- 作者: Mario Mateus Sugizaki; Robson Francisco Carvalho; Flavio Ferrari Aragon; Carlos Roberto Padovani; Katashi Okoshi; Marina Politi Okoshi; Silmeia Garcia Zanati; Maeli Dal Pai-Silva; Ethel Lourenzi Barbosa Novelli; Antonio Carlos Cicogna
- 作者服務機構: 1 Department of Internal Medicine — School of Medicine, Faculdade de Medicina de Botucatu, UNESP, Rubido Junior, SjN, 18618-000, Botucatu, SP, Brazil; ; 2 Department of Biochemistry, ; 3 Department of Morphology, ; 4 Department of Biostatistic, State University Julio Mesquita Filho@, UNESP, Botucatu, Sao Paulo, Brazil
- 中文摘要: --
- 英文摘要: Previous works from our laboratory have revealed that food restriction (FR) promotes discrete myocardial dysfunction in young rats. We examined the effects of FR on cardiac function, in vivo and in vitro, and ultrastructural changes in the heart of middle-aged rats. Twelve-month-old Wistar-Kyoto rats were fed a control (C) or restricted diet (daily intake reduced to 50% of the control group) for 90 days. Cardiac performance was studied by echocardiogram and in isolated left ventricular (LV) papillary muscle by isometric contraction in basal condition, after calcium chloride (5.2 mM) and beta-adrenergic stimulation with isoproterenol (10^-6 M). FR did not change left ventricular function, but increased time to peak tension, and decreased maximum rate of papillary muscle tension development. Inotropic maneuvers promoted similar effects in both groups. Ultrastructural alterations were seen in most FR rat muscle fibers and included, absence and/or disorganization of myofilaments and Z line, hyper-contracted myofibrils, polymorphic and swollen mitochondria with disorganized cristae, and a great quantity of collagen fibrils. In conclusion, cardiac muscle sensitivity to isoproterenol and elevation of extracellular calcium concentration is preserved in middle-aged FR rats. The intrinsic muscle performance depression might be related to morphological damage.
- 中文關鍵字: --
- 英文關鍵字: food restriction, myocardial ultrastructure, papillary muscle, rat, ventricular function