豚鼠心脏氧反常损伤机制及药物保护

MECHANISM AND DRUG PROTECTION OF OXYGEN PARADOX INJURY IN GUINEA PIG HEART

本文在离体灌流豚鼠心脏模型上研究了氧反常损伤的机制。结果表明：缺氧４０ｍｉｎ时，心肌钠，钾－三磷酸腺苷酶（Ｎａ~＋，Ｋ~－ＡＴＰａｓｅ）活性下降２４％（Ｐ＜０．０５），钙（Ｃａ^（２＋））含量升高２８％（Ｐ＜０．０５），丙二醛（ＭＤＡ）含量无明显变化。复氧２ｍｉｎ时，Ｎａ＋，Ｋ＋－ＡＴＰａｓｅ活性下降４８％，与缺氧４０ｍｉｎ相比有显著差异，Ｃａ^（２＋）和ＭＤＡ含量分别增加９０％和４３％；复氧２０ｍｉｎ时，Ｎａ~＋，Ｋ~＋－ＡＴＰａｓｅ活性下降７２％，Ｃａ^（２＋）和ＭＤＡ含量分别增加７．２倍和３．７倍。复氧２０～３０ｓ即有·ＯＨ和Ｏ－２产生，在复氧３ｍｉｎ时达高峰。结果提示，氧自由基可能是氧反常损伤的初始原因；小壁胺（３μＭ）和地尔硫（３μＭ）能不同程度地减轻氧反常损伤。

A model of isolated perfused guinea pig heart was used to investigate the mechanism of oxygen paradox injury. The results showed that after 40 min anoxia,myocardial Na+, K+-ATPase activity decreased by 24% (p<0.05), Ca^(2+) content increased by 28%(p<0. 05), MDA level had no significant change. After 2 min reoxygenation, Na+, K+- ATPase activity decreased further by 48%, which had significant difference compared with that of 40 min anoxia. Myocardial Ca￣(2+) and MDA contents increased by 90% and 43%,respectively. After 20 min reoxygenation, Na+, K+-ATPase activity decreased by 72%, Ca￣(2+) and MDA contents increased 7. 2 times and 3. 7 times of control values, respectively. OH and O-2 generated 20-30 sec and peaked at 3 min after reoxygenation. The results suggest that oxygen free radicals might be involved in oxygen paradox injury. Berbamine(2μM) and diltiazem(3μM) could alleviate this injury to some extent.