The hemodynamics of isoproterenol-induced cardiac failure in the rat.
In virgin, male Sprague-Dawley rats, subcutaneous injections of 2.5 mg/kg or 250 mg/kg isoproterenol increased heart rate and aortic dF/dt and decreased total peripheral resistance. The net systemic response was an arterial hypotension. The larger dose of isoproterenol initially produced a greater hypotension; reflex compensatory responses followed. Cardiac failure occurred by 24 hours post-isoproterenol. The extent of cardiac failure was isoproterenol dose dependent. By gross inspection of the epicardial surface of the hearts of the isoproterenol-treated rats, anatomical injury also appeared to be isoproterenol dose dependent. The data presented in this study support the existing theory that isoproterenol-induced myocardial damage is due to a relative myocardial hypoxia produced by artereial hypotension and myocardial hyperactivity. The data also indicate that reflex responses to arterial hypotension occur and may be detrimental. Cardiac failure is produced by massive quantities of isoproterenol, and the degree of cardiac failure is dose dependent.
D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D002302:Cardiac Output / Q000187:drug effects; D002319:Cardiovascular System / Q000187:drug effects; D006333:Heart Failure / Q000209:etiology* / Q000503:physiopathology; D006339:Heart Rate / Q000187:drug effects; D006439:Hemodynamics / Q000187:drug effects*; D006801:Humans; D007545:Isoproterenol; D009206:Myocardium / Q000473:pathology; D051381:Rats; D014655:Vascular Resistance / Q000187:drug effects
D007545:Isoproterenol