Objective To explore the effect of Bushen decoction on Na+-K+ATPase 、Ca2+-Mg2+ATPase and succinate dehydrogenase(SDH) in rats with heart failure. Methods 60 heart failure rats were established by ligating left anterial descending coronary artery. Theywere randomly divided into model group, sham operation group, trimetazidine group, Bushen low-dose group, Bushen middle-dose groupand Bushen high-dose group with 10 rats in each group. They were gavaged 2 weeks after modeling for 8 weeks, hemodynamic changes includingleft ventricular systolic pressure (LVSP), left ventricular diastolic pressure (LVEDP), and the maximum rate left ventricular pressurerised or decreased (±LVdp/dtmax) were recorded as well as the level of Na+-K+ATP ase、Ca2+-Mg2+ATPase and SDH through the spectrophotometer.Results Compared with the sham operation group, the LVSP and + LVdp/dtmax of rats in model group decreased (P<0.05), LVEDPand -LVdp/dtmax increased (P<0.05). After Bushen intervention, contractility and diastolic function of myocardial of rats in middle and highdose group were better than model group (P<0.01), especially in high dose group. Na+-K+ATP ase、Ca2+-Mg2+ATPase and SDH activity werehigher in Bushen groups than the model group, but lower than the sham operation group. With the increase of the doses, Na+-K+ATP ase、Ca2+-Mg2+ATPase and SDH activity gradually increased. Conclusion Bushen decoction can improve the cardiac function of rats with heartfailure that may be associated with Na+-K+ATPase, Ca2+-Mg2+ATPase and SDH activity.

Objective:To improve the differential awareness of lead porsoning.Methods:A case with stomachache, anemia, myasthenia, and abnormal urine color was described. The diagnosis and treatment were analyzed and discussed.Results:A middle-aged female was admitted with a 9-month medical history, compalnied with rash, stomachache. She also had evidence of hemolytic anemia,nervous system and kidneys imvolvement, and Lab test showed a significantly elevated blood lead level. It was considered to be in line with multiple organ system damage caused by lead poisoning.Conclusion:Lead poisoning can mimic the clinical presentations of rheumatic diseases, resulting in multiple system ivolvement. When the patient's clinical manifestation cannot be fully explained, some special situations should be considered, such as toxic testing.

Objective To establish an improved type Ⅱ cardio-renal syndrome rat model and evaluate it.Methods Twenty male SD rats were randomly divided into sham and model groups with 7 rats in the sham group and 13 rats in the model group.The model group received the method of squeezing the heart under a small animal anesthesia machine to permanently ligate the left anterior descending branch of the coronary artery to cause myocardial infarction.One week later,unilateral nephrectomy(right nephrectomy)was performed.The rats underwent cardiac echocardiography,pathological staining,and blood and urine tests at 6 weeks to verify model establishment.Results Compared with the sham group,the cardiac function assessed by echocardiography and the endogenous creatinine clearance rate in the model group rats were significantly decreased(P<0.01),and the levels of brain natriuretic peptide,blood creatinine,urea nitrogen,and 24 h urine protein in the model group were significantly increased(P<0.01).HE staining revealed a disordered myocardial arrangement,glomerular atrophy,and inflammatory cell infiltration in model group rats.Picric acid-Sirius red staining showed a significant increase in myocardial collagen fibers,an irregular arrangement of renal tubules,and a large amount of collagen deposition in model group rats.The positive staining area ratio was also significantly increased(P<0.01).Conclusions This improved modeling method provided a typeⅡcardio-renal syndrome rat model with s simple operation,minimal surgical trauma,and low mortality rate.This model simulates the early onset of cardiac and renal function damage and pathological changes in type Ⅱ CRS,laying the foundation for systematic and in-depth research on the pathogenesis and pathological mechanism of type Ⅱ cardio-renal syndrome.