Ludatscher R M, Hashmonai M, Monies-Chass I, Schramek A
Acta Anat (Basel). 1981;111(4):320-7. doi: 10.1159/000145483.
Ultrastructural muscle changes resulting from temporary anoxia and their evolution were studied in dogs. Ischaemia of the hind limb was produced by subcutaneous ligation of all muscles of the thigh and clamping of the femoral artery. Revascularization was obtained by declamping and removal of the muscle ligature. The period of ischaemia ranged from 4 1/2 to 7 h, the latter being the upper limit allowing functional recovery after revascularization. 6-7 h of ischaemia revealed focal degenerative changes of varied intensity. These consisted of enlarged mitochondria with ruptured cristae, small pads of glycogen granules and accumulation of lipid vacuoles. The tubules of sarcoplasmic reticulum contained dense, fine-granular material. Focal myofibrillar destruction and disruption of the Z line were encountered in half of the cases. The myofibrillar damage was more severe 9 days after revascularization of the muscles. The functional recovery of the ischaemic limbs in the present study may be due to the focal nature of these changes.
对犬类因暂时性缺氧导致的超微结构肌肉变化及其演变进行了研究。通过皮下结扎大腿所有肌肉并夹闭股动脉来造成后肢缺血。通过松开夹子和去除肌肉结扎线实现血管再通。缺血时间为4.5至7小时，后者是血管再通后功能恢复的上限。缺血6 - 7小时显示出不同强度的局灶性退行性变化。这些变化包括线粒体肿大、嵴破裂、糖原颗粒小垫以及脂质空泡积聚。肌浆网的小管含有致密的细颗粒物质。半数病例中出现局灶性肌原纤维破坏和Z线断裂。肌肉血管再通9天后，肌原纤维损伤更为严重。本研究中缺血肢体的功能恢复可能归因于这些变化的局灶性特点。
