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Adenosine infusion during early reperfusion failed to limit myocardial infarct size in a collateral deficient species

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...

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Published in:Cardiovascular research 1991-11, Vol.25 (11), p.943-949
Main Authors: Goto, Mahiko, Miura, Tetsuji, Iliodoromitis, Efstathios K, O'Leary, Edward L, Ishimoto, Row, Yellon, Derek M, Iimura, Osamu
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container_end_page 949
container_issue 11
container_start_page 943
container_title Cardiovascular research
container_volume 25
creator Goto, Mahiko
Miura, Tetsuji
Iliodoromitis, Efstathios K
O'Leary, Edward L
Ishimoto, Row
Yellon, Derek M
Iimura, Osamu
description 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.
doi_str_mv 10.1093/cvr/25.11.943
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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). 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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). 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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.</abstract><cop>England</cop><pub>Oxford University Press</pub><pmid>1813123</pmid><doi>10.1093/cvr/25.11.943</doi><tpages>7</tpages></addata></record>
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source Oxford University Press:Jisc Collections:Oxford Journal Archive: Access period 2024-2025
subjects adenosine
Adenosine - therapeutic use
Animals
Blood Pressure - drug effects
Collateral Circulation - physiology
Male
myocardial infarct size
Myocardial Infarction - drug therapy
Myocardial Infarction - pathology
Myocardial Reperfusion Injury - prevention & control
Myocardium - pathology
rabbit
Rabbits
reperfusion
title Adenosine infusion during early reperfusion failed to limit myocardial infarct size in a collateral deficient species
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