Effect of low-dose ketamine on inflammatory response in off-pump coronary artery bypass graft surgery

Cho, J. E.; Shim, Jæ Kwang; Choi, Yong Seon; Kim, D. H.; Hong, Stephanie; Kwak, Young Lan

doi:10.1093/bja/aen325

Cited by 34 publications

(23 citation statements)

References 27 publications

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“…[79][80][81] The use of ketamine in cardiac surgery was associated with decreased inflammation, opioid sparing, and improved patient satisfaction postoperatively. [82][83][84][85][86][87][88][89][90] Its use in the prevention of chronic poststernotomy pain has not been studied.…”

Section: Acetaminophenmentioning

confidence: 99%

Chronic Poststernotomy Pain

Kleiman

Sanders

Nemergut

et al. 2017

Regional Anesthesia and Pain Medicine

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Chronic pain following median sternotomy is common after cardiac surgery. If left untreated, chronic sternal pain can reduce quality of life, affecting sleep, mood, activity level, and overall satisfaction. This has a significant societal effect given the large number of cardiac surgeries annually. Although a number of pathophysiologic processes and risk factors are assumed to contribute, the exact cause and major risk factors remain unknown. Moreover, the treatment of chronic poststernotomy pain is often inadequate, relying on opioids and other medications that provide minimal benefit to the patient and have significant adverse effects. Indeed, little is known regarding the prevention of chronic pain development following sternotomy. This review aims to present the current, limited data regarding the incidence, risk factors, treatment, and prevention of chronic poststernotomy pain and to identify areas of future research to improve management of this common complaint following cardiac surgery.

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Section: Acetaminophenmentioning

confidence: 99%

Chronic Poststernotomy Pain

Kleiman

Sanders

Nemergut

et al. 2017

Regional Anesthesia and Pain Medicine

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“…In another randomized, placebo-controlled trial with two doses of ketamine (0.25 or 0.5 mg/kg) vs. placebo in on-pump CABG patients during general anesthesia cardiac induction, both ketamine doses suppressed the elaboration of several pro-inflammatory markers/cytokines—C-reactive protein (CRP), IL-6, and IL-10 (but not IL-8)—with concomitant sympathomimetic effects (Bartoc et al 2006). Yes, in off-pump CABG, ketamine did not decrease serum levels of pro-inflammatory cytokines—CRP, IL-6, tumor necrosis factor-alpha (TNFα), and cardiac enzymes—in the perioperative period (Cho et al 2009). To date, there have not been any studies examining levels of pro-inflammatory mediators in response to subanesthetic-dose ketamine for major depression, but this is an area of active investigation by many groups studying ketamine as a rapidly acting anti-depressant in both the preclinical and clinical realms.…”

Section: Ketamine and Inflammationmentioning

confidence: 99%

Glutamate and its receptors in the pathophysiology and treatment of major depressive disorder

et al. 2013

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Monoaminergic neurotransmitter (serotonin, norepinephrine and dopamine) mechanisms of disease dominated the research landscape in the pathophysiology and treatment of major depressive disorder (MDD) for more than 50 years and still dominate available treatment options. However, the sum of all brain neurons that use monoamines as their primary neurotransmitter is <20 %. In addition, most patients treated with monoaminergic antidepressants are left with significant residual symptoms and psychosocial disability not to mention side effects, e.g., sexual dysfunction. In the past several decades, there has been greater focus on the major excitatory neurotransmitter in the human brain, glutamate, in the pathophysiology and treatment of MDD. Although several preclinical and human magnetic resonance spectroscopy studies had already implicated glutamatergic abnormalities in the human brain, it was rocketed by the discovery that the N-methyl-D-aspartate receptor antagonist ketamine has rapid and potent antidepressant effects in even the most treatment-resistant MDD patients, including those who failed to respond to electroconvulsive therapy and who have active suicidal ideation. In this review, we will first provide a brief introduction to glutamate and its receptors in the mammalian brain. We will then review the clinical evidence for glutamatergic dysfunction in MDD, the discovery and progress-to-date with ketamine as a rapidly acting antidepressant, and other glutamate receptor modulators (including proprietary medications) for treatment-resistant depression. We will finally conclude by offering potential future directions necessary to realize the enormous therapeutic promise of glutamatergic antidepressants.

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“…Though corticosteroids have been shown to reduce the serum inflammatory markers, [20,21] neither systemic nor inhaled corticosteroids have been shown to offer clinical benefits measured in terms of pulmonary dysfunction, oxygenation, duration of mechanical ventilation, hemodynamic benefit, or improvement in pain control in patients undergoing CPB. [5,22,23] In addition, Cho et al, have studied 50 patients undergoing off-pump CABG and concluded that administration of 0.5 mg/kg of ketamine at induction of general anesthesia did not result in significant changes in serum levels of CRP, IL 6, TNF alpha and cardiac enzymes [24] even though off-pump CABG has been shown to induce marked and similar inflammatory response as that of CPB. [18,25] Ketamine has been shown not to decrease the IL-6 levels in the tracheobronchial aspirate of infants undergoing cardiac surgery.…”

Section: Resultsmentioning

confidence: 99%