ABSTRACT
Objective To evaluate the effect of high-level spinal cord injury (SCI) on the myocardial energy metabolism in rats.Methods Sixty healthy male Sprague-Dawley rats,weighing 250-300 g,were randomly divided into 2 groups (n=30 each) using a random number table:sham operation (group S) and SCI group.SCI was induced in anesthetized rats by dropping a 10 g weight onto C7 spinal cord from 5 cm height falling freely inside a vertical hollow glass tube.At 6,12,24,48 and 72 h after SCI,6 rats in each group were chosen and arterial blood samples were taken for measurement of serum creatine kinase (CK) and creatine kinase isoenzyme-MB (CK-MB) activities.The rats were then sacrificed and myocardial specimens were obtained for examination of myocardial ultrastructure and for determination of ATP weight ratio,levels of Na+-K+-ATPase,Ca2+-Mg2+-ATPase,non-esterified fatty acids (NEFA) and lactic acid (LD),and expression of peroxisome proliferator-activated receptor alpha (PPARα) mRNA and protein (using fluorescent quantitative PCR and Western blot).Results Compared with group S,the serum CK and CK-MB activities were significantly increased,the ATP weight ratio,activities of Na+-K+-ATPase and Ca2+-Mg2+-ATPase and levels of NEFA and LD were decreased,and the expression of PPAR-α mRNA and protein was down-regulated in SCI group.No pathological changes of myocardium were found in group S,and the pathological changes of myocardium were obvious in SCI group.Conclusion High-level SCI can lead to decrease in the myocardial energy metabolism in rats,and down-regulated expression of PPARα is involved in the mechanism.
ABSTRACT
Objective To investigate the effect of creatine phosphate sodium on myocardial protection and calcium-sensitive receptor (CaSR) expression following high-level spinal cord injury.Methods Thirty healthy male SD rats weighing 250-300 g were assigned to sham operation,12-hour injury,24-hour injury,12-hour injury followed by a single intraperitoneal injection of creatine phosphate sodium,and 24-hour injury followed by a single intraperitoneal injection of creatine phosphate sodium according to the random number table,with 6 rats in each group.High-level spinal cord injury was induced at C7 segment by dropping a 10 g weight falling freely along the hollow glass tube from a 5 cm height.Level of blood troponin Ⅰ (cTnⅠ) was measured.Myocardial tissues were collected to study ultrastructure of myocardial cells under transmission electron microscope and CaSR expression using fluorescence quantitative PCR and Western blotting.Results cTnⅠ level was (0.031 ±0.002) U/L and (0.026 ± 0.001) U/L in 12-and 24-hour injury groups,but it was reduced to (0.023 ± 0.002) U/L and (0.018 ± 0.006) U/L at the same time point in treatment groups (P ＜ 0.05).Whereas either in injnry or treatment groups,cTnⅠ level was higher than (0.004 ± 0.002) U/L in sham operation group (P ＜ 0.05).CaSR mRNA level was (0.991 ±0.146) × 10-3 and (1.245 ±0.204) × 10-3 in 12-and 24-hour injury gronp and decreased to (0.880 ± 0.096) × 10-3 and (0.782 ± 0.138) × 10 3 at the same time point in treatment groups (P ＜ 0.05),but all were higher than (0.437 ± 0.065) × 10-3 in sham operation group (P ＜ 0.05).CaSR protein expressed in 12-and 24-hour injury group was (0.627 ±0.066) × 10 3 and (0.809 ±0.154) ×10 3 and lowered to (0.505 ±0.176) × 10-3 and (0.524 ±0.138) × 10-3 at the same time point in treatment groups,but all were higher than (0.331 ± 0.102) × 10-3 in sham operation group (P ＜ 0.05).Transmission electron microscopy demonstrated normal myocardial ultrastructure in sham operation group but impairment in injury groups,but the impairment was significantly improved in treatment groups.Conclusion Creatine phosphate sodium can decrease cTnⅠ level,attenuate the damage to myocardial ultrastructure and down-regulate CaSR after high-level spinal cord injury.