Aussedat J, Verdys M, Rossi A
Can J Physiol Pharmacol. 1985 Sep;63(9):1159-64. doi: 10.1139/y85-190.
[14C]inosine in a range of concentrations of 20 microM to 1 mM was administered to the isolated perfused rat heart for 30 min. The incorporation of the nucleoside into myocardial adenine nucleotides increased for extracellular concentrations of the precursor up to 50 microM, reaching a plateau at 60 nmol . g-1 X 30 min-1 with concentrations ranging between 50 and 200 microM. The supply of 500 microM and 1 mM of inosine induced a further increase in cardiac adenine nucleotide synthesis to about 200 nmol . g-1 X 30 min-1. When supplied during low flow ischaemia (0.5 mL . min-1, 30 min.), 1 mM of inosine protected the heart against ATP degradation, while 100 microM of inosine was inefficacious. In the presence of 1 mM of inosine on reperfusion the adenine nucleotide content of the heart was similar to that observed in the absence of the nucleoside. The incorporation of [14C]inosine into adenine nucleotides was, in this last condition, below the value measured before ischaemia. Inosine administration was effective in protecting the heart against ischaemic breakdown of glycogen and favoured postischaemic restoration of glycogen stores.
将一系列浓度在20微摩尔至1毫摩尔之间的[14C]肌苷给予离体灌注大鼠心脏30分钟。对于细胞外浓度高达50微摩尔的前体，核苷掺入心肌腺嘌呤核苷酸的量增加，在50至200微摩尔的浓度范围内，以60纳摩尔·克-1×30分钟-1达到平台期。供应500微摩尔和1毫摩尔的肌苷可使心脏腺嘌呤核苷酸合成进一步增加至约200纳摩尔·克-1×30分钟-1。在低流量缺血（0.5毫升·分钟-1，30分钟）期间供应时，1毫摩尔的肌苷可保护心脏免受ATP降解，而100微摩尔的肌苷则无效。在再灌注时存在1毫摩尔肌苷的情况下，心脏的腺嘌呤核苷酸含量与在不存在该核苷时观察到的相似。在最后这种情况下，[14C]肌苷掺入腺嘌呤核苷酸的量低于缺血前测得的值。给予肌苷可有效保护心脏免受缺血性糖原分解，并有利于缺血后糖原储备的恢复。
