3,5,3'-TRIIODO-L-THYRONINE PRETREATMENT WITH CARDIOPLEGIC ARREST AND CHRONIC LEFT-VENTRICULAR DYSFUNCTION

Background. The active form of thyroid hormone, T-3, may be an importa nt determinant of left ventricular (LV) function after hypothermic car dioplegic arrest and rewarming, particularly in patients with preexist ing LV dysfunction. Thus, the present project tested the hypothesis th at T-3 pretreatment will. improve myocyte contractile performance afte r hypothermic cardioplegic arrest and rewarming in the setting of chro nic LV dysfunction. Methods. Control LV porcine myocytes (n = 160) and cardiomyopathic LV (rapid pacing for 3 weeks at 240 beats/min) myocyt es (n = 100) were treated with or without 80 pmol/L T-3. Myocytes then were maintained in normothermic conditions (2 hours at 37 degrees C i n media) or exposed to hypothermic cardioplegic arrest ([K+], 24 mmol/ L; 2 hours at 4 degrees C) with subsequent rewarming. Results. After c ardioplegic arrest and rewarming, T-3 pretreatment increased myocyte v elocity of shortening by 41% in control myocytes and by 35% in cardiom yopathic myocytes when compared to untreated myocytes. Furthermore, T- 3 pretreatment followed by beta-adrenergic receptor stimulation with i soproterenol (25 nmol/L) improved myocyte velocity of shortening by 24 % in control myocytes and 90% in cardiomyopathic myocytes after hypoth ermic cardioplegic arrest and rewarming, as compared with untreated my ocytes. Conclusions. In summary, this study provides evidence to sugge st that preemptive treatment with T-3 may improve LV pump function and beta-adrenergic responsiveness after hypothermic cardioplegic arrest and rewarming in patients with underlying LV dysfunction.