1.EXPERIMENTAL STUDY OF MYOCARDIAL ISCHEMIA AND HEMODYNAMIC CHANGES DURING PULMONARY LOBECTOMY IN DOG WITH OR WITHOUT CORONARY ARTERY STENOSIS
Li ZHANG ; Shiwen WANG ; Dalia LI
Medical Journal of Chinese People's Liberation Army 1983;0(02):-
To determine the effect of pulmonary lobectomy on myocardial blood supply and hemodynamics, 18 dogs were randomized into 3 groups. The dogs in group A and C were subjected to about 75% occlusion of the left anterior descending coronary artery. One week later, dogs in group C were sacrificed by arterial bleeding, while dogs in group A and B underwent right upper pulmonary lobectomy, and extremity ECG, blood routine, blood gas, hemodynamics and morphological changes of the myocardium were examined. The results showed that pulmonary lobectomy could result in or worsen myocardial ischemia. There was significant decrease in PO 2 , SaO 2 ; and CI, and significant elevation of LVEDP, PCWP and MPAP. There were more elevation of LVEDP and less decrease in CI after lobectomy in group A compared with group B. It suggested that pulmonary lobectomy could intensify myocardial ischemi and indace hemodynamic disturbances by lowering PO 2 and SaO 2 , especially where there was coronary artery stenosis before the operation.
2.Neuroprotective effect and the mechanism of Shenzao jiannao oral liquid on Alzheimer ’s disease model mice
Xian JIN ; Jicong CHEN ; Yuying XIN ; Honghe XIAO ; Yan LI ; Yan DENG ; Jingxian YANG
China Pharmacy 2022;33(7):836-841
OBJECTIVE To study the neuroprotective effects of Shenzao jianna o oral liquid (SZJN)on Alzheimer ’s disease (AD)model mice and its mechanism. METHODS The mice were randomly divided into sham operation group ,model group , Donepezil hydrochloride tablet group (0.65 mg/kg),SZJN low-dose ,medium-dose and high-dose groups (0.3,1.5 and 7.5 g/kg, calculated by crude drug quantity ),with 12 mice in each group ,half male and half female. Each group was given relevant medicine(intragastric administration of water at constant volume in sham operation group and model group ),twice a day ,for consecutive 28 d. On the 15th day of administration ,intracerebroventricular injection of β-amyloid 1-42(Aβ1-42)combined with intraperitoneal injection of scopolamine hydrobromide were used to induce AD model. Morris water maze was used to detect the learning and memory ability of mice. HE staining and Nissl staining were used to evaluate the pathological changes of brain tissue in mice. The levels of MDA and SOD in brain tissue of mice were detected. The phosphorylation level of cyclic adenosine monophosphate response element binding protein (CREB) and expression of brain-derived neurotrophic factor (BDNF) in hippocampal tissues were detected by Western blot. RESULTS Compared with sham operation group ,the escape latency of the model group was significantly prolonged ,and the number of crossing the platform and the percentage of residence time in the target quadrant were significantly reduced (P<0.01). The level of SOD in brain tissue ,the phosphorylation level of CREB and the expression level of BDNF in hippocampus decreased significantly (P<0.01),while the level of MDA increased significantly (P< 0.01). In hippocampal CA 1 area and cortical tissue ,nerve cells showed significantly decreased number ,the disordered arrangement and large gap ;the shape of nucleus was irregular and deeply stained ,and Nissl body was blurred ,loosely arranged and the number decreased. Compared with model group ,the escape latency of mice in each dose group of SZJN was significantly shortened ,and the times of crossing the platform and the percentage of residence time in the target quadrant were significantly jing- increased(P<0.01). Above indexes of brain tissue in mice were reversed sig nificantly in SZJN high-dose group (P<0.01),and pathological damage of brain tiss ue was improved. CONCLUSIONS SZJN can significantly improve the learning and memory ability of AD model mice ,and alleviate the pathological injury and oxidative stress of brain tissue ,which may be related to the activation of CREB/BDNF signaling pathway.