The activation pattern of the antioxidant enzymes in the right ventricle of rat in response to pressure overload is of heart failure type.

Aline Ecarnot-Laubriet, Luc Rochette, Catherine Vergely, Pierre Sicard, Jean-Raymond Teyssier
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引用次数: 32

Abstract

In the left ventricle subjected to pressure overload activity, the antioxidant enzymes increased at the hyperfunctional stage. During the transition to heart failure, these enzymes are down-regulated, oxidative stress increases, and apoptosis progresses. Maladaptative activation of the antioxidant enzymes at an early stage may contribute to the intrinsic vulnerability of right ventricle to pressure overload. The authors studied changes in expression and activity of the enzymes manganese and copper-zinc superoxide dismutases, glutathione peroxidase, and catalase in the right ventricle of rat following induction of pulmonary hypertension by injection of monocrotaline. Increase in the manganese superoxide dismutase was delayed to the late failing stage, activity of glutathione peroxidase was depressed throughout, and only catalase was activated at the early stage before returning to control levels. This inability to activate antioxidant enzymes may contribute to the deleterious consequences of pressure overload on right ventricle systolic function.

大鼠右心室抗氧化酶在压力负荷下的激活模式为心力衰竭型。
在承受压力过载活动的左心室,抗氧化酶在功能亢进阶段增加。在向心力衰竭过渡的过程中,这些酶被下调,氧化应激增加,细胞凋亡进展。早期抗氧化酶的不适应激活可能导致右心室对压力过载的内在脆弱性。研究了大鼠右心室锰、铜锌超氧化物歧化酶、谷胱甘肽过氧化物酶、过氧化氢酶等酶在肺动脉高压诱导下的表达和活性变化。锰超氧化物歧化酶的增加延迟到衰竭晚期,谷胱甘肽过氧化物酶的活性一直被抑制,只有过氧化氢酶在恢复到对照水平之前在早期被激活。这种不能激活抗氧化酶可能导致压力过载对右心室收缩功能的有害后果。
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