Propranolol and experimental myocardial infarction: substrate effects.
Propranolol is known to decrease ischaemic damage in developing myocardial infarction. Besides acting on mechanical parameters which help determine the balance of oxygen supply and oxygen demand in the ischaemic tissue, propranolol decreases the myocardial uptake of free fatty acids and increases that of glucose. It is suggested that propranolol may favourably alter developing myocardial infarction in dogs by altering the supply of substrates reaching the ischaemic zone. However, propranolol also decreases enzyme release from isolated rat hearts with coronary ligation at a relative constant arterial free fatty acid concentration. Propranolol causes more marked depression of mechanical function and of heart rate in hearts perfused with free fatty acids than with glucose. It is suggested that the glucose-promoting and anti-lipolytic actions of propranool might be important not only in decreasing infarct size but also in helping to prevent undesirable side effects in hearts with experimental myocardial infarction.
D000818:Animals; D004285:Dogs; D004734:Energy Metabolism / Q000187:drug effects; D005230:Fatty Acids, Nonesterified / Q000378:metabolism; D005947:Glucose / Q000378:metabolism; D006321:Heart / Q000187:drug effects; D006339:Heart Rate / Q000187:drug effects; D006801:Humans; D007773:Lactates / Q000378:metabolism; D009203:Myocardial Infarction / Q000188:drug therapy / Q000378:metabolism*; D009206:Myocardium / Q000378:metabolism*; D010101:Oxygen Consumption / Q000187:drug effects; D011433:Propranolol / Q000494:pharmacology* / Q000627:therapeutic use; D051381:Rats
D005230:Fatty Acids, Nonesterified; D007773:Lactates; D011433:Propranolol; D005947:Glucose