Deterioration of myocardial injury due to dexmedetomidine administration after myocardial ischaemia

Mimuro, Soichiro; Katoh, Takasumi; Suzuki, Akira; Yu, Shuchun; Adachi, Yushi; Uraoka, Masahiro; Sano, Hideki; Sato, Shigehito

doi:10.1016/j.resuscitation.2010.07.021

Cited by 33 publications

(26 citation statements)

References 16 publications

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“…However, previous studies have reported that administration of dexmedetomidine after reperfusion did not exert a direct protective effect on left ventricular dysfunction, and even increased myocardial infarct size in isolated rat hearts (13,43). Contrary to our secondary hypothesis, the results of the present study indicated that postconditioning with dexmedetomidine was also able to attenuate H/R injury of cardiomyocytes.…”

Section: Discussionmentioning

confidence: 81%

“…Our previous studies have demonstrated that dexmedetomidine was able to reduce cardiovascular events and mortality in patients undergoing cardiac surgery (8,9). Previous experiments on animals have also demonstrated benefits of dexmedetomidine when administered before ischemia (10–12); however, its use at reperfusion was reported to increase the myocardial infarct size (13). The capacity for dexmedetomidine to protect cardiac tissues against I/R injury requires further investigation.…”

Section: Introductionmentioning

confidence: 99%

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Dexmedetomidine attenuates hypoxia/reoxygenation injury in primary neonatal rat cardiomyocytes

Peng

Qiu

et al. 2017

Experimental and Therapeutic Medicine

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Systemic administration of dexmedetomidine provides cardioprotection against ischemia/reperfusion (I/R) injury; however, the direct effects of dexmedetomidine on cardiomyocytes have not been clarified. The present study investigated the effects of dexmedetomidine on primary neonatal rat cardiomyocytes under hypoxic/reoxygenation (H/R) conditions. In order to simulate in vivo I/R injury, primary neonatal rat cardiomyocytes were cultured under hypoxic conditions for 1 h and subsequently reoxygenated for 24 h. The effects of preconditioning with dexmedetomidine 2 h before hypoxia and postconditioning during reoxygenation were also examined. Cellular viability and activity were analyzed by monitoring the dynamic response profile of living cells using a real-time cell analyzer system. A special scaled index, defined as the normalized cell index (NCI), was used to minimize the influence of inter-experimental variations. The dose-effect curve was generated from the area under the time-course curve values of NCI. H/R exposure markedly decreased cell viability and activity. Furthermore, no cytotoxicity was associated with a clinically relevant concentration of dexmedetomidine. Preconditioning with dexmedetomidine concentration-dependently ameliorated the reductions in NCI in cardiomyocytes following H/R injury. Additionally, postconditioning with dexmedetomidine improved the reductions in NCI at concentrations between 3 and 200 nM. Finally, the effect of 3–40 nM dexmedetomidine postconditioning was greater than preconditioning. These results indicated that preconditioning and postconditioning with dexmedetomidine attenuated H/R injury in primary neonatal rat cardiomyocytes at the cellular level.

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Section: Discussionmentioning

confidence: 81%

Section: Introductionmentioning

confidence: 99%

Dexmedetomidine attenuates hypoxia/reoxygenation injury in primary neonatal rat cardiomyocytes

Peng

Qiu

et al. 2017

Experimental and Therapeutic Medicine

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“…27 In a myocardial ischemia/reperfusion model, dexmedetomidine administration before ischemia reduced the infarct size, 28 whereas administration after ischemia deteriorated myocardial injury. 29 In addition, only when administered before injury, dexmedetomidine attenuated tolllike receptor 4 expression which mediates the renal ischemia/ reperfusion injury 6 and attenuated kidney ischemia/reperfusion injury and inflammatory response. 30 Therefore, early intervention of dexmedetomidine before the ischemic insult seems to be critical for its organ-protective effects against ischemia/reperfusion injury, although it was administered only postoperatively in most studies.…”

Section: Discussionmentioning

confidence: 99%

Perioperative dexmedetomidine reduces the incidence and severity of acute kidney injury following valvular heart surgery

Cho¹,

Shim

Soh³

et al. 2016

Kidney International

122

112

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Acute kidney injury (AKI) following cardiac surgery is closely interrelated with hemodynamic instability and sympathetic activity, and adversely influences prognosis. Here, we investigated in a randomized placebo-controlled trial whether dexmedetomidine, an α2 adrenoreceptor agonist, could prevent AKI after valvular heart surgery. Two hundred patients undergoing valvular heart surgery were randomly assigned to equal placebo or treatment groups. Dexmedetomidine was infused at a rate of 0.4 μg/kg/h starting immediately after anesthetic induction and continuing for 24 h after surgery. We then assessed the incidence of AKI during the first 48 postoperative hours, hemodynamic variables, and a composite of major morbidity end points. The incidence of AKI, based on Acute Kidney Injury Network criteria, was significantly lower in the treatment group compared with the control group (14 vs. 33%). The dexmedetomidine group exhibited a significantly lower incidence of a composite of major morbidity end points (21 vs. 38%) and a significantly shorter length of intensive care unit stay (3 [2, 3] days vs. 3 [2, 4] days) compared with the control group. Thus, perioperative infusion of dexmedetomidine effectively reduced both the incidence and severity of AKI, and improved outcome in patients undergoing valvular heart surgery without untoward hemodynamic side effects.

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“…Nevertheless, its cardioprotective effects still remain to be fully elucidated. In this context, Dex has shown detrimental effects in the myocardium when used as a post-conditioning rather than a pre-conditioning agent [48]. This observation lead Cai et al to hypothesize that the protective effect of Dex depends on timing [10].…”

Section: Discussionmentioning

confidence: 99%

Dexmedetomidine protects the heart against ischemia-reperfusion injury by an endothelial eNOS/NO dependent mechanism

Riquelme

Westermeier

Hall

et al. 2016

Pharmacological Research

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Deterioration of myocardial injury due to dexmedetomidine administration after myocardial ischaemia

Abstract: Dexmedetomidine administration does not influence haemodynamics or CF, but does increase the cardiac infarct size. α-2 Adrenergic stimulation may induce this mechanism.

Cited by 33 publications

References 16 publications

Dexmedetomidine attenuates hypoxia/reoxygenation injury in primary neonatal rat cardiomyocytes

Dexmedetomidine attenuates hypoxia/reoxygenation injury in primary neonatal rat cardiomyocytes

Perioperative dexmedetomidine reduces the incidence and severity of acute kidney injury following valvular heart surgery

Dexmedetomidine protects the heart against ischemia-reperfusion injury by an endothelial eNOS/NO dependent mechanism

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