An investigation of arterial insufficiency in rat hindlimb. An enzymic, mitochondrial and histological study.
An investigation of arterial insufficiency in rat hindlimb. An enzymic, mitochondrial and histological study.
复制标题
大鼠后肢动脉供血不足的研究。
作者：
D. J. Hayes;R. Challiss;G. Radda
动脉功能不全的小动物模型已被用来研究在腓肠肌，跖肌和比目鱼肌的低灌注肢体的酶的变化。在单侧股动脉结扎诱导动脉功能不全后7天，己糖激酶，磷酸化酶和6-磷酸果糖激酶的最大活性显着增加，而柠檬酸合酶和2-酮戊二酸脱氢酶的活性保持不变。在单侧动脉结扎后8-10周，己糖激酶、磷酸化酶和6-磷酸果糖激酶的类似增加仍然明显，尽管只有己糖激酶仍然显著高于对侧对照值。未观察到氧化酶活性的增强。结果进行了讨论与其他研究组报告的动脉功能不全患者的酶适应相矛盾的结果。
A small animal model of arterial insufficiency has been used to investigate enzymic alterations in the gastrocnemius, plantaris and soleus muscles of the hypoperfused limb. At 7 days after induction of arterial insufficiency by unilateral femoral artery ligation, there were significant increases in the maximal activities of hexokinase, phosphorylase and 6-phosphofructokinase, whereas the activities of citrate synthase and 2-oxoglutarate dehydrogenase remained unchanged. Similar increases in hexokinase, phosphorylase and 6-phosphofructokinase were still apparent 8-10 weeks after unilateral artery ligation, although only hexokinase remained significantly higher than contralateral control values. No enhancement of oxidative enzyme activities was observed. The results are discussed in relation to the conflicting findings reported by other groups investigating enzymic adaptations in patients with arterial insufficiency.