甲基强的松龙对体外循环下心脏瓣膜置换患者肾功能的影响

背景与目的:有研究表明甲基强的松龙可减轻体外循环所致的肺损伤,但其对体外循环患者术后肾功能损害的作用尚不十分清楚。本文探讨甲基强的松龙是否有效抑制体外循环心内直视术中的炎症反应,并对肾脏有保护作用。方法:随机选取40例体外循环下择期行心脏瓣膜置换手术的患者,年龄30～55岁,心功能Ⅱ～Ⅲ级,随机分为甲基强的松龙组和对照组,每组20例。甲基强的松龙(MPS)组于体外循环前以甲基强的松龙10mg/kg预冲,对照组(NS)以等量的生理盐水代替。于CPB前(T1),CPB结束后2h(T2)、CPB结束后12h(T3),CPB结束后24h(T4),等时点留取中心静脉血和尿液,以酶联免疫吸附实验(ELISA)法检测炎性介质(IL-6、TNF-α、IL-10);取尿上清液检测反映肾功能的早期敏感指标:尿-N-乙酰氨基-葡萄糖苷酶(NAG)、尿α1-微球蛋白(α1-MG)、尿视黄醇结合蛋白(RBP)的水平。结果:CPB前两组炎性介质和肾功检测指标,差异均无统计学意义(P>0.05),而CPB结束后,两组炎性介质的水平和肾功各项指标均较术前增高。与NS相比,MP组T2~T4时点IL-6水平明显降低(P<0.05)。在T2~T3时点TNF-α的水平明显低于对照组(P<0.05)。两组IL-10的水平在CPB后均增加,但在T2~T3时点MP组升高幅度明显高于NS组(P<0.05)。与NS比较,MP组在CPB后各时点尿NAG、α1-MG、RBP的水平均明显降低(P<0.05)。结论:CPB可导致全身炎性反应及肾功能损伤;甲基强的松龙可减轻炎性反应,同时对肾功能有一定的保护作用。     

Linkage reprogramming by tailor-made E3s reveals polyubiquitin chain requirements in DNA-damage bypass

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The interface of hypothalamic–pituitary–adrenocortical axis and circulating brain natriuretic peptide in prediction of cardiopulmonary performance during physical stress

Brain natriuretic peptide (NT-pro-BNP) was implicated in the regulation of hypothalamic–pituitary–adrenocortical (HPA) responses to psychological stressors. However, HPA axis activation in different physical stress models and its interface with NT-pro-BNP in the prediction of cardiopulmonary performance is unclear. Cardiopulmonary test on a treadmill was used to assess cardiopulmonary parameters in 16 elite male wrestlers (W), 21 water polo player (WP) and 20 sedentary age-matched subjects (C). Plasma levels of NT-pro-BNP, cortisol and adrenocorticotropic hormone (ACTH) were measured using immunoassay sandwich technique, radioimmunoassay and radioimmunometric techniques, respectively, 10 min before test (1), at beginning (2), at maximal effort (3), at 3rd min of recovery (4). In all groups, NT-pro-BNP decreased between 1 and 2; increased from 2 to 3; and remained unchanged until 4. ACTH increased from 1 to 4, whereas cortisol increased from 1 to 3 and stayed elevated at 4. In all groups together, ΔNT-pro-BNP2/1 predicted peak oxygen consumption (B = 37.40, r = 0.38, p = 0.007); cortisol at 3 predicted heart rate increase between 2 and 3 (r = −0.38,B = −0.06, p = 0.005); cortisol at 2 predicted peak carbon-dioxide output (B = 2.27, r = 0.35, p < 0.001); ΔACTH3/2 predicted peak ventilatory equivalent for carbon-dioxide (B = 0.03, r = 0.33, p = 0.003). The relation of cortisol at 1 with NT-pro-BNP at 1 and 3 was demonstrated using logistic function in all the participants together (for 1/cortisol at 1 B = 63.40, 58.52; r = 0.41, 0.34; p = 0.003, 0.013, respectively). ΔNT-pro-BNP2/1 linearly correlated with ΔACTH4/3 in WP and W (r = −0.45, −0.48; p = 0.04, 0.04, respectively). These results demonstrate for the first time that HPA axis and NT-pro-BNP interface in physical stress probably contribute to integrative regulation of cardiopulmonary performance.