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Clenbuterol-induced myocyte necrosis occurred against a background of zero damage in control muscles. In the heart, the clenbuterol-induced necrosis was not uniform, being more abundant in the left subendocardium and peaking 2. 4 mm from the apex. Clenbuterol treatment of failing rat hearts, alone or in combination with mechanical unloading, improves LV function at the whole-heart and cellular levels by affecting cell morphology, excitation–contraction coupling, and myofilament sensitivity to calcium. We have investigated the dose- and time-dependency of myocyte apoptosis and necrosis induced by the beta2-adrenergic receptor agonist, clenbuterol, with the aim of determining whether myocyte apoptosis and necrosis are two separate processes or a continuum of events. In the heart, the clenbuterol-induced necrosis was not uniform, being more abundant in the left subendocardium and peaking 2. 4 mm from the apex. 4 mm from the apex), dose (5 mg clenbuterol/kg), and sampling time (12 h) were optimized, maximum cardiomyocyte necrosis was found to be 1. It is conceivable that, like the less selective -ARagonist isoproterenol (3, 27), clenbuterol may inducecell death and necrosis in the heart. Indeed, clen-buterol has previously been shown to induce generalhistological damage in the soleus muscle of the rat inresponse to a dose of 2 mg/kg administered via drink-ing water (36). The incidence of apoptosis in both the heart and soleus muscle reached a maximum 4 h after administration of clenbuterol, whereas the peak incidence of necrosis occurred around 12 h to 15 h. = 4, in each group) received a single injection of 5 mg of clenbuterol kg and were killed at specific time points over a 24-h period They follow strict quality control measures and provide the necessary information about the product, including dosage, side effects, and cycle length, clenbuterol heart necrosis.
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