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Adenosine infusion during early reperfusion failed to limit myocardial infarct size in a collateral deficient species
M Goto1, T Miura, E K Iliodoromitis
1Second Department of Internal Medicine, Sapporo Medical College, Japan.
Insights
Adenosine did not limit myocardial infarct size in rabbits, even with lignocaine. This study investigated adenosine
Area of Science:
- Cardiovascular Research
- Myocardial Infarction
- Pharmacology
Background:
- Adenosine and lignocaine may protect against reperfusion injury and limit infarct size in canines.
- Rabbit hearts differ from canine hearts due to lack of xanthine oxidase and significant coronary collaterals.
Purpose of the Study:
- To evaluate the cardioprotective effects of intravenous adenosine in rabbit hearts.
- To determine if adenosine, with or without lignocaine, limits myocardial infarct size in rabbits.
Main Methods:
- Rabbits underwent 30-minute coronary artery occlusion followed by reperfusion.
- Adenosine (high or low dose) with or without lignocaine was administered before reperfusion.
- Infarct size was assessed after 3 or 72 hours of reperfusion.
Main Results:
- High-dose adenosine significantly reduced blood pressure and caused coronary steal.
- Neither high nor low doses of adenosine, with or without lignocaine, reduced infarct size.
- Infarct size remained comparable across all treatment and control groups.
Conclusions:
- Intravenous adenosine does not limit myocardial infarct size in the rabbit model.
- Adenosine's lack of efficacy may be due to species-specific differences in cardiac physiology.
- Adenosine and lignocaine combination did not provide cardioprotection in this rabbit study.
Study Objective:
Intracoronary or intravenous adenosine during reperfusion in combination with lignocaine may attenuate "reperfusion injury" and limit myocardial infarct size in the canine heart. The aim of this study was to test whether intravenous adenosine also protects myocardium in the rabbit heart, which lacks xanthine oxidase and significant coronary collaterals in contrast to the canine heart.
Design:
Five groups of rabbits underwent a 30 min occlusion of the circumflex coronary artery, followed by reperfusion. In adenosine treated groups, either a high dose of adenosine (0.37 mg.kg-1.min-1) with lignocaine treatment (5 mg intravenously 1 min before coronary occlusion and before reperfusion) or a low dose (0.15 mg.kg-1.min-1) of adenosine with or without lignocaine was infused for 60 min starting 5 min before the onset of reperfusion. Group 1 was untreated, while group 2 received a high dose of adenosine with lignocaine. These groups were reperfused for 3 h. Group 3 was untreated, group 4 received a low dose of adenosine, and group 5 a low dose of adenosine and lignocaine. These groups were reperfused for 72 h.
Experimental Material:
60 anaesthetised open chest rabbits were used. Groups 1 and 2 were killed after 3 h coronary reperfusion. Groups 3, 4, and 5 recovered from surgery for 72 h and were then killed for further study.
Measurements And Main Results:
The high dose of adenosine reduced mean blood pressure to 44% of baseline value and diminished reactive hyperaemia in the area at risk by "coronary steal". The low dose of adenosine did not significantly alter systemic blood pressure or heart rate. Infarct size did not differ between groups 1 and 2, at 39.7(SD 20.1)% of area at risk v 33.2(15.9)% (by tetrazolium staining), nor between groups 3, 4, and 5: 50.3(12.6)% v 52.7(15.6)% v 47.8(9.3)% (by histology).
Conclusion:
Neither a high dose nor a low dose of adenosine limited myocardial infarct size in the rabbit heart even when adenosine was combined with lignocaine treatment.