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Pharmacological delayed preconditioning against ischaemia-induced ventricular arrhythmias: effect of an adenosine
R Tissier1, R Souktani, O Parent de Curzon
1Département de Pharmacologie, Faculté de Médecine Paris Sud and INSERM E 00.01, 63, rue Gabriel Péri, 94276 Le Kremlin-Bicêtre Cedex, France.
Insights
Delayed preconditioning using an adenosine A(1)-receptor agonist (A(1)-DPC) or ischaemia-induced delayed preconditioning (I-DPC) reduced infarct size but did not prevent ventricular arrhythmias during ischaemia-reperfusion in rabbits.
Area of Science:
- Cardiology
- Pharmacology
- Ischaemia-Reperfusion Injury
Background:
- Delayed preconditioning strategies aim to protect the heart against ischaemia-reperfusion injury.
- Adenosine A(1)-receptor agonists are investigated for their cardioprotective potential.
- Ventricular arrhythmias are a critical complication of myocardial ischaemia and reperfusion.
Purpose of the Study:
- To compare the anti-arrhythmic effects of pharmacological delayed preconditioning (A(1)-DPC) with ischaemia-induced delayed preconditioning (I-DPC).
- To evaluate the efficacy of N(6)-cyclopentyladenosine, an adenosine A(1)-receptor agonist, in preventing ventricular arrhythmias.
- To assess the impact of these preconditioning methods on infarct size during ischaemia-reperfusion.
Main Methods:
- Conscious rabbits underwent a two-day protocol involving either saline control, I-DPC, or A(1)-DPC (100 or 400 microg kg(-1)).
- On day two, animals were subjected to 30-minute coronary artery occlusion followed by reperfusion.
- Ventricular arrhythmias were quantified using an arrhythmia score, and infarct size was measured as a percentage of the area at risk.
Main Results:
- Both I-DPC and A(1)-DPC significantly reduced infarct size compared to the control group.
- Neither I-DPC nor A(1)-DPC altered the incidence or severity of ventricular arrhythmias during ischaemia and reperfusion.
- Pharmacological and ischaemia-induced delayed preconditioning failed to provide anti-arrhythmic protection in this model.
Conclusions:
- Delayed preconditioning, whether pharmacological or ischaemia-induced, effectively reduces infarct size in a rabbit model of ischaemia-reperfusion.
- However, these preconditioning methods do not offer protection against ventricular arrhythmias.
- Further research is needed to develop strategies that provide both infarct size reduction and anti-arrhythmic effects.
Abstract:
1. The goal of this study was to investigate the effects of the delayed pharmacological preconditioning produced by an adenosine A(1)-receptor agonist (A(1)-DPC) against ventricular arrhythmias induced by ischaemia and reperfusion, compared to those of ischaemia-induced delayed preconditioning (I-DPC). 2. Eighty-nine instrumented conscious rabbits underwent a 2 consecutive days protocol. On day 1, rabbits were randomly divided into four groups: 'Control' (saline, i.v.), 'I-DPC' (six 4-min coronary artery occlusion/4-min reperfusion cycles), 'A(1)-DPC(100)' (N(6)-cyclopentyladenosine, 100 microg kg(-1), i.v.), and 'A(1)-DPC(400)' (N(6)-cyclopentyladenosine, 400 microg kg(-1), i.v.). On day 2, i.e., 24 h later, the incidence and severity of ventricular arrhythmias during a 30-min coronary artery occlusion and subsequent reperfusion were analysed in all animals, using an arrhythmia score. 3. I-DPC, A(1)-DPC(100) and A(1)-DPC(400) significantly reduced the infarct size (34+/-5, 42+/-3 and 43+/-7% of the area at risk, respectively) as compared to Control (55+/-3% of the area at risk). 4. During both ischaemia and reperfusion, neither the incidence nor the severity of ventricular arrhythmias were altered by A(1)-DPC(100), A(1)-DPC(400) or I-DPC as compared to Control. 5. Thus, despite reduction of infarct size induced by delayed preconditioning, A(1)-DPC as well as I-DPC failed to exert any anti-arrhythmic effect in the conscious rabbit model of ischaemia-reperfusion.
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