title: Severe, short-term food restriction improves cardiac function following ischemia/reperfusion in perfused rat hearts.
abstract: The purpose of this study was to clarify the characteristics of improved ischemic tolerance induced by severe, short-term food restriction in isolated, perfused rat hearts. Male Wistar (8 week-old) rats were given a food intake equivalent to a 70% reduction on the food intake of ad-libitum fed rats for 11 days (FR group and AL group, respectively). After this period, hearts were isolated and perfused in the Langendorff mode, and subjected to 20 min of global ischemia followed by 30 min of reperfusion. Although the coronary flow rate in the FR group (63.0 +/- 3.1 ml/min/g dry weight) was higher than that in the AL group (47.1 +/- 1.3 ml/min/g dry weight) during preischemic perfusion, the lactate release into the coronary effluent and absolute values of +dP/dt and -dP/dt in the FR group (2422 +/- 161 and -1282 +/- 51) were inversely lower than in the AL group (2971 +/- 156 and -1538 +/- 74, respectively). An increase in ischemic contracture was suppressed in the FR group. Following reperfusion, cardiac function, high-energy phosphate content, and intracellular pH, as measured by 31P-nuclear magnetic resonance spectroscopy, had recovered to a much greater degree in the FR group than in the AL group. The serum T3 level was significantly lower in the FR group (2.7 +/- 0.1 pg/ml) than in the AL group (3.6 +/- 0.1 pg/ml), and the levels of triglycerides, free fatty acids, insulin, and glucose were also significantly lower in the FR group than in the AL group. The protein expressions of myocyte enhancer factor 2A, Na(+), K(+)-ATPase, and phospholamban in the cardiac tissue were higher in the FR group than in the AL group. These results suggested that severe, short-term food restriction improves ischemic tolerance in rat hearts via altered expression of functional proteins induced by low serum T3 levels, decreased coronary conductance, and change in metabolic flux.
authors.affiliation: Department of Laboratory Medicine, National Defense Medical College, Tokorozawa, Saitama, Japan. grd1418@kmh.gr.jp
authors.forename: Tadashi
authors.initials: T
authors.lastname: Yamagishi
authors.forename: Motoaki
authors.initials: M
authors.lastname: Bessho
authors.forename: Shigeki
authors.initials: S
authors.lastname: Yanagida
authors.forename: Kenya
authors.initials: K
authors.lastname: Nishizawa
authors.forename: Masatoshi
authors.initials: M
authors.lastname: Kusuhara
authors.forename: Fumitaka
authors.initials: F
authors.lastname: Ohsuzu
authors.forename: Seiichi
authors.initials: S
authors.lastname: Tamai
mesh_terms: D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D015153:Blotting, Western; D002118:Calcium / Q000378:metabolism; D031204:Caloric Restriction; D003402:Creatine Kinase / Q000378:metabolism; D004195:Disease Models, Animal; D004734:Energy Metabolism; D005227:Fatty Acids / Q000378:metabolism; D005947:Glucose / Q000378:metabolism; D006019:Glycolysis; D006863:Hydrogen-Ion Concentration; D007328:Insulin / Q000378:metabolism; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D019344:Lactic Acid / Q000378:metabolism; D009682:Magnetic Resonance Spectroscopy; D008297:Male; D009200:Myocardial Contraction; D015428:Myocardial Reperfusion Injury / Q000378:metabolism / Q000503:physiopathology / Q000517:prevention & control*; D009206:Myocardium / Q000201:enzymology / Q000378:metabolism*; D010477:Perfusion; D051381:Rats; D017208:Rats, Wistar; D013997:Time Factors; D014280:Triglycerides / Q000378:metabolism; D014284:Triiodothyronine / Q000378:metabolism; D016277:Ventricular Function, Left; D017725:Ventricular Pressure
chemical_list: D005227:Fatty Acids; D007328:Insulin; D014280:Triglycerides; D014284:Triiodothyronine; D019344:Lactic Acid; D000255:Adenosine Triphosphate; D007770:L-Lactate Dehydrogenase; D003402:Creatine Kinase; D005947:Glucose; D002118:Calcium