ABSTRACT
Objective: To explore the impact of renal function injury on diagnostic value of NT-proBNP in patients with heart failure (HF). Methods: A total of 420 patients with cardiovascular disease at (50-75) years of age were divided into 2 groups based on left ventricular ejection fraction (LVEF): Control group, the patients with normal cardiac function, LVEF≥40%,n=232 and HF group, LVEFeGFR≥60 ml/min·1.73m2), Moderate renal injury (60>eGFR≥30 ml/min·1.73m2) and Severe renal injury (eGFR Results: Compared with Control group, HF group had increased blood level of NT-proBNP,P0.05, while it was much higher in Moderate and Severe renal injury subgroups than Normal renal function subgroup,P Conclusion: Moderate to severe renal function injury could increase circulating level of NT-proBNP and therefore, the cut-off value of NT-proBNP for HF diagnosis should be elevated accordingly in patients of HF combing renal injury.
ABSTRACT
In order to investigate the protective effect of hypoxic preconditioning on the cerebral ischemia-reperfusion injury, the expression of Bcl-2 and Bax was detected by using immunohistochemical staining after 3 h cerebral ischemia followed by 1, 6, 12, 24 and 48 h reperfusion respectively in rats treated with or without hypoxic preconditioning before cerebral ischemia. In addition,the apoptosis of neural cells and the behavioral scores for neurological functions recovery were evaluated by TUNEL staining and "crawvling method", respectively. Compared with control group (cerebral ischemia-reperfusion without hypoxic preconditioning), the expression of Bcl-2 was significantly increased, but that of Bax decreased in the hypoxic preconditioning group (cerebral ischemiareperfusion with hypoxic preconditioning), both P＜0. 05. The pre-treatment with hypoxic preconditioning could reduce the apoptosis of neural cells and promote the neurological function recovery as compared to control group. It was suggested that hypoxic preconditioning may have protective effects on the cerebral ischemia-reperfusion injury by inhibiting the apoptosis of neural cells, increase the expression of Bcl-2 and decrease the expression of Bax.