The protective effects of dexmedetomidine on ischemic brain injury: A meta-analysis

Jiang, Lianxiang; Hu, Meizhu; Lu, Yan; Cao, Yukun; Chang, Ying; Zhang, Dai

doi:10.1016/j.jclinane.2017.04.003

Cited by 88 publications

(74 citation statements)

References 39 publications

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“…Dex is a novel highly selective adrenergic receptor agonist that displays strong intrinsic activity, short elimination half-life and distribution half-life (17). Recent studies have demonstrated that Dex has protective effects on the heart, kidney, central nervous system, respiratory system and small intestine (18,19). Presently, the protective effects of Dex on hepatic injury have received increased attention.…”

Section: Discussionmentioning

confidence: 99%

Dexmedetomidine activates the PI3K/Akt pathway to inhibit hepatocyte apoptosis in rats with obstructive jaundice

et al. 2019

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Obstructive jaundice (OJ) is a common disease in clinical surgery. The present study aimed to determine the effects of dexmedetomidine (Dex) on hepatocyte apoptosis in rats with OJ and also to explore the underlying mechanism. A total of 30 adult male Sprague Dawley rats were randomly divided into 3 groups: Sham group, bile duct ligation (BDL) group, and BDL+Dex group. The serum liver function index, expression levels of serum inflammatory factor interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α), and the liver pathological changes were compared amongst groups. The serum liver function index and expression levels of inflammatory factors in the BDL group and BDL+Dex group were higher compared with the sham group. The serum liver function index and expression levels of inflammatory factors were lower in the BDL+Dex group compared with the BDL group. The severity of hepatic injury was diminished in the BDL+Dex group compared with the BDL group. Compared with the sham group, the hepatocyte apoptosis rate increased significantly in the BDL group and BDL+Dex group. The present findings suggested that Dex improved the liver function of rats with OJ, reduced the production of inflammatory factors and inhibited the apoptosis of hepatocytes. Dex demonstrated a protective effect on liver damage potentially via activation of the phosphoinositide 3-kinase/protein kinase B signaling pathway.

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Section: Discussionmentioning

confidence: 99%

Dexmedetomidine activates the PI3K/Akt pathway to inhibit hepatocyte apoptosis in rats with obstructive jaundice

et al. 2019

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“…Studies have shown that inflammatory pathways mediated by neuroendocrine hormones and proinflammatory cytokines is implicated in the pathophysiology of ischemic brain injury. Alpha2-adrenoceptor agonist, dexmedetomidine, is used as neuroprotectant in anesthetic procedures (Jiang et al, 2017). However, meta-analyses to evaluate the neuroprotection of dexmedetomidine against ischemic brain injury are still lacking.…”

Section: Dex In Neurological Injurymentioning

confidence: 99%

Dexmedetomidine Improves Cardiovascular and Ventilatory Outcomes in Critically Ill Patients: Basic and Clinical Approaches

et al. 2020

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Dexmedetomidine (DEX) is a highly selective a2-adrenergic agonist with sedative and analgesic properties, with minimal respiratory effects. It is used as a sedative in the intensive care unit and the operating room. The opioid-sparing effect and the absence of respiratory effects make dexmedetomidine an attractive adjuvant drug for anesthesia in obese patients who are at an increased risk for postoperative respiratory complications. The pharmacodynamic effects on the cardiovascular system are known; however the mechanisms that induce cardioprotection are still under study. Regarding the pharmacokinetics properties, this drug is extensively metabolized in the liver by the uridine diphosphate glucuronosyltransferases. It has a relatively high hepatic extraction ratio, and therefore, its metabolism is dependent on liver blood flow. This review shows, from a basic clinical approach, the evidence supporting the use of dexmedetomidine in different settings, from its use in animal models of ischemia-reperfusion, and cardioprotective signaling pathways. In addition, pharmacokinetics and pharmacodynamics studies in obese subjects and the management of patients subjected to mechanical ventilation are described. Moreover, the clinical efficacy of delirium incidence in patients with indication of non-invasive ventilation is shown. Finally, the available evidence from DEX is described by a group of Chilean pharmacologists and clinicians who have worked for more than 10 years on DEX.

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“…The potential mechanism might be that dexmedetomidine reduces the release of inflammatory mediators and neuroendocrine hormones. 24 Zhang et al 25 reported that dexmedetomidine improved the short-term outcome of lung tissues of rats with sepsis. However, until now, the effects of dexmedetomidine on the outcome of postoperative HICH patients were unknown.…”

Section: Dexmedetomidine Was Beneficial For the Outcome Of Postoperatmentioning

confidence: 99%

Dexmedetomidine is superior to midazolam for sedation and cerebral protection in postoperative hypertensive intracerebral hemorrhage patients: a retrospective study

Gong

Zhang

et al. 2020

J Int Med Res

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Objective Dexmedetomidine has a good sedative effect and does not affect the judgment of the patient's consciousness level. However, its effectiveness for sedation and cerebral protection after craniotomy in hypertensive intracerebral hemorrhage (HICH) patients is unknown. Methods A retrospective study of 164 postoperative HICH patients who underwent sedation with dexmedetomidine or midazolam was conducted. The Ramsay sedation score, mean arterial pressure (MAP), heart rate (HR), pulse oxygen saturation (SpO2), and respiratory rate were measured at the indicated time points. Human soluble protein-100β (S-100β) and neuron-specific enolase (NSE) levels were also compared between the two groups. Results Dexmedetomidine treatment showed a significantly better effect than midazolam on decreasing the frequency of apparent agitation. The MAP and HR, but not the SpO2, were significantly decreased and lower than those in midazolam group. Detection of plasma S-100β and NSE proteins revealed a significant decrease in the dexmedetomidine group compared with the midazolam group. The 6-month follow-up evaluation indicated a significantly better prognosis of postoperative HICH patients treated with dexmedetomidine than for those treated with midazolam. Conclusions Dexmedetomidine is effective for sedation in postoperative HICH patients and may be beneficial for their outcome.

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The protective effects of dexmedetomidine on ischemic brain injury: A meta-analysis

Cited by 88 publications

References 39 publications

Dexmedetomidine activates the PI3K/Akt pathway to inhibit hepatocyte apoptosis in rats with obstructive jaundice

Dexmedetomidine activates the PI3K/Akt pathway to inhibit hepatocyte apoptosis in rats with obstructive jaundice

Dexmedetomidine Improves Cardiovascular and Ventilatory Outcomes in Critically Ill Patients: Basic and Clinical Approaches

Dexmedetomidine is superior to midazolam for sedation and cerebral protection in postoperative hypertensive intracerebral hemorrhage patients: a retrospective study

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