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目的:动态观察内毒素（LPS）诱导新生大鼠心肌cAMP、cGMP和超微结构改变及Dex对其的影响,探讨Dex的保护作用。方法:7日龄新生大鼠117只,随机分组（n=9）,对照组（A,生理盐水）,LPS组（B,LPS 5mg/kg）;治疗组（C,LPS5mg/kg+Dex 5mg/kg）。各组在注射后2、4、6、24h处死留取心肌,放免法检测cAMP和cGMP含量,电镜现察超微结构;同时测血糖和血气。结果:①cAMP:B组2h显著增高（P<0.05）后渐下降;24h最低;C组2h增高,但低于B组（P<0.05）,24h显著高于A、B两组;②cGMP:B组渐增高24h显著高于A、C两组;C组2h显著增高（P<0.05）,6h后下降至24h显著低于B组（P<0.05）;③心肌形态学:B组24h严重损害,C组仅轻微异常;④血糖、血气出组示应激性高血糖和继发性低血糖;血气:B组24h显著异常。结论:LPS诱导后新生大鼠心肌cAMP下降,cGMP增高,心肌损害严重,内环境紊乱,Dex通过间接调节心肌细胞第二信使对心肌有部分保护作用。
OBJECTIVE: To dynamically observe the changes of cAMP, cGMP and ultrastructure induced by endotoxin (LPS) in neonatal rat myocardium and the effect of Dex on the protective effect of Dex. Methods: One hundred and seven newborn rats were randomly divided into three groups: control group (A, normal saline) and LPS group (B, LPS 5 mg / kg) / kg). The hearts were sacrificed at 2, 4, 6, 24 hours after injection. The levels of cAMP and cGMP were determined by radioimmunoassay. The ultrastructure was observed by electron microscopy. Blood glucose and blood gas were measured simultaneously. Results: ①cAMP: group B increased significantly at 2h (P <0.05), but gradually decreased at 24h; lowest at 24h; increased at 2h in group C but lower than that at group B (P <0.05) (P <0.05). After 6 hours and then decreased to 24 hours, it was significantly lower than that in group B (P <0.05). ③ Myocardial morphology: 24h severe damage in group B , C group only slight abnormalities; ④ blood glucose, blood gas to excrete stress hyperglycemia and secondary hypoglycemia; blood gas: B group was significantly abnormal 24h. CONCLUSION: LPS-induced myocardial cAMP is decreased, cGMP is increased, myocardial damage is severe, and the internal environment is disturbed. Dex indirectly protects the myocardium by indirectly regulating the second messenger of cardiomyocytes.