Ischemic injury and repair process after transection in hypothyroid rat muscles.

Hindlimb ischemia for 4 h, followed by reperfusion, resulted in necrosis of most soleus muscle in euthyroid rats, whereas only slight damage occurred in hypothyroid rats. Muscle repair after transection of the tibialis anterior muscle of hypothyroid rats showed delayed debris removal, initial retardation of myotube formation, and a higher incidence of aberrant sarcomeres in newly formed muscle fibers by electron microscopy. The protective mechanism against ischemia in hypothyroid muscles can probably be attributed to decreased degradation of high-energy phosphates, reduced formation of substrates for xanthine oxidase during ischemia, and attenuated generation of harmful oxygen free radicals during reperfusion. Initial delay of myotube formation seems to reflect retarded proliferation of muscle precursor cells. Prolonged occurrence of aberrant sarcomeres in hypothyroidism is perhaps due to a delay or imbalance in the synthesis of proteins that assemble sarcomeres. These findings demonstrate the significant roles of thyroid hormones in ischemic injury and muscle repair.