title: Inotropic interventions during myocardial "stunning" in the pig.
abstract: To study the effects of inotropic interventions on myocardial "stunning," we subjected pigs to 12 minutes of left anterior descendents (LAD) coronary artery occlusion followed by 2 hours of reperfusion. Measurements were made of segmental shortening (SS%), myocardial blood flow (MBF), adenine nucleotides, the extent of ultrastructural damage, and granulocyte accumulation. Three groups of pigs were compared: control (CON) (N = 6), isoproterenol infused (ISO) (N = 6), and pretreated with triiodothyronine (T3) (30 micrograms/kg ip) (N = 5). Inotropic reserve was tested with a bolus of Ca++. During reperfusion, SS% in the CON reperfused segments showed a relatively constant decrement of 75% throughout the reperfusion period but no alteration in the inotropic reserve. In the ISO group, SS% was maintained at preocclusion levels, but there was a small but significant decrease in the inotropic reserve. In the T3 group, SS% was reduced more than 90% and showed no response to the Ca++. Myocardial blood flow was maintained at control levels in the CON and ISO groups during reperfusion but was greatly reduced in the T3 group. The ATP was reduced 36% in CON, 39% in ISO, and further reduced to 87% of control in the T3 group. Mitochondrial damage in the CON and ISO groups was 5 and 10%, respectively, and reversible, but there was 86% irreversible damaged mitochondria in the T3 group. Using a monoclonal antibody against pig granulocytes, the presence and quantitation of adherent granulocytes were determined. There was no accumulation of granulocytes. These data suggest that some forms of myocardial adrenergic augmentation during stunning may have adverse consequences. Thus, the strength, duration, and types of stimulation may be critical to the preservation of the myocardium in the treatment of myocardial stunning.
authors.affiliation: Department of Pathology, University of California, San Diego School of Medicine, La Jolla 93093.
authors.forename: F C
authors.initials: FC
authors.lastname: White
authors.forename: G
authors.initials: G
authors.lastname: Boss
mesh_terms: D000244:Adenosine Diphosphate / Q000378:metabolism; D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D000911:Antibodies, Monoclonal; D002118:Calcium / Q000494:pharmacology; D005260:Female; D007545:Isoproterenol / Q000494:pharmacology*; D008297:Male; D008854:Microscopy, Electron; D009200:Myocardial Contraction / Q000187:drug effects*; D015425:Myocardial Reperfusion; D015428:Myocardial Reperfusion Injury / Q000473:pathology / Q000503:physiopathology*; D009206:Myocardium / Q000648:ultrastructure*; D009504:Neutrophils / Q000473:pathology; D013552:Swine; D014284:Triiodothyronine / Q000494:pharmacology*
chemical_list: D000911:Antibodies, Monoclonal; D014284:Triiodothyronine; D000244:Adenosine Diphosphate; D000255:Adenosine Triphosphate; D007545:Isoproterenol; D002118:Calcium