Prolonged depletion of ATP and of the adenine nucleotide pool due to delayed resynthesis of adenine nucleotides following reversible myocardial ischemic injury in dogs.
Prolonged depletion of ATP and of the adenine nucleotide pool due to delayed resynthesis of adenine nucleotides following reversible myocardial ischemic injury in dogs.
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犬可逆性心肌缺血损伤后，由于腺嘌呤核苷酸的再合成延迟，导致 ATP 和腺嘌呤核苷酸库的长期消耗。
DOI：
10.1016/0022-2828(81)90219-4
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发表时间：
1981
影响因子：
5
通讯作者：
Jennings,RB
中科院分区：
文献类型：
--
作者：
Reimer,KA;Hill,ML;Jennings,RB
在开胸犬中，通过旋动脉闭塞诱导严重缺血15分钟后，65%的ATP和50%的总腺嘌呤核苷酸（Adenine Nucleotide，NAD）池从内膜下心肌中丢失[12]。然而，如果受影响的组织用冠状动脉血再灌注，这种损伤是可逆的。在本实验中，我们评估了缺血性损伤15分钟后不同时期的动脉复流对ATP和ATP Ad再合成的影响。阻断旋动脉15 min，再灌注20或60 min，或24或96 h。在切除心脏前10秒，将回旋动脉再闭塞，并静脉内注射荧光染料硫代黄素S，以鉴定缺血或已缺血的再灌注组织。缺血15 min后ATP含量从5.42 ± 0.33 μmol/g下降到2.08 ± 0.21 μmol/g，下降了62%，总核苷酸含量下降了50%。ATP含量略有恢复，在第一个20分钟的再灌注，但仍然显着抑制至少24小时，因为腺嘌呤核苷酸的初始耗尽，因为最小的抢救或novosynthesis发生在受伤的肌肉在此期间。到第4天，ATP和总腺嘌呤核苷酸仍略有下降，但已恢复到对照组的88%和91%。电解质的变化和增加菊粉扩散空间，这是不可逆的损伤心肌再灌注20或60分钟的特点，没有观察到。再灌注24或96 h的心脏也未见组织坏死。这些观察结果表明，ATP和腺嘌呤核苷酸的显着抑郁症和这些代谢产物的缓慢恢复发生在心肌，但可逆性损伤的细胞活力。
After 15 min of severe ischemia induced by circumflex artery occlusion in open-chest dogs, 65% of the ATP and 50% of the total adenine nucleotide (ΣAd) pool is lost from the subendocardial myocardium [12]. Nevertheless, this injury is reversible if the affected tissue is reperfused with coronary arterial blood. In the present experiment, we assessed the effects of various periods of arterial reflow following 15 min of ischemic injury, on resynthesis of ATP and ΣAd. The circumflex artery was occluded for 15 min and reperfused for 20 or 60 min, or 24 or 96 h. Ten seconds prior to excision of the heart, the circumflex artery was reoccluded and the fluorescent dye thioflavine S was injected intravenously in order to identify the ischemic or the reperfused tissue which had been ischemic. The mean ATP after 15 min of ischemia was reduced 62% from 5.42 ± 0.33 to 2.08 ± 0.21 μmol/g; and the total nucleotide content was reduced by 50%. ATP content recovered slightly during the first 20 min of reperfusion but remained markedly depressed for at least 24 h because of the initial depletion of adenine nucleotides and because minimal salvage orde novosynthesis occurred in the injured muscle during this time period. By 4 days, ATP and total adenine nucleotides were still slightly depressed but had recovered to 88% and 91% of control. Electrolyte changes and an increased inulin diffusible space, which are characteristic of irreversibly injured myocardium reperfused for 20 or 60 min, were not observed. Also tissue necrosis was absent in the hearts reperfused for 24 or 96 h. These observations indicate that the marked depression of ATP and adenine nucleotides and the slow recovery of these metabolites occurred in myocardium which nevertheless was reversibly injured in terms of cellular viability.