Corydalis yanhusuo W. T. Wang has also been used in China for the treatment of a variety of cardiovascular diseases, and l-THP is once again believed to be the main active principle. More recent studies have suggested that another important mechanism of l-THP protection against global cerebral ischaemia-reperfusion injury is through reducing apoptosis by modulating the expression of heat shock protein 70, bcl-2 and bax. Additionally, ethanolic extracts of Corydalis yanhusuo W. T. Wang administered orally have been reported to protect against heart failure following induction of myocardial infarction in rats. We hypothesized that l-THP protects the myocardium from ischaemia-reperfusion injury following acute coronary artery occlusion. Myocardial infarction, and consequent loss of functional myocardium, is a major cause of heart failure. Despite interventional treatment or thrombolysis, prognosis remains poor in patients with large infarct area and/or severe left ventricular dysfunction. As well as the damage MK-0683 structure caused by ischaemia, a further volume of functional myocardium is lost immediately after reperfusion, and this reperfusion damage is a major determinant of post-myocardial infarction. Cardioprotection before reperfusion may confer some benefit in reducing myocardial I/R injury, and certain drugs such as statins and angiotensin receptor blockers, have been shown to decrease cardiovascular morbidity and mortality when administered before elective cardiac surgery or percutaneous coronary intervention. The results of the present study indicate that the infarct size of lTHP-treated rats was significantly reduced compared with untreated rats whilst cardiac function was significantly improved, following myocardial ischaemia and subsequent reperfusion. Moreover, this effect was explained, in large part, by a decrease in myocardial NO production. NO plays a crucial role in many aspects of the pathophysiology of heart failure. NO has often been described as a ‘double-edged’ sword; NO inhibits I/R injury, represses inflammation, and prevents left ventricular remodeling, whereas excess NO and coexistence of reactive oxygen species with NO are injurious. NO donors have also been reported to increase cardiomyocyte death and to switch the nature of cell death from apoptosis to necrosis, in a concentrationdependent manner. The detrimental effect of excessive NO is attributable to its action on mitochondria. NO inhibits the mitochondrial respiratory chain, resulting in inhibition of ATP production, as well as increase in production of reactive oxygen species and an increase in susceptibility to cell death. During reperfusion, due to disturbance in the redox state of the cells, excess NO can combine with superoxide anion, resulting in formation of the reactive radical peroxynitrite, which inhibits mitochondrial respiration at multiple sites, and also causes mitochondrial permeability transition pore opening. This in turn leads to membrane lipid peroxidation and in the interruption of normal signalling pathways.