OBJECTIVE: Therapeutic angiogenesis has become a promising approach for treating ischemic heart disease (IHD). The present study aims to investigate the effects of Qishen Granule (QSG) on angiogenesis in myocardial ischemia (MI) and the potential mechanism. METHODS: In vivo study was conducted on rat model of myocardial infarction. QSG was performed daily at a dose of 2.352 g/kg for four weeks. Cardiac function was assessed by echocardiogram and pro-angiogenic effects were evaluated by Laser Doppler and CD31 expression. Oxygen-glucose deprivation (OGD) was applied in cultured human umbilical vein endothelial cells (HUVECs). Cell viability, wound healing and tube formation assay were used to test functions of HUVECs. ELISA and Western blots were used to assess protein expressions of bone morphogenetic protein 2-delta-like 4-notch homolog 1 (BMP2-Dll4-Notch1) signaling pathway. RESULTS: The results showed that QSG improved heart function, cardiac blood flow and microvessel density in myocardial ischemic rats. In vitro, QSG protected HUVECs by promoting the cell viability and tube formation. QSG upregulated bone morphogenetic protein-2 (BMP2) and downregulated delta-like 4 (Dll4) and notch homolog 1 (Notch1) expressions both in rats and HUVECs. CONCLUSION QSG protected against MI by promoting angiogenesis through BMP2-Dll4-Notch1 pathway. BMP2 might be a promising therapeutic target for IHD.

AIM: To observe the effect of acute normovolemic hemodilution (ANH) autologous blood transfusion on the EEG bispectral index and muscle relaxation in elderly patients undergoing orthopedic surgery to explore the influence of autologous blood transfusion containing anesthetic components on the quality and safety of postoperative anesthesia recovery. METHODS: Forty patients, aged 65-75, weighing 55-80 kg, ASA grade I-II, with an estimated intraoperative blood loss of more than 600 mL, were selected for elective orthopedic surgery. The patients were randomly divided into two groups (n=20): group A was given acute normovolemic hemodilution (ANH), and the target value of Hct was 28%-30% after induction of anesthesia; group B was the control group which was given routine fluid infusion during operation without ANH. Bispectral index (BIS), TOF values and plasma concentrations of propofol and cisatracurium were measured at the beginning of autotransfusion (T

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.

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.