Effects of intracerebroventricular application of the delta opioid receptor agonist [d-Ala2, d-Leu5] enkephalin on neurological recovery following asphyxial cardiac arrest in rats

Gao, Changjun; Li, J.-P.; Wang, W.; Lü, B.-C.; Niu, Le; Zhu, Chao; Wei, Yanyan; Zhang, T.; Wu, Shuo; Chai, Weidong; Li, Y.-Q.

doi:10.1016/j.neuroscience.2010.02.025

“…57 The synthetic ␦-opioid receptor agonist d-Ala (2)-d-Leu (5) enkephalin (DADLE), has also been tested in CA. 58 In an isolated working rat-heart model, pharmacological activation of delta-opioid receptors using DADLE offered myocardial protection similar to that conferred by ischaemic preconditioning. However, the evidence for cardioprotection with DADLE was not uniform among species.…”

Section: ␦-Opioid Agonistsmentioning

confidence: 97%

“…␦-Opioids agonists Animals/rat-heart model Reduction of myocardial metabolism during ischaemia, amelioration of myocardial dysfunction and increased survival post-ROSC. [56][57][58] Thombolysis Humans No treatment benefit from routine use in OHCA patients. May be useful in selected patients with STEMI and pulmonary embolism [61][62][63] Neurotensin Animals Prolonged decrease of body temperature.…”

Section: Humans Nrtsmentioning

confidence: 99%

Emerging pharmaceutical therapies in cardiopulmonary resuscitation and post-resuscitation syndrome

Charalampopoulos

¹

,

Νικολάου

²

2011

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“…DADLE induces hibernation in ground squirrels in situations were κ and μ agonists have failed [46]. It has also been reported that DADLE treatment protects the brain against focal [48] and global cerebral ischemia [49][50][51], making DADLE a promising neuroprotective candidate.…”

Section: Opioid Receptor Activatorsmentioning

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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“…DADLE induces hibernation in ground squirrels in situations were κ and μ agonists have failed [46]. It has also been reported that DADLE treatment protects the brain against focal [48] and global cerebral ischemia [49-51], making DADLE a promising neuroprotective candidate.…”

Section: Drug-induced Hypothermia In Ischemic Strokementioning

confidence: 99%

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

Zhang

¹

,

Wang

²

,

Zhao

³

et al. 2013

CNSNDDT

View full text Add to dashboard Cite

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.

show abstract

Effects of intracerebroventricular application of the delta opioid receptor agonist [d-Ala2, d-Leu5] enkephalin on neurological recovery following asphyxial cardiac arrest in rats

Cited by 35 publications

References 41 publications

Emerging pharmaceutical therapies in cardiopulmonary resuscitation and post-resuscitation syndrome

Emerging pharmaceutical therapies in cardiopulmonary resuscitation and post-resuscitation syndrome

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

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

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