Key result
Remifentanil preconditioning significantly reduced myocardial infarct size from 34.9% to 20.7%, an effect that was abolished by A1 and A2B adenosine receptor antagonists.
Why the study?
Does remifentanil preconditioning reduce infarct size in isolated rat hearts, and is this effect mediated by cross-talk between opioid and adenosine receptors?
Does remifentanil preconditioning reduce infarct size in isolated rat hearts, and is this effect mediated by cross-talk between opioid and adenosine receptors?
Remifentanil preconditioning protects against myocardial ischemia-reperfusion injury in rat hearts through a mechanism involving cross-talk between opioid receptors and A1 and A2B adenosine receptors.
Answers are grounded in this paper and cite their sources.
Supports opioid-adenosine receptor cross-talk in rat cardioprotection; hypothesis-generating and requires confirmation before clinical consideration.
The purpose of this study was to determine whether there is a cross-talk between opioid receptors (OPRs) and adenosine receptors (ADRs) in remifentanil preconditioning (R-Pre) and, if so, to investigate the types of ADRs involved in the cross-talk. Isolated rat hearts received 30 min of regional ischemia followed by 2 hr of reperfusion. OPR and ADR antagonists were perfused from 10 min before R-Pre until the end of R-Pre. The heart rate, left ventricular developed pressure (LVDP),velocity of contraction (+dP/dtmax), and coronary flow (CF) were recorded. The area at risk and area of necrosis were measured. After reperfusion, the LVDP, +dP/dtmax,and CF showed a significant increase in the R-Pre group compared with the control group (no intervention before or after regional ischemia). These increases in the R-Pre group were blocked by naloxone, a nonspecific ADR antagonist, an A1 ADR antagonist, and an A2B ADR antagonist. The infarct size was reduced significantly in the R-Pre group compared with the control group. The infarct-reducing effect in the R-Pre group was blocked by naloxone, the nonspecific ADR antagonist, the A1 ADR antagonist, and the A2B ADR antagonist. The results of this study demonstrate that there is cross-talk between ADRs and OPRs in R-Pre and that A1 ADR and A2B ADR appear to be involved in the cross-talk.
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Lee et al. (2015) studied Ischemia-reperfusion injury (n=64). Remifentanil preconditioning vs. No intervention was evaluated on Area of necrosis as a percentage of the area at risk (AN/AR) (p=<0.01). Remifentanil preconditioning significantly reduced myocardial infarct size from 34.9% to 20.7%, an effect that was abolished by A1 and A2B adenosine receptor antagonists.
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