Heliox and oxygen reduce infarct volume in a rat model of focal ischemia

Pan, Y. Albert; Zhang, Haibo; VanDeripe, Donald R.; Cruz‐Flores, Salvador; Panneton, W. Michael

doi:10.1016/j.expneurol.2007.03.023

Cited by 55 publications

(45 citation statements)

References 18 publications

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“…Furthermore, other gases may potentially be added to the neuroprotective gas mixture to enhance neuronal survival and function. The anesthethic gas, xenon (50% inhaled concentration) has been found to augment neuroprotection afforded by hypothermia in the neonatal rat hypoxia/ischemia model (31,32), and helium (70% He/30% O 2 ) provided excellent neuroprotection in adult rat stroke models (33,34).…”

Section: Discussionmentioning

confidence: 99%

Hydrogen is neuroprotective and preserves cerebrovascular reactivity in asphyxiated newborn pigs

et al. 2010

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Section: Discussionmentioning

confidence: 99%

Hydrogen is neuroprotective and preserves cerebrovascular reactivity in asphyxiated newborn pigs

et al. 2010

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“…The results of another rodent study suggest that heliox (30% oxygen and 70% helium-a biological inert gas) is more potent than NBO in reducing infarct volumes after transient focal stroke. 20 As compared with the control group (30% oxygen/70% nitrogen), NBO-treated rats showed 56% and 70% reduction in total and cortical infarct volumes, and heliox-treated rats showed 87% and nearly 100% reduction of total and cortical infarct volumes. The authors speculate that helium diffuses into mitochondria and facilitates the egress of nitrogen, thereby enhancing mitochondrial uptake of oxygen and restoring cellular energy levels.…”

Section: Gasesmentioning

confidence: 99%

Advances in Emerging Nondrug Therapies for Acute Stroke 2007

Singhal

2008

Stroke

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N umerous clinical trials of thrombolytic and neuroprotective drugs for stroke have been conducted over the last 2 decades. The NINDS trial of intravenous tissue plasminogen activator remains the most notable success. Intra-arterial thrombolysis appears promising, but in the absence of phase III clinical trial data, this approach remains investigational. Numerous pharmaceutical drugs targeting 1 or more cell death pathways have failed to show efficacy. Despite failure, these prior attempts have provided insights regarding critical issues such as proper clinical trial design and the need for more rigorous preclinical drug testing in order to improve the translational leap from bench to bedside.More recently, accumulating data suggest that "non-drug" approaches toward stroke therapy might also provide new opportunities in addition to more traditional pharmaceutical therapies. As testimony to the growing importance of these alternate and sometimes complementary methods, there has been a proliferation of device trials, and the NINDS, through its key 'Specialized Program of Translational Research in Acute Stroke' [SPOTRIAS] initiative, 1 has funded trials of therapeutic hypothermia, caffeinol, and normobaric hyperoxia, among others. Although this brief survey focuses on emerging gas and device therapies for ischemic stroke, it should be noted that several other 'non-drug' approaches, including physiological strategies (eg, hypothermia, glucose regulation), and natural agents (eg, albumin, magnesium), continue to be tested in ongoing trials. GasesIncreasing brain tissue oxygenation has long been considered a logical stroke treatment strategy. Although initial efforts using hyperbaric oxygen (HBO) chambers were unsuccessful, the realization that early trials had numerous methodological shortcomings has led to a resurgence of interest in hyperoxia. 2 As a potential treatment, oxygen has distinct advantages over pharmaceutical drugs: it easily diffuses across the blood-brain barrier to reach target tissues, may act via multiple pathways, and high concentrations of oxygen in brain might be well tolerated.In the past year, several groups have explored normobaric oxygen therapy (NBO, or inhaled high-flow oxygen) because of its obvious practical benefits. It is widely available, simple to administer, and noninvasive. Recent data suggest that NBO may have rapid effects in stroke and can be started promptly after symptom onset. The results of animal 3,4 and human 5 studies suggest that NBO slows down the process of ischemic cell death after stroke. This "stopping the stroke clock" effect may provide an opportunity to extend the time window for thrombolysis. 6 While most prior studies have shown efficacy in models of transient focal stroke, a new study suggests that NBO may even be protective in permanent cortical ischemia. 7 Other studies published this past year have started clarifying NBO's mechanisms. First, although it was believed that NBO (unlike other oxygen delivery methods) does not significantly raise brain tissue o...

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“…There has been a surge of recent interest in the use of inert gases for neuroprotection against ischemic brain injury [107][108][109]. Helium is one such example; it is a colorless, nontoxic and cost-efficient gas without anesthetic properties [110].…”

Section: Gaseous Hypothermiamentioning

confidence: 99%

“…On the other hand, Qu et al found that administration of sodium hydrosulfide, a H 2 S donor, increased the H 2 S level in brain cortex and enlarged infarct volume in rats [106]. In these studies, body temperature was maintained at 37±0.5°C during anesthesia and not monitored thereafter [106].There has been a surge of recent interest in the use of inert gases for neuroprotection against ischemic brain injury [107][108][109]. Helium is one such example; it is a colorless, nontoxic and cost-efficient gas without anesthetic properties [110].…”

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confidence: 99%

Drug-Induced Hypothermia in Stroke Models: Does it Always Protect?

Zhang¹,

Wang²,

Zhao³

et al. 2013

CNSNDDT

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Ischemic stroke is a common neurological disorder lacking a cure. Recent studies show that therapeutic hypothermia is a promising neuroprotective strategy against ischemic brain injury. Several methods to induce therapeutic hypothermia have been established; however, most of them are not clinically feasible for stroke patients. Therefore, pharmacological cooling is drawing increasing attention as a neuroprotective alternative worthy of further clinical development. We begin this review with a brief introduction to the commonly used methods for inducing hypothermia; we then focus on the hypothermic effects of eight classes of hypothermia-inducing drugs: the cannabinoids, opioid receptor activators, transient receptor potential vanilloid, neurotensins, thyroxine derivatives, dopamine receptor activators, hypothermia-inducing gases, adenosine, and adenine nucleotides. Their neuroprotective effects as well as the complications associated with their use are both considered. This article provides guidance for future clinical trials and animal studies on pharmacological cooling in the setting of acute stroke. KeywordsBrain ischemia; Hypothermic; Neuroprotection; Pharmacological cooling Send correspondence to: Dr. Feng Zhang, Department of Neurology, University of Pittsburgh School of Medicine, 3500 Terrace Street, Pittsburgh, PA, 15213, USA, Telephone: 412-383-7604, Fax: 412-648-1239, zhanfx2@upmc.edu NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscript 1. Hypothermia and strokes IntroductionTherapeutic hypothermia is defined as a 2-6°C reduction of core body temperature [1][2][3] and is a promising neuroprotective approach against brain injury induced by strokes. In hemorrhagic stroke, hypothermia reduces brain edema [4,5] and improves neurologic function [4][5][6][7]. In ischemic stroke, hypothermia is also protective, which has been proven in randomized clinical trials in human cardiac arrest and in animal studies of focal and global ischemia [8,9]. However, the impact of hypothermia on patients with acute ischemic stroke still needs to be explored [10]. During the past decades, studies on hypothermia and ischemic stroke have suggested that the required amplitude of protective hypothermia depends on its time of initiation relative to stroke onset, duration, and depth of hypothermia [1,9,11]. Optimal protection is typically gained when hypothermia is induced as early as possible after stroke onset, with a mild-to-moderate hypothermia of 32 to 35°C that lasts at least one to two hours [1, 2, 12-14]. Protective mechanism of hypothermia in ischemic strokeAlthough hypothermia is effective in protecting against experimental models of ischemic stroke, the precise protective mechanisms are not yet fully understood. It has been suggested that the protective mechanisms are multifold, including reductions in metabolic rate, cerebral blood flow, blood-brain barrier damage, as well as decreases in excitotoxicity, apoptosis, inflammation and free radical production [15]. On average, hypothermia red...

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Heliox and oxygen reduce infarct volume in a rat model of focal ischemia

Cited by 55 publications

References 18 publications

Hydrogen is neuroprotective and preserves cerebrovascular reactivity in asphyxiated newborn pigs

Hydrogen is neuroprotective and preserves cerebrovascular reactivity in asphyxiated newborn pigs

Advances in Emerging Nondrug Therapies for Acute Stroke 2007

Drug-Induced Hypothermia in Stroke Models: Does it Always Protect?

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