Clonidine Improves Recovery from Myocardial Stunning in Conscious Chronically Instrumented Dogs

MeiBner, Andreas; Weber, Thomas P.; Aken, Hugo Van; Zbieranek, Kai; Rolf, Norbert

doi:10.1213/00000539-199811000-00005

Cited by 10 publications

(5 citation statements)

References 26 publications

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“…In addition, we suggest that the greater improvement in terms of functional recovery is mediated by an increase in endo/epi blood flow ratio. These results are consistent with previous studies using other α 2 -adrenergic agonists, such as mivazerol or clonidine (8,9). It is likely that the effects of a factor other than α 2 -adrenergic agonist activity are only small, even with the use of high-dose DEX in this study.…”

Section: Discussionsupporting

confidence: 93%

“…Several studies reported that intravenous administration of clonidine, an α 2 -adrenergic agonist, and DEX could prevent a myocardial ischemia-induced NE release in anesthetized dogs (9,19,20). Mivazerol, α 2 -adrenergic agonist, also suppressed the increase of plasma NE concentration and preserved myocardial blood flow in the inner layers during coronary artery stenosis in anesthetized dogs (10).…”

Section: Discussionmentioning

confidence: 99%

“…Meissner et al (9) showed that clonidine improved recovery from myocardial stunning and attenuated increases in catecholamine plasma levels in dogs. Thus it is considered that α 2 -adrenergic agonists exert myocardial protection resulting from the attenuation of the catecholamine response to ischemic stress and redistributing myocardial blood flow.…”

Section: Discussionmentioning

confidence: 99%

“…Miura et al (6) also reported that the elevation of NE concentration during ischemia was markedly attenuated by ischemic preconditioning. α 2 -Adrenergic agonists have been reported to have protective effects on the ischemic myocardium such as coronary artery stenosis or myocardial stunning, and attenuate plasma NE levels, and preserve myocardial blood flow in the inner layers in the laboratory (7)(8)(9). It is well known that the central sympatholytic effect of α 2 -adrenergic agonists may be beneficial during myocardial ischemia.…”

Section: Introductionmentioning

confidence: 99%

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Direct Protective Effects of Dexmedetomidine Against Myocardial Ischemia-Reperfusion Injury in Anesthetized Pigs

Yamada

Cho

Hara

et al. 2012

Shock

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Systemic administration of α2-adrenergic agonists has been shown to protect ischemic myocardium, but the direct effects on ischemia-reperfused myocardium have not yet been clarified. This study was carried out to determine the effects of intracoronary dexmedetomidine (DEX) on the myocardial ischemia-reperfusion injury in anesthetized pigs. In open-chest pigs, the left anterior descending coronary artery was perfused through an extracorporeal circuit from the carotid artery. They received intracoronary infusion of DEX at a rate of 1 ng · mL(-1) (group LD, n = 9), 10 ng · mL(-1) (group MD, n = 9), or 100 ng · mL(-1) (group HD, n = 9) of coronary blood flow or vehicle (group C, n = 12) for 30 min before ischemia. Myocardial stunning was produced by 12-min ischemia of the perfused area of left anterior descending coronary artery and 90-min reperfusion. The effect on reperfusion-induced arrhythmias was evaluated using the incidence of ventricular tachycardia or fibrillation after reperfusion. Regional myocardial contractility was evaluated with segment shortening (%SS). Dexmedetomidine significantly reduced the incidence of reperfusion-induced ventricular arrhythmias. Dexmedetomidine significantly improved the recovery of percentage segment shortening at 90 min after reperfusion (32.6% ± 3.1% in group C, 58.2% ± 2.1% in group LD, 61.1% ± 1.8% in group MD, and 72.0% ± 2.0% in group HD). Dexmedetomidine suppressed the increase in plasma norepinephrine concentration after reperfusion. The results indicate that DEX would exert the protective effect against ischemia-reperfusion injury by the direct action on the myocardium, which is not mediated through the central nervous system.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Direct Protective Effects of Dexmedetomidine Against Myocardial Ischemia-Reperfusion Injury in Anesthetized Pigs

Yamada

Cho

Hara

et al. 2012

Shock

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“…Clinical evidence suggests that induced autonomic nervous system modulation during perioperative administration of DEX is associated with a trend towards improved cardiac outcomes following non-cardiac surgery. 1–4 Previous experiments on animals have shown the benefits of DEX administration in the ischemic heart. 5–7 Cardioprotective effects have also been reported in global ischemia of isolated rat hearts.…”

Section: Introductionmentioning

confidence: 99%

The efficacy and mechanism of dexmedetomidine in myocardial apoptosis via the renin–angiotensin–aldosterone system

Wang

Zhang

et al. 2014

J Renin Angiotensin Aldosterone Syst

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Introduction: Pharmacological preconditioning limits myocardial infarct size after ischemia/reperfusion. Dexmedetomidine is an α2-adrenergic receptor agonist used in anesthesia that may have cardioprotective properties against ischemia/reperfusion injury. We investigated whether dexmedetomidine induces cardioprotection against myocardial apoptosis injury. Methods: In order to assess the role of dexmedetomidine on myocardial apoptosis, we established a grave scalding rat model. Blood and myocardial tissue from the ventriculus sinister were harvested, then troponin, myocardial apoptosis, and expression of caspase-12, GRP78, and CHOP were assessed. Results: Dexmedetomidine significantly reduced myocardial apoptosis, improved functional recovery, and reversed myocardial injury induced by grave scalding. The heart rate in the five groups studied was significantly different (p < 0.05). The number of buffy-stained nucleoli in the myocardial cell was highest in the simple scald group. The expression of caspase-12 obviously increased in the simple scald group. The expression of GRP78 and CHOP increased in the simple scald and scald and 50 μg/kg dexmedetomidine groups (p < 0.05). Conclusions: The results show that dexmedetomidine (DEX) produces cardioprotection against myocardial apoptosis injury. DEX is not only a useful sedative, but also plays a pivotal role in anesthetic cardioprotection. The potential benefits of DEX protection in high risk cardiovascular patients undergoing surgery are enormous.

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A comparison of α-methylnorepinephrine, vasopressin and epinephrine for cardiac resuscitation

et al. 2003

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Clonidine Improves Recovery from Myocardial Stunning in Conscious Chronically Instrumented Dogs

Cited by 10 publications

References 26 publications

Direct Protective Effects of Dexmedetomidine Against Myocardial Ischemia-Reperfusion Injury in Anesthetized Pigs

Direct Protective Effects of Dexmedetomidine Against Myocardial Ischemia-Reperfusion Injury in Anesthetized Pigs

The efficacy and mechanism of dexmedetomidine in myocardial apoptosis via the renin–angiotensin–aldosterone system

A comparison of α-methylnorepinephrine, vasopressin and epinephrine for cardiac resuscitation

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