{"title":"Contribution of sodium channel and sodium/hydrogen exchanger to sodium accumulation in the ischemic myocardium","authors":"Kouichi Tanonaka, Ayako Takasaki, Hiroshi Kajiwara, Satoshi Takeo","doi":"10.1016/S0306-3623(00)00057-4","DOIUrl":null,"url":null,"abstract":"<div><p>Contribution of sodium channels and sodium/hydrogen exchangers (NHEs) to sodium accumulation during ischemia in the ischemic/reperfused heart was examined.</p><p>Ischemia increased the myocardial sodium. Reperfusion elicited a further increase in the myocardial sodium, which was associated with little recovery of the left ventricular developed pressure (LVDP) of the perfused heart.</p><p>Treatment with tetrodotoxin or dimethylamirolide (DMA) dose-dependently attenuated the ischemia- and reperfusion-induced increase in myocardial sodium and enhanced the post-ischemic recovery of the LVDP.</p><p>There was an inverse relationship between the increase in myocardial sodium during ischemia and the post-ischemic recovery of the LVDP.</p><p>The myocardial sodium accumulation during ischemia is mainly attributed to sodium influx through sodium channels and NHEs.</p></div>","PeriodicalId":12607,"journal":{"name":"General Pharmacology-the Vascular System","volume":"34 3","pages":"Pages 167-174"},"PeriodicalIF":0.0000,"publicationDate":"2000-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0306-3623(00)00057-4","citationCount":"15","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"General Pharmacology-the Vascular System","FirstCategoryId":"1085","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0306362300000574","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 15
Abstract
Contribution of sodium channels and sodium/hydrogen exchangers (NHEs) to sodium accumulation during ischemia in the ischemic/reperfused heart was examined.
Ischemia increased the myocardial sodium. Reperfusion elicited a further increase in the myocardial sodium, which was associated with little recovery of the left ventricular developed pressure (LVDP) of the perfused heart.
Treatment with tetrodotoxin or dimethylamirolide (DMA) dose-dependently attenuated the ischemia- and reperfusion-induced increase in myocardial sodium and enhanced the post-ischemic recovery of the LVDP.
There was an inverse relationship between the increase in myocardial sodium during ischemia and the post-ischemic recovery of the LVDP.
The myocardial sodium accumulation during ischemia is mainly attributed to sodium influx through sodium channels and NHEs.
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