妊娠期高血压(HDCP)是妊娠期的特发疾病,以妊娠20周后出现高血压、水肿、蛋白尿为主要表现的全身各器官和系统损害的一种妊娠期并发症,严重影响母婴健康,是孕产妇和围生儿患病及死亡的主要原因之一[1,2].降压治疗是HDCP的重要治疗手段,目的是预防子痫、心脑血管意外和胎盘早剥等严重母胎并发症,保证母儿安全,有效改善妊娠结局.我国2015年HDP诊治指南[3]参考了国际指南并结合我国国情建议:收缩压≥160 mmHg和(或)舒张压≥110 mmHg(1 mmHg=0.133 kPa)给予降压药物治疗,目标血压控制在130~155/80~105 mmHg,合并器官功能损伤,应控制130~139/80~89 mmHg,降压过程应平稳,避免过度波动,且血压不应低于130/80 mmHg,以保证子宫-胎盘的血流灌注[4].
《中国心力衰竭诊断和治疗指南》是根据国内外最新临床研究成果,参考欧美国家发布的指南,结合我国国情及临床实践,对心衰的分类、诊断、预防、治疗和管理等做出了全面的阐述和推荐.2018年指南在2014年的基础上进行了更新,新指南对正性肌力药在临床应用中的推荐也做了完善及相应调整.
OBJECTIVE:To study the role and mechanism of myocardial apoptosis after short-term and long-term exercise preconditioning. METHODS:Forty-eight male SD rats were randomly divided into control group (C), exhaust group (E), short-exercise preconditioning (S-EP) and long-term exercise preconditioning group (L-EP). Short-term and long-term exercise preconditioning were conducted for 3 days and 3 weeks of repeated intermittent swimming training program. The changes of myocardial cells were observed under light microscope. The serum levels of ischemia-modified albumin(IMA) and creatine kinase-isoenzyme(CK-MB) were detected by ELISA. Real time fluorescence quantitative PCR and Western blot were used to detect the expressions of tumor necrosis factor-α(TNF-α),Caspase-8, Caspase-3 genes and proteins in myocardial tissue. The apoptosis of cardiomyocytes was observed by TUNEL method. RESULTS:Compared with group C, group E had serious myocardial injury. The levels of serum IMA, CK-MB and the expressions of TNF-α, Caspase-8 and Caspase-3 in myocardium were increased (P<0.05). Compared with group E, serum CK-MB and TNF-α and Caspase-8 mRNA in S-EP group were significantly lower than those in group E (P<0.05), but there was no significant difference in serum IMA and Caspase-3 mRNA and protein (P>0.05). The levels of serum IMA, CK-MB and TNF-α, Caspase-8 and Caspase-3 mRNA in L-EP group were significantly lower than those in control group (P<0.05). The apoptosis of cardiomyocytes in group E was obvious. Short-term and long-term exercise preconditioning could inhibit apoptosis. Compared with S-EP group, the apoptosis of L-EP group was significantly decreased. CONCLUSIONS:Short-term and long-term exercise preconditioning can reduce myocardial injury after exhaustive exercise, but short-term exercise preconditioning does not alter the expression of Caspase protease. Long-term exercise preconditioning significantly inhibits Caspase-8, 3 mRNA expression and reduces protein synthesis. The inhibitive effects of long-term exercise preconditioning on myocardial cell apoptosis were stronger than those of short-term exercise preconditioning.