Gilmour R F, Williams E S, Farmer B B, Zipes D P
Am J Physiol. 1981 Oct;241(4):H505-12. doi: 10.1152/ajpheart.1981.241.4.H505.
It has been proposed that electrophysiological changes following coronary artery occlusion result from inhibition of the adenine nucleotide translocase and that these changes can be reduced by carnitine infusion or reproduced by infusion of K+-atractyloside. In the present study, we recorded bipolar electrograms during serial 3- to 5-min occlusions of the left anterior descending coronary artery in open-chest, anesthetized dogs. DL-Carnitine (100-200 mg/kg iv) prior to coronary artery occlusion did not significantly alter ischemia-induced electrogram changes. L-Carnitine (100 mg/min ia) distal to the site of occlusion during coronary artery occlusion partially reversed ischemia-induced electrogram changes, but these effects resembled those produced by intra-arterial infusion of NaCl. During normal perfusion, intra-arterial infusion of K+-atractyloside (750 mumol/10 min) or equimolar KCl produced similar reversible flattening of perfused zone electrograms. Sodium atractyloside (750 mumol/10 min ia) did not produce electrogram changes. We conclude that 1) carnitine does not attenuate ischemia-induced electrogram changes in this model and 2) K+-atractyloside-induced electrogram changes are primarily due to K+.
有人提出，冠状动脉闭塞后的电生理变化是由于腺嘌呤核苷酸转位酶受到抑制所致，并且这些变化可通过输注肉碱而减轻，或通过输注K+-苍术苷而重现。在本研究中，我们在开胸、麻醉的犬身上，于左前降支冠状动脉连续闭塞3至5分钟期间记录双极电图。在冠状动脉闭塞前静脉注射DL-肉碱（100 - 200 mg/kg）并未显著改变缺血诱导的电图变化。在冠状动脉闭塞期间，于闭塞部位远端动脉内注射L-肉碱（100 mg/min）可部分逆转缺血诱导的电图变化，但这些效应类似于动脉内输注NaCl所产生的效应。在正常灌注期间，动脉内输注K+-苍术苷（750 μmol/10 min）或等摩尔的KCl可使灌注区电图产生类似的可逆性平坦化。动脉内注射苍术苷钠（750 μmol/10 min）未产生电图变化。我们得出结论：1）在该模型中肉碱不会减轻缺血诱导的电图变化；2）K+-苍术苷诱导的电图变化主要归因于K+。
