Abstract
BackgroundDesflurane during early reperfusion has been shown to postcondition human myocardium, in vitro. We investigated the role of adenosine and bradykinin receptors, and generation of radical oxygen species in desflurane-induced postconditioning in human myocardium.MethodsWe recorded isometric contraction of human right atrial trabeculae hanged in an oxygenated Tyrode's solution (34 degrees Celsius, stimulation frequency 1 Hz). After a 30-min hypoxic period, desflurane 6% was administered during the first 5 min of reoxygenation. Desflurane was administered alone or with pretreatment of N-mercaptopropionylglycine, a reactive oxygen species scavenger, 8-(p-Sulfophenyl)theophylline, an adenosine receptor antagonist, HOE140, a selective B2 bradykinin receptor antagonist. In separate groups, adenosine and bradykinin were administered during the first minutes of reoxygenation alone or in presence of N-mercaptopropionylglycine. The force of contraction of trabeculae was recorded continuously. Developed force at the end of a 60-min reoxygenation period was compared (mean ± standard deviation) between the groups by a variance analysis and post hoc test.ResultsDesflurane 6% (84 ± 6% of baseline) enhanced the recovery of force after 60-min of reoxygenation as compared to control group (51 ± 8% of baseline, P < 0.0001). N-mercaptopropionylglycine (54 ± 3% of baseline), 8-(p-Sulfophenyl)theophylline (62 ± 9% of baseline), HOE140 (58 ± 6% of baseline) abolished desflurane-induced postconditioning. Adenosine (80 ± 9% of baseline) and bradykinin (83 ± 4% of baseline) induced postconditioning (P < 0.0001 vs control), N-mercaptopropionylglycine abolished the beneficial effects of adenosine and bradykinin (54 ± 8 and 58 ± 5% of baseline, respectively).ConclusionsIn vitro, desflurane-induced postconditioning depends on reactive oxygen species production, activation of adenosine and bradykinin B2 receptors. And, the cardioprotective effect of adenosine and bradykinin administered at the beginning of reoxygenation, was mediated, at least in part, through ROS production.
Highlights
Desflurane during early reperfusion has been shown to postcondition human myocardium, in vitro
The objectives of our study were to determine whether: 1) reactive oxygen species (ROS) generation, and adenosine and bradykinin receptor stimulation may be involved in desfluraneinduced PostC, 2) adenosine and bradykinin given at the beginning of reoxygenation mimic PostC, 3) adenosine and bradykinin receptors’ activation was followed by myocardial PostC via ROS production
Mechanisms involved in desflurane-induced PostC were studied in presence of desflurane 6%, because we have previously shown that 6% was effective to induce PostC in human myocardium, in vitro
Summary
Desflurane during early reperfusion has been shown to postcondition human myocardium, in vitro. We investigated the role of adenosine and bradykinin receptors, and generation of radical oxygen species in desflurane-induced postconditioning in human myocardium. It has been shown that adenosine and bradykinin postconditioned isolated rabbit [10] and rat hearts [11], via stimulation of adenosine and B2 receptors. The involvement of adenosine and bradykinin receptors in anesthetic-induced PostC remains unknown, whereas these receptors were shown to be involved in anesthetic-induced preconditioning [12]. Only two studies suggested that ROS were involved in isofluraneinduced PostC in mouse myocardium in vivo [3], and in sevoflurane-induced PostC in isolated rat hearts [8]
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