权益分类	功能权益	普通用户	{{item.name}}会员
{{category.name}}	{{benefitItem.name}}

The role of nitric oxide in ischemia/reperfusion damage in the heart

一氧化氮在心脏缺血/再灌注损伤中的作用

基本信息

批准号：
07457019
负责人：
ABIKO Yasushi
金额：
$ 4.93万
依托单位：
Asahikawa Medical College
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (B)
财政年份：
1995
资助国家：
日本
起止时间：
1995 至 1996
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-07457019/
关键词：
Myocardium ischemia reperfusion damage oxygen radicals Lysophosphatidylcholine Palmitoylcarnitin Nitric oxide 心筋保護 dilazep K-7259 NO ラット摘出心臓 L-NAME

项目摘要

Ischemia of the heart produces damage on the heart by a decrease in blood (oxygen) supply and/or an increase in oxygen demand of the myocardium. Reperfusion damage, however, occurs when blood supply increases after ischemia. We postulate that it is toxic substances, i. e., ischemic poisons, that inflict damage to the cell during ischemia/reperfusion. The ischemic poisons include oxygen radicals, lysophospholipids and acylcarnitines.The present study was designed to answer to the following two questions. First, do the ischemic poisons inflict an ischemia-like damage to the myocardium and do anti-ischemic drugs attenuate the myocardial damage induced by ischemic poisons? Second, are nitric oxide involved in the production of myocardial damage induced by ischemic poisons?We confirmed that H_2O_2, lysophosphatidylcholine (LPC) and palmitoylcarnitine (PALCAR) produced the ischemia-like damage to the myocardium, and some anti-ischemic substances including dilazep, K-7259 and d-propranolol attenuated the myocardial damage induced by ischemic poisons.We then measured NO_2 and NO_3 in the perfusate in the isolated, perfused rat heart in the hope that dilazep and K-7259 will change the concentrations of NO_2 and NO_3 in the perfusate. However, both dilazep and K-7259 did not modify the concentrations of NO_2 and NO_3 in the perfusate. We also examined whether N^G-L-arginine (L-NAME) attenuates the myocardial damage induced by PALCAR.L-NAME attenuated the PALCAR-induced myocardial damage, but the effect of L-NAME was not reversed by L-arginine. Therefore, we conclude that nitric oxide may not mainly contribute to ischemia/reperfusion damage in the heart.

心脏缺血通过血液（氧）供应的减少和/或心肌的氧需求的增加而对心脏产生损伤。然而，再灌注损伤发生在缺血后血液供应增加时。我们假设它是有毒物质，即。例如，缺血性毒物，在缺血/再灌注期间对细胞造成损害。缺血性毒物包括氧自由基、溶血磷脂和酰基肉毒碱。首先，缺血性毒物是否对心肌造成缺血样损伤，抗缺血药物是否减轻缺血性毒物引起的心肌损伤？第二，一氧化氮是否参与缺血性毒物引起的心肌损伤？我们证实H_2O_2、溶血磷脂酰胆碱（LPC）和棕榈酰卡尼汀（PALCAR）可引起心肌缺血样损伤，而一些抗缺血药物如地拉卓、K-7259和d-心得安可减轻缺血性毒物引起的心肌损伤。目的：观察地拉卓和K-7259对大鼠心脏灌流液中NO_2和NO_3浓度的影响。但地拉卓和K-7259均不改变灌流液中NO_2和NO_3的浓度。我们还研究了N^G-L-精氨酸（L-NAME）是否减轻PALCAR诱导的心肌损伤，L-NAME可减轻PALCAR诱导的心肌损伤，但L-NAME的作用不能被L-Arg逆转。因此，我们得出结论，一氧化氮可能不是主要的缺血/再灌注损伤的心脏。