Effects of sodium salicylate on ischemia/reperfusion injury in isolated rat hearts

Zhousheng Xiao, Y. X. Fang, X. Chen

Research output: Contribution to journalArticle

Abstract

This study was designed to examine the effects of sodium salicylate (SA) on ischemia reperfusion injury in isolated perfused rat hearts. After 30 min ischemia and 30 min reperfusion, myocardial function was impaired, as shown by 29%, 23% and 46% decreases in the left ventricular pressure (LVP), the maximal rate of left ventricular pressure rise (LV dp/dt(max)) and coronary flow (CF), respectively, and Ca2+ content of myocardial tissue was markedly elevated. However, pretreatment with SA significantly deteriorated reperfusion-induced damages in a dose-dependent manner. Ca2+ content of myocardial tissue in the presence of SA was higher compared to control. The effect of SA was attenuated or abolished by EDTA (0.1 mmol·L-1) and 3% BSA, respectively. These results suggest that SA deteriorates ischemia-reperfusion injury in isolated perfused rat hearts and that the mechanism may be related to facilitation of calcium overload on myocardial tissue.

Original languageEnglish (US)
Pages (from-to)187-190
Number of pages4
JournalChinese Journal of Pharmacology and Toxicology
Volume8
Issue number3
StatePublished - Jan 1 1994

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Sodium Salicylate
Salicylates
Reperfusion Injury
Rats
Ventricular Pressure
Tissue
Myocardial Reperfusion
Edetic Acid
Ischemia
Calcium

All Science Journal Classification (ASJC) codes

  • Toxicology
  • Pharmacology

Cite this

Effects of sodium salicylate on ischemia/reperfusion injury in isolated rat hearts. / Xiao, Zhousheng; Fang, Y. X.; Chen, X.

In: Chinese Journal of Pharmacology and Toxicology, Vol. 8, No. 3, 01.01.1994, p. 187-190.

Research output: Contribution to journalArticle

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abstract = "This study was designed to examine the effects of sodium salicylate (SA) on ischemia reperfusion injury in isolated perfused rat hearts. After 30 min ischemia and 30 min reperfusion, myocardial function was impaired, as shown by 29{\%}, 23{\%} and 46{\%} decreases in the left ventricular pressure (LVP), the maximal rate of left ventricular pressure rise (LV dp/dt(max)) and coronary flow (CF), respectively, and Ca2+ content of myocardial tissue was markedly elevated. However, pretreatment with SA significantly deteriorated reperfusion-induced damages in a dose-dependent manner. Ca2+ content of myocardial tissue in the presence of SA was higher compared to control. The effect of SA was attenuated or abolished by EDTA (0.1 mmol·L-1) and 3{\%} BSA, respectively. These results suggest that SA deteriorates ischemia-reperfusion injury in isolated perfused rat hearts and that the mechanism may be related to facilitation of calcium overload on myocardial tissue.",
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