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

Br J Anaesth. 2009 Jan;102(1):23-8. doi: 10.1093/bja/aen325. Epub 2008 Nov 20.

Abstract

Background: Off-pump coronary artery bypass graft surgery (OPCAB) is still associated with a marked systemic inflammatory response. The aim of this study was to investigate whether pre-emptive, low dose of ketamine, which has been reported to have anti-inflammatory activity in on-pump coronary artery bypass surgery, could reduce inflammatory response in low-risk patients undergoing OPCAB.

Methods: In this prospective randomized-controlled trial, 50 patients with stable angina and preserved myocardial function undergoing OPCAB were randomly assigned to receive either 0.5 mg kg(-1) of ketamine (Ketamine group, n=25) or normal saline (Control group, n=25) during induction of anaesthesia. Inflammatory markers including C-reactive protein (CRP), interleukin (IL)-6, tumour necrosis factor-alpha (TNF-alpha), and cardiac enzymes were measured previous to induction (T1), 4 h after surgery (T2), and the first and second days after the surgery (T3 and T4).

Results: There were no significant intergroup differences in the serum concentrations of the CRP, IL-6, and TNF-alpha and cardiac enzymes. Pro-inflammatory markers and cardiac enzymes, except TNF-alpha, were all increased after the surgery compared with baseline values in both groups.

Conclusions: Low-dose ketamine administered during anaesthesia induction did not exert any evident anti-inflammatory effect in terms of reducing the serum concentrations of pro-inflammatory markers in low-risk patients undergoing OPCAB.

Publication types

  • Randomized Controlled Trial

MeSH terms

  • Aged
  • Anesthetics, Dissociative / therapeutic use*
  • Coronary Artery Bypass, Off-Pump / adverse effects*
  • Female
  • Humans
  • Inflammation Mediators / blood*
  • Interleukin-6 / blood
  • Ketamine / therapeutic use*
  • Male
  • Middle Aged
  • Prospective Studies
  • Systemic Inflammatory Response Syndrome / blood
  • Systemic Inflammatory Response Syndrome / etiology
  • Systemic Inflammatory Response Syndrome / prevention & control*
  • Tumor Necrosis Factor-alpha / blood

Substances

  • Anesthetics, Dissociative
  • Inflammation Mediators
  • Interleukin-6
  • Tumor Necrosis Factor-alpha
  • Ketamine