hydrogen sulfide/hemorragia

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Neuroprotective Effects of Hydrogen Sulfide Against Early Brain Injury and Secondary Cognitive Deficits Following Subarachnoid Hemorrhage.

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Although the neuroprotective effects of hydrogen sulfide (H2 S) have been demonstrated in several studies, whether H2 S protects against early brain injury (EBI) and secondary cognitive dysfunction in subarachnoid hemorrhage (SAH) model remains unknown. This study was undertaken to evaluate the

Hydrogen sulfide ameliorates subarachnoid hemorrhage-induced neuronal apoptosis via the ROS-MST1 pathway.

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BACKGROUND Hydrogen sulfide (H2S) has shown a neuroprotective role in several cerebrovascular diseases. This study aimed to explore the underlying mechanisms of H2S in early brain injury after subarachnoid hemorrhage (SAH). METHODS One hundred seventy-seven male Sprague-Dawley rats were employed in

A hypothesis: hydrogen sulfide might be neuroprotective against subarachnoid hemorrhage induced brain injury.

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Gases such as nitric oxide (NO) and carbon monoxide (CO) play important roles both in normal physiology and in disease. Recent studies have shown that hydrogen sulfide (H2S) protects neurons against oxidative stress and ischemia-reperfusion injury and attenuates lipopolysaccharides (LPS) induced

Hydrogen Sulfide Reduces Cognitive Impairment in Rats After Subarachnoid Hemorrhage by Ameliorating Neuroinflammation Mediated by the TLR4/NF-κB Pathway in Microglia

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Background and Aims: Cognitive impairment is one of the major complications of subarachnoid hemorrhage (SAH) and is closely associated with neuroinflammation. Hydrogen sulfide (H₂S) has been shown to have an anti-inflammatory effect and reduce cognitive impairment in

Surviving blood loss using hydrogen sulfide.

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BACKGROUND Reduced metabolic activity improves outcome in many clinical and experimental models of injury and diseases that result in insufficient blood supply. Recently, we demonstrated that inhaled hydrogen sulfide gas can be used to reversibly reduce metabolic activity in mice. We hypothesize

Exogenous hydrogen sulfide protects against traumatic hemorrhagic shock via attenuation of oxidative stress.

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OBJECTIVE This study was designed to investigate the protective effects of exogenous hydrogen sulfide (H(2)S) on trauma-hemorrhagic shock (T-H). METHODS Forty-eight male Sprague-Dawley rats were anesthetized, while 32 were subjected to both midline laparotomy and hemorrhagic shock (35-40 mmHg for 90

Effects of hydrogen sulfide on hemodynamics, inflammatory response and oxidative stress during resuscitated hemorrhagic shock in rats.

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BACKGROUND Hydrogen sulfide (H2S) has been shown to improve survival in rodent models of lethal hemorrhage. Conversely, other authors have reported that inhibition of endogenous H2S production improves hemodynamics and reduces organ injury after hemorrhagic shock. Since all of these data originate

Intravenous hydrogen sulfide does not induce hypothermia or improve survival from hemorrhagic shock in pigs.

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Several laboratory studies suggested that induced hypothermia during hemorrhagic shock improves survival. Inhaled hydrogen sulfide (H2S) induced hypothermia and decreased metabolism in mice and rats but not in piglets. We tested the hypothesis that i.v. H2S will induce hypothermia, reduce oxygen

Neuroprotective Effects of Early Brain Injury after Subarachnoid Hemorrhage in Rats by Calcium Channel Mediating Hydrogen Sulfide

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The present study explored the modulating apoptosis effect of hydrogen sulfide (H₂S) in subarachnoid hemorrhage (SAH) rats and its exact mechanism. A rat SAH model established by intravascular puncturing was used for the present study. After giving NaHS (donor of H₂S), an

Exogenous Hydrogen Sulfide Offers Neuroprotection on Intracerebral Hemorrhage Injury Through Modulating Endogenous H2S Metabolism in Mice.

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Hydrogen sulfide (H₂S), an important endogenous signaling molecule, has a significant neuroprotective role in the central nervous system. In this study, we examined the protective effects of exogenous H₂S against intracerebral hemorrhage (ICH), as well as its underlying

Biological Effects of Hydrogen Sulfide and Its Protective Role in Intracerebral Hemorrhage

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Intracerebral hemorrhage (ICH) has extremely high morbidity and mortality, substantially impacting public health. Studying the pathophysiological mechanisms of ICH is a complicated undertaking, and there remains a lack of effective medical treatment for improving ICH survival rates and promoting

Hydrogen Sulfide Attenuates Tissue Plasminogen Activator-Induced Cerebral Hemorrhage Following Experimental Stroke.

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Tissue plasminogen activator (tPA), the only approved drug for the treatment of ischemic stroke, increases the risk of cerebral hemorrhage. Here, we investigated whether the newly identified gaso-transmitter hydrogen sulfide (H2S), when used in combination with tPA, reduced the hemorrhagic

Hydrogen Sulfide Ameliorates Early Brain Injury Following Subarachnoid Hemorrhage in Rats.

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Increasing studies have demonstrated the neuroprotective effect of hydrogen sulfide (H2S) in central nervous system (CNS) diseases. However, the potential application value of H2S in the therapy of subarachnoid hemorrhage (SAH) is still not well known. This study was to investigate the potential

Hydrogen sulfide attenuates brain edema in early brain injury after subarachnoid hemorrhage in rats: Possible involvement of MMP-9 induced blood-brain barrier disruption and AQP4 expression.

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This study investigated the effect of H2S on brain edema formation and the possible underlying mechanisms in early brain injury (EBI) of SAH using the endovascular perforation model. 96 male rats were randomly divided into four groups: sham group, SAH+vehicle group, SAH+low-dosage NaHS group, and

An exogenous hydrogen sulphide donor, NaHS, inhibits the apoptosis signaling pathway to exert cardio-protective effects in a rat hemorrhagic shock model.

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Hydrogen sulfide (H2S) has been reported to be interwined in multiple systems, specifically in the cardiovascular system. However, the mechanisms underlying remain controversial. In the present study, we assessed the cardio-protective effects of H2S in the rat hemorrhagic shock model. Hemorrhagic

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