Sato T, Imanishi S, Arita M, Shimada T
Department of Physiology, Oita Medical University, Japan.
Heart Vessels. 1993;8(2):71-8. doi: 10.1007/BF01744386.
Elastase (ELA) is an enzyme catalyzing the digestion of elastin, an essential constituent of elastic fibers. Using isolated guinea pig papillary muscles, we examined the effect of ELA (3 x 10(-7) -3 x 10(-4) g/ml) on resting tension (RT) and twitch tension (TT). The effects of ELA on elastic fibers located in the subendocardium were examined histologically. A relatively high concentration of ELA (3 x 10(-4) g/ml) increased TT transiently, with progressive decreases in RT. In contrast, a relatively low concentration (3 x 10(-5) g/ml) decreased both TT and RT straightforwardly. Much lower concentrations (3 x 10(-6) -3 x 10(-7) g/ml) did not reveal significant effects. The ELA-induced increases in TT were unaffected in the presence of atenolol (10(-5) g/ml), ouabain (10(-7) M) or ryanodine (10(-6)M). ELA did not increase the maximum rate of rise of slow action potentials recorded using standard microelectrodes. ELA (3 x 10(-5) g/ml) decreased the maximum TT obtained at optimal RT or Lmax, and decreased the slope of the ascending and descending limbs of the TT-RT relation curve (Frank-Starling's). Electron-microscopic findings revealed that subendocardial elastin was mostly digested at ELA concentrations of 3 x 10(-5) -3 x 10(-4) g/ml. These findings suggest that the decrease of RT by ELA may be, at least in part, caused by a decomposition of the elastic fibers. On the other hand, the increase of TT by ELA could not be attributed to a release of endogenous catecholamine, an inhibition of Na+, K(+)-pump, a release of Ca2+ from sarcoplasmic reticulum, or an increase of slow inward current.
弹性蛋白酶(ELA)是一种催化弹性蛋白消化的酶,弹性蛋白是弹性纤维的重要组成部分。我们使用分离的豚鼠乳头肌,研究了ELA(3×10⁻⁷ - 3×10⁻⁴ g/ml)对静息张力(RT)和收缩张力(TT)的影响。通过组织学方法研究了ELA对心内膜下弹性纤维的作用。相对较高浓度的ELA(3×10⁻⁴ g/ml)可使TT短暂增加,同时RT逐渐降低。相比之下,相对较低浓度(3×10⁻⁵ g/ml)则直接降低TT和RT。更低的浓度(3×10⁻⁶ - 3×10⁻⁷ g/ml)未显示出显著影响。在存在阿替洛尔(10⁻⁵ g/ml)、哇巴因(10⁻⁷ M)或ryanodine(10⁻⁶ M)的情况下,ELA诱导的TT增加不受影响。ELA并未增加使用标准微电极记录的慢动作电位的最大上升速率。ELA(3×10⁻⁵ g/ml)降低了在最佳RT或Lmax时获得的最大TT,并降低了TT-RT关系曲线(弗兰克-斯塔林曲线)上升和下降支的斜率。电子显微镜检查结果显示,在心内膜下弹性蛋白在ELA浓度为3×10⁻⁵ - 3×10⁻⁴ g/ml时大多被消化。这些发现表明,ELA导致的RT降低可能至少部分是由弹性纤维的分解引起的。另一方面,ELA导致的TT增加不能归因于内源性儿茶酚胺的释放、Na⁺、K⁺-泵的抑制、肌浆网中Ca²⁺的释放或慢内向电流的增加。