title: Assessment of hemodynamic function and tolerance to ischemia in the absence or presence of calcium antagonists in hearts of isoproterenol-treated, exercise-trained, and sedentary rats.
abstract: The effects of cardiac hypertrophy on the structure, function and tolerance to ischemia of rat hearts have been investigated. Multiple injections of low doses of isoproterenol (ISO) resulted in an increase of heart weight/body weight ratio by 60%, and a decrease of myocardial creatine kinase activity by 25%, as compared to normal rats. Compared to age-matched control rats, rats submitted to a swimming program had a higher heart weight by 20%, but similar values of heart weight to body weight ratio. In isolated perfusion, the functional capacities of hearts from ISO-treated rats were severely depressed compared to normal rat hearts whereas exercise-trained rat hearts performed as well or even better than control hearts. The functional recovery of ISO-treated hearts following cardioplegia-induced arrest for 20 min at 37 degrees C was significantly worse than the recovery of normal hearts, but hearts of exercise-trained rats showed a significantly better recovery than control hearts. Exercise training results in improvement of myocardial blood supply resulting in better preservation of the heart during ischemia, compared to normal hearts. Addition of a combination of verapamil and diltiazem to the cardioplegic solution followed by ischemic arrest for 20 min at 37 degrees C resulted for ISO-treated rat hearts in an improved recovery of cardiac output (99%) compared to cardioplegia in the absence of these drugs (72%). In exercise-trained and control rat hearts, calcium antagonists improved the recovery from cardioplegic arrest of cardiac output from 90% to 92% and from 71% to 87%, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: Department of Thoracic Surgery, University Hospital, Leiden, The Netherlands.
authors.forename: C J
authors.initials: CJ
authors.lastname: Brinkman
authors.forename: A
authors.initials: A
authors.lastname: van der Laarse
authors.forename: G J
authors.initials: GJ
authors.lastname: Los
authors.forename: A P
authors.initials: AP
authors.lastname: Kappetein
authors.forename: J J
authors.initials: JJ
authors.lastname: Weening
authors.forename: H A
authors.initials: HA
authors.lastname: Huysmans
mesh_terms: D000818:Animals; D006332:Cardiomegaly / Q000139:chemically induced / Q000503:physiopathology*; D002314:Cardioplegic Solutions; D003402:Creatine Kinase / Q000378:metabolism; D004110:Diltiazem / Q000494:pharmacology*; D005355:Fibrosis; D006324:Heart Arrest, Induced; D006439:Hemodynamics / Q000187:drug effects*; D007545:Isoproterenol; D009206:Myocardium / Q000201:enzymology / Q000473:pathology; D009929:Organ Size; D010806:Physical Education and Training; D051381:Rats; D014700:Verapamil / Q000494:pharmacology*
chemical_list: D002314:Cardioplegic Solutions; D014700:Verapamil; D003402:Creatine Kinase; D004110:Diltiazem; D007545:Isoproterenol