TY - JOUR
T1 - The cardioprotective effect of dexmedetomidine on global ischaemia in isolated rat hearts
AU - Okada, Hisako
AU - Kurita, Tadayoshi
AU - Mochizuki, Toshiaki
AU - Morita, Koji
AU - Sato, Shigehito
N1 - Copyright:
Copyright 2008 Elsevier B.V., All rights reserved.
PY - 2007/9
Y1 - 2007/9
N2 - Aim: Dexmedetomidine is a highly specific and selective α-2 adrenergic agonist that is now widely used in the intensive care setting. Many intensive care unit (ICU) patients are at risk of respiratory or cardiac arrest. This study was conducted to determine whether dexmedetomidine exhibits a cardioprotective effect on global ischaemia and subsequent myocardial infarction. Methods: Isolated rat hearts were subjected to 30 min of global ischaemia followed by 120 min reperfusion, with administration of 0, 1 and 10 nM dexmedetomidine during the pre-ischaemic period (n = 7 each group). Secondly, 1 μM yohimbine, an α-2 antagonist, was given during the pre-ischaemic period, alone or in combination with 10 nM dexmedetomidine (n = 7 each group). Results: Dexmedetomidine administration reduced coronary flow significantly (103.6 ± 4.7%, 77.9 ± 3.7, 63.7 ± 6.1%, of the baseline values for 0, 1 and 10 nM dexmedetomidine, respectively), and yohimbine administration reversed this effect (88.0 ± 2.2%). Dexmedetomidine improved the infarct size at each concentration (45.3 ± 3.6, 30.2 ± 3.3, and 21.2 ± 2.3% of the total left ventricular mass for 0, 1, and 10 nM dexmedetomidine, respectively), which was also reversed by yohimbine (43.6 ± 1.4%). Conclusion: Dexmedetomidine exhibited a cardioprotective effect on global ischaemia in the isolated rat heart model, which was mediated by α-2 adrenergic stimulation.
AB - Aim: Dexmedetomidine is a highly specific and selective α-2 adrenergic agonist that is now widely used in the intensive care setting. Many intensive care unit (ICU) patients are at risk of respiratory or cardiac arrest. This study was conducted to determine whether dexmedetomidine exhibits a cardioprotective effect on global ischaemia and subsequent myocardial infarction. Methods: Isolated rat hearts were subjected to 30 min of global ischaemia followed by 120 min reperfusion, with administration of 0, 1 and 10 nM dexmedetomidine during the pre-ischaemic period (n = 7 each group). Secondly, 1 μM yohimbine, an α-2 antagonist, was given during the pre-ischaemic period, alone or in combination with 10 nM dexmedetomidine (n = 7 each group). Results: Dexmedetomidine administration reduced coronary flow significantly (103.6 ± 4.7%, 77.9 ± 3.7, 63.7 ± 6.1%, of the baseline values for 0, 1 and 10 nM dexmedetomidine, respectively), and yohimbine administration reversed this effect (88.0 ± 2.2%). Dexmedetomidine improved the infarct size at each concentration (45.3 ± 3.6, 30.2 ± 3.3, and 21.2 ± 2.3% of the total left ventricular mass for 0, 1, and 10 nM dexmedetomidine, respectively), which was also reversed by yohimbine (43.6 ± 1.4%). Conclusion: Dexmedetomidine exhibited a cardioprotective effect on global ischaemia in the isolated rat heart model, which was mediated by α-2 adrenergic stimulation.
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U2 - 10.1016/j.resuscitation.2007.01.032
DO - 10.1016/j.resuscitation.2007.01.032
M3 - Article
C2 - 17391832
AN - SCOPUS:34547455307
VL - 74
SP - 538
EP - 545
JO - Resuscitation
JF - Resuscitation
SN - 0300-9572
IS - 3
ER -