Varela A, Carregal M, Bruno-Magnasco C, Espósito S, Savino E A
Cátedra de Fisiología, Facultad de Farmacia y Bioquímica, Universidad de Buenos Aires, Argentina.
Rev Esp Fisiol. 1992 Jun;48(2):107-13.
The aim of the investigation was to assess whether endogenous triacylglycerol contributes to the maintenance of the contractile and pacemaker activities of the isolated atria from fed and fasted rats. To attain this information, the atria were treated with methylpalmoxirate which is a potent inhibitor of carnitine palmitoyltransferase I. In the presence of glucose, methylpalmoxirate abolished the lipolysis without affecting peak developed tension or the atrial rate. When exposed to a substrate-free medium containing 2-deoxyglucose, the atria displayed a progressive fall of the pacemaker frequency, a pronounced decay of contractile strength and the appearance of contracture. These derangements appeared faster in the atria from fed rats coinciding with a smaller triacylglycerol mobilization. Methylpalmoxirate suppressed triacylglycerol breakdown, increased the contracture strength, accelerated the fall of the atrial rate and in a significant number of fasted atria it led to a complete cessation of the spontaneous contractions. The decline of the peak tension was not altered by the inhibitor, probably because the contractile strength was too weak in the glucose-free medium, so that additional negative inotropic effects were not detectable. These data suggest that exogenous glucose in addition to that derived from glycogen meet the atrial energy requirements when the fatty acid oxidation is hindered. The deleterious effects exerted by methylpalmoxirate after the glucose metabolism was eliminated indicate that endogenous triacylglycerol supports, at least partly, the atrial functions.
本研究的目的是评估内源性三酰甘油是否有助于维持喂食和禁食大鼠离体心房的收缩和起搏活动。为了获得这一信息，用肉碱棕榈酰转移酶I的强效抑制剂甲基棕榈酰氧肟酸处理心房。在有葡萄糖存在的情况下，甲基棕榈酰氧肟酸消除了脂解作用，而不影响最大收缩张力或心房率。当暴露于含有2-脱氧葡萄糖的无底物培养基中时，心房起搏频率逐渐下降，收缩强度明显衰减，并出现挛缩。这些紊乱在喂食大鼠的心房中出现得更快，这与较小的三酰甘油动员相吻合。甲基棕榈酰氧肟酸抑制三酰甘油分解，增加挛缩强度，加速心房率下降，并且在大量禁食心房中导致自发收缩完全停止。抑制剂未改变峰值张力的下降，可能是因为在无葡萄糖培养基中收缩强度太弱，以至于额外的负性肌力作用无法检测到。这些数据表明，当脂肪酸氧化受到阻碍时，除了糖原衍生的葡萄糖外，外源性葡萄糖满足心房的能量需求。在葡萄糖代谢消除后，甲基棕榈酰氧肟酸产生的有害作用表明内源性三酰甘油至少部分支持心房功能。
