Infusion of the β-adrenergic blocker esmolol attenuates myocardial dysfunction in septic rats*

Suzuki, Takeshi; Morisaki, Hiroshi; Serita, Ryohei; Yamamoto, Michiko; Kotake, Yoshifumi; Ishizaka, Akitoshi; Takeda, Junzo

doi:10.1097/01.ccm.0000182796.11329.3b

Cited by 152 publications

(133 citation statements)

References 42 publications

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“…However, they failed to provide any supporting data, and one may argue that anti-inflammatory effects would unlikely have occurred this swiftly, i.e., after only four hours of treatment (12)(13)(14)(15).…”

Section: Study Design and Findingsmentioning

confidence: 99%

Heart rate reduction may be a major determinant of vascular tone in esmolol-treated septic shock patients—although still remains to be confirmed!

Kimmoun¹,

Wei

Lévy³

et al. 2016

J. Thorac. Dis.

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Section: Study Design and Findingsmentioning

confidence: 99%

Heart rate reduction may be a major determinant of vascular tone in esmolol-treated septic shock patients—although still remains to be confirmed!

Kimmoun¹,

Wei

Lévy³

et al. 2016

J. Thorac. Dis.

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“…High levels of circulating catecholamines due to ongoing endogenous and pharmacological adrenergic stimulation may partially explain the discrepancy between maintained cardiac contractility in vivo, that clinicians observe at the bedside, and the profound decrease in cardiac contractility seen under laboratory conditions, for example in ex vivo models of cultured myocardial cells [80] and isolated perfused hearts [81]. Adrenergic downregulation, however, results in a reduced cardiac reserve that is unraveled by a reversible hypo-responsiveness to dobutamine in patients with septic shock [82].…”

Section: Underlying Mechanismsmentioning

confidence: 99%

“…In septic animals, β-blockers reduced heart rate though stroke volume was preserved [81,141]. The longer duration of diastole may perhaps allow better diastolic filling.…”

Section: Beta-blockers In Sepsismentioning

confidence: 99%

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The Heart in Sepsis: From Basic Mechanisms to Clinical Management

Rudiger¹,

Singer

2013

CVP

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Septic shock is characterized by circulatory compromise, microcirculatory alterations and mitochondrial damage, which all reduce cellular energy production. In order to reduce the risk of major cell death and a diminished likelihood of recovery, adaptive changes appear to be activated. As a result, cells and organs may survive in a non-functioning hibernation-like condition. Sepsis-induced cardiac dysfunction may represent an example of such functional shutdown. Sepsis-induced myocardial dysfunction is common, corresponds to the severity of sepsis, and is reversible in survivors. Its mechanisms include the attenuation of the adrenergic response at the cardiomyocyte level, alterations of intracellular calcium trafficking and blunted calcium sensitivity of contractile proteins. All these changes are mediated by cytokines. Treatment includes preload optimization with sufficient fluids. However, excessive volume loading is harmful. The first line vasopressor recommended at present is norepinephrine, while vasopressin can be started as a salvage therapy for those not responding to catecholamines. During early sepsis, cardiac output can be increased by dobutamine. While early administration of catecholamines might be necessary to restore adequate organ perfusion, prolonged administration might be harmful. Novel therapies for sepsis-induced cardiac dysfunction are discussed in this article. Cardiac inotropy can be increased by levosimendan, istaroxime or omecamtiv mecarbil without greatly increasing cellular oxygen demands. Heart rate reduction with ivabradine reduces myocardial oxygen expenditure and ameliorates diastolic filling. Beta-blockers additionally reduce local and systemic inflammation. Advances may also come from metabolic interventions such as pyruvate, succinate or high dose insulin substitutions. All these potentially advantageous concepts require rigorous testing before implementation in routine clinical practice. While early administration of catecholamines might be necessary to restore adequate organ perfusion and pressure, prolonged administration might be harmful.Novel therapies for sepsis-induced cardiac dysfunction are discussed in this article. Cardiac inotropy can be increased by levosimendan, istaroxime or omecamtiv mecarbil without greatly increasing cellular oxygen demands. Heart rate reduction with ivabradine will reduce myocardial oxygen expenditure and ameliorate diastolic filling. Beta-blockers additionally reduce local and systemic inflammation. Advances may also come from metabolic interventions such as pyruvate, succinate or high dose insulin substitutions. However, all these potentially advantageous concepts require rigorous testing before implementation in routine clinical practice.-3 -Alain Rudiger & Mervyn Singer: The heart in sepsis

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“…Excessive adrenergic stimulation is harmful to the heart (3). In animal studies, esmolol, a selective beta-1-adrenergic blocker, improves cardiac contractility, stroke volume (SV) and vascular responsiveness to norepinephrine (4)(5)(6). In patients with septic shock who were initially stabilized, Morelli et al showed that esmolol infusion reduced heart rate, increased SV and reduced norepinephrine requirements (7).…”

mentioning

confidence: 99%

Beta-blockers in septic shock: a magnifying glass on the relation heart vessel

2016

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Infusion of the β-adrenergic blocker esmolol attenuates myocardial dysfunction in septic rats*

Abstract: Esmolol infusion in sepsis improved oxygen utilization of myocardium and preserved myocardial function.

Cited by 152 publications

References 42 publications

Heart rate reduction may be a major determinant of vascular tone in esmolol-treated septic shock patients—although still remains to be confirmed!

Heart rate reduction may be a major determinant of vascular tone in esmolol-treated septic shock patients—although still remains to be confirmed!

The Heart in Sepsis: From Basic Mechanisms to Clinical Management

Beta-blockers in septic shock: a magnifying glass on the relation heart vessel

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