title: Functional and metabolic responses to ischemia in the isolated perfused hypothyroid rat heart.
abstract: It has been demonstrated that the V3 cardiac myosin isozyme has a higher efficiency and consumes less oxygen in doing mechanical work than the V1 myosin isozyme. The purpose of the present study is to investigate the functional and metabolic responses to ischemia following reperfusion of the hypothyroid heart, in which ventricular myosin isozyme is shifted from V1 predominance to V3 predominance. The heart was perfused by the working heart method for 15 min, and then global ischemia was induced for 10, 20 and 30 min with pacing at a rate of 320/min until cardiac cessation. The ischemic heart was reperfused for 30 min. The extent of recovery of pressure-rate product after reperfusion, following 20 min of ischemia in the hypothyroid heart, was higher than that in the control heart (p less than 0.01). The level of adenosine triphosphate (ATP) declined more slowly in the hypothyroid heart than in the control heart. The level of ATP and energy charge potential in the hypothyroid heart reperfused after 20 min of ischemia were higher than those in the reperfused control heart (p less than 0.01, p less than 0.05, respectively), though they did not differ from each other in preischemia. There were no significant differences in the levels of tissue lactate between the 2 hearts during ischemia and reperfusion. The recovery rate of the coronary flow of the 2 hearts did not differ from each other significantly. These data suggest that there is probability of the V3 predominant heart recovering from ischemic damage to the metabolism and cardiac function better than the V1 predominant heart because the transformation of myocardium, due to an increase in V3 into a slower but more efficiently working muscle results in conservation of tissue ATP during ischemia.
authors.affiliation: First Department of Internal Medicine, Asahikawa Medical College, Japan.
authors.forename: M
authors.initials: M
authors.lastname: Abe
authors.forename: H
authors.initials: H
authors.lastname: Obata
authors.forename: H
authors.initials: H
authors.lastname: Tanaka
mesh_terms: D000255:Adenosine Triphosphate / Q000378:metabolism*; D000818:Animals; D003327:Coronary Disease / Q000150:complications / Q000378:metabolism*; D004195:Disease Models, Animal; D007037:Hypothyroidism / Q000150:complications*; D008297:Male; D015425:Myocardial Reperfusion; D009218:Myosins / Q000378:metabolism*; D010477:Perfusion; D051381:Rats; D011919:Rats, Inbred Strains
chemical_list: D000255:Adenosine Triphosphate; D009218:Myosins