Varela A, Carregal M, Espósito S, Bruno-Magnasco C, Savino E A
Cátedra de Fisiología, Facultad de Farmacia y Bioquímica, Buenos Aires, Argentina.
Arch Int Physiol Biochim Biophys. 1994 Mar-Apr;102(2):125-8. doi: 10.3109/13813459408996119.
The aim of the investigation was to assess whether endogenous triacylglycerol contributes to the maintenance of the atrial functions. To attain this information, the atria from fed and fasted rats were treated with oxfenicine which is a cardioselective inhibitor of carnitine palmitoyltransferase I. In the presence of glucose, oxfenicine suppressed lipolysis without affecting the pacemaker and contractile activities. When exposed to 2-deoxyglucose in a substrate-free medium, the atria displayed a progressive fall of the contractile strength and pacemaker rate. The dysfunctions appeared faster in the atria from fed rats coinciding with a smaller triacylglycerol mobilization. Under this condition, oxfenicine abolished the triacylglycerol breakdown, increased the fall in the peak tension, elicited a rise in the resting tension and accelerated the decline of the pacemaker rate, leading in a significant number of atria to a complete cessation of the spontaneous contractions. These effects proceeded faster in the fed rats atria. Present data suggest that glucose oxidation is sufficient to meet the atrial energy demand when the fatty acid catabolism is impeded. The noxious effects of oxfenicine, attained after the glucose metabolism was eliminated, lend direct evidence to the notion 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心房功能。为获取这一信息，对喂食和禁食大鼠的心房用奥芬尼辛进行处理，奥芬尼辛是肉碱棕榈酰转移酶I的心脏选择性抑制剂。在有葡萄糖存在的情况下，奥芬尼辛抑制脂肪分解，而不影响起搏和收缩活动。当在无底物培养基中暴露于2-脱氧葡萄糖时，心房的收缩强度和起搏频率逐渐下降。喂食大鼠心房的功能障碍出现得更快，这与较小的三酰甘油动员相吻合。在这种情况下，奥芬尼辛消除了三酰甘油的分解，增加了峰值张力的下降，引起静息张力升高，并加速了起搏频率的下降，导致大量心房完全停止自发收缩。这些效应在喂食大鼠的心房中进展更快。目前的数据表明，当脂肪酸分解代谢受到阻碍时，葡萄糖氧化足以满足心房的能量需求。在消除葡萄糖代谢后奥芬尼辛产生的有害作用，直接证明了内源性三酰甘油至少部分支持心房功能这一观点。
