Venditti Paola, Bari Angela, Di Stefano Lisa, Agnisola Claudio, Di Meo Sergio
Dipartimento delle Scienze Biologiche, Sezione di Fisiologia, Università Federico II di Napoli, V. Mezzocannone 8, I80134 Naples, Italy.
Pflugers Arch. 2008 Jan;455(4):667-76. doi: 10.1007/s00424-007-0328-x. Epub 2007 Aug 16.
We investigated whether swim training modifies the effect of T(3) treatment on rat heart response to ischemia-reperfusion. Homogenates of Langendorff preparations perfused for 25 min after 20-min ischemia were used for biochemical determinations and isolation of mitochondrial fractions. Oxidative damage and antioxidant levels of homogenates, O(2) consumption and H(2)O(2) release rates, oxidative damage, and susceptibility to Ca(2+)-induced swelling of mitochondria were determined. During reperfusion, hyperthyroid hearts displayed significant tachycardia and low inotropic recovery. This pattern was improved by training, which also attenuated tissue oxidative damage and glutathione depletion. Similar training effects were shown in euthyroid preparations. Moreover, training reduced mitochondrial H(2)O(2) production and oxidative damage in hyperthyroid and euthyroid hearts and susceptibility to Ca(2+)-induced swelling only in the hyperthyroid ones. Rates of mitochondrial O(2) consumption were not different in sedentary and trained hyperthyroid rats. However, determination of the oxidative capacity suggested that, in the sedentary rats, O(2) consumption was conditioned by oxidative damage mitochondria have suffered, whereas in trained rats, it was due to changes in mitochondrial characteristics. The above results suggest that moderate training is able to reduce hyperthyroid heart susceptibility to oxidative damage and dysfunction modifying mitochondrial population.
我们研究了游泳训练是否会改变T(3)治疗对大鼠心脏缺血再灌注反应的影响。在20分钟缺血后灌注25分钟的Langendorff标本匀浆用于生化测定和线粒体组分的分离。测定了匀浆的氧化损伤和抗氧化水平、O(2)消耗和H(2)O(2)释放速率、氧化损伤以及线粒体对Ca(2+)诱导肿胀的敏感性。在再灌注期间，甲状腺功能亢进的心脏表现出明显的心动过速和低收缩性恢复。这种模式通过训练得到改善，训练还减轻了组织氧化损伤和谷胱甘肽消耗。在甲状腺功能正常的标本中也显示出类似的训练效果。此外，训练降低了甲状腺功能亢进和甲状腺功能正常的心脏中线粒体H(2)O(2)的产生和氧化损伤，并且仅在甲状腺功能亢进的心脏中降低了对Ca(2+)诱导肿胀 的敏感性。久坐不动和经过训练的甲状腺功能亢进大鼠的线粒体O(2)消耗率没有差异。然而，氧化能力的测定表明，在久坐不动的大鼠中，O(2)消耗受线粒体所遭受的氧化损伤的影响，而在经过训练的大鼠中，这是由于线粒体特征的变化。上述结果表明适度训练能够降低甲状腺功能亢进心脏对氧化损伤和功能障碍的易感性，通过改变线粒体群体来实现。
