric air for 24 hours and then STZ (3 mg/kg) was bilaterally infused in lateral ventricles of the brain. Two weeks later Morris Water Maze (MWM) test was performed to assess spatial learning and memory consolidation. Results: STZ increased escape latency (P<0.05), distance and number of crossed quadrants (P<0.05) especially on 1st and 2nd days. However, hyperoxia preconditioning significantly attenuated STZ-induced learning and memory deficits during training sessions in the MWM (P<0.05). Preconditioning also increased time spent and swimming distance in the target quadrant in probe test (P<0.05). However, hyperoxia preconditioning had no effect on the swimming speed. Conclusion: Hyperoxia preconditioning significantly attenuated STZ-induced impairments in spatial learning and memory. These results suggest that hyperoxia may have a potential therapeutic effect at the early stage of AD and possibly the prevention of memory deficits.


Ekram Mohammadi, Mohammad Reza Bigdeli,
Volume 19, Issue 2 (5-2015)
Abstract

Introduction: The purpose of this study was to determine Na-Ca exchanger 2, 3 (NCX2, 3) protein level changes during 2, 5, 10, 15 days after induction of normobaric hyperoxia (HO) preconditioning. Materials and Methods: Rats were divided in two experimental groups. The first group was exposed to 95% inspired HO for 4 h/day for 6 consecutive days (HO). The second group acted as control, and was exposed to 21% oxygen in the same chamber. Each main group was subdivided to middle cerebral artery occlusion (MCAO-operated) and intact (without any surgery) subgroups. After 2, 5, 10 and 15 days from pretreatment, MCAO-operated subgroups were subjected to 60 min of right MCAO. After 24 hours reperfusion, neurologic deficit score (NDS) and infarct volume (IV) were measured in MCAO-operated subgroups. The NCX 2, 3 expression levels of core, penumbra and subcortex regions were assessed in sham-operated and intact subgroups. Results: Expression of NCX 2, 3 proteins were increased in penumbra (P=0.000, P=0.002), core (P=0.001, P=0.033) and just NCX3 was increased in subcortex (P=0.033) during preconditioning with HO. Neurologic deficit score and infarct volume were decreased with HO preconditioning. These effects of hyperoxia disappeared gradually during 15 days after pretreatment. Conclusion: Although further studies are needed to clarify the mechanisms of time course of neuroprotection, HO durable effects on NCX2, 3 expression, IV and NDS are consistent with an active role in the genesis of ischemic neuroprotection.
Firoozeh Alavian, Sohrab Hajizadeh, Mohammad Javan, Mohammad Reza Bigdeli,
Volume 21, Issue 2 (5-2017)
Abstract

Introduction: Recent studies have shown that intermittent normobaric hyperoxia (HO) protects the rat brain from ischemia reperfusion injury. However, the exact mechanism of this kind of protection in vivo is not known. In this study, the effect of HO on expression of TNFR1 and TNFR2 in a stroke model was investigated. Methods: In this experimental study, rats were divided into 4 groups: normoxia – sham, hyperoxia – sham, normoxia – stroke and hyperoxia –stroke for each factor (TNFR1 or TNFR2). Hyperoxia groups were exposed to 95% inspired oxygen for 4 h/day and 6 consecutive days. Oxygen concentration in the control groups was 21% (normoxia, room air). After 24h, the rats were subjected to 60 min of right middle cerebral artery occlusion (MCAO). After 24h reperfusion, neurological deficit scores (NDS) and TNFR1, 2 brain levels using Western Blot were assessed. Results: Preconditioning with HO decreased NDS. Also, followed by stroke and reperfusion, TNFR1 levels significantly increased; while there was no significant difference in hyperoxia groups compared with normoxia groups in the cortex, HO significantly reduced TNFR1 expression in subcortex. On the other hand, groups of stroke compared to sham groups significantly expressed lower levels of TNFR2 in the cortex and subcortex. There was no significant difference in hyperoxia groups compared with normoxia groups in these areas. Conclusion: Although additional studies will be required to further elucidate precise mechanisms of ischemic tolerance, it seems that HO is associated with the expression of TNFR1 in subcortex, consistent with an active role in the genesis of ischemic protection.



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