AIM: To investigate the effect of L-phenyla lanine on vascular remodeling in hypertensive rats. METHODS: Vascular remodeling was measured by laser scanning conf ocal microscopy (LSCM) in mesenteric resistance arteries isolated from spontaneo usly hypertensive rat (SHR) and normotensive Wistar-Kyoto (WKY) rat. The effect of L-phenylalanine on the hypertensive vascular remodeling was observed. The thi rd most distal first-order branches of mesenteric resistance arteries from SHR a nd WKY were studied. The arteries were fixed under pressure. The segments were s tained with the nuclear dye propidium iodide. The diameter, wall thickness and o rientation angle of smooth muscle cells were measured with LSCM. RESULTS: Compared with WKY, SHR arteries showed: (1) smaller lum en, (2) increased wall thickness, (3) disorganized orientation angle of smooth m uscle cells. L-phenylalanine treatment induced specific changes in the lumen, wa ll thickness and the orientation angle of smooth muscle cells. CONCLUSIONS: Hypertension induces vascular remodeling of the bra nches of mesenteric arteries from SHR. L-phenylalanine inhibits the vascular rem odeling process of hypertension.

Two main impact factors on accuracy of electronic balance are discussed based on its working principle:acceleration of gravity and temperature variation.Through analysis of interacting variables in acceleration of gravity and electronic balance measurement results,the method of builtin standard weight compensation and its shortages are brought forward and attach the compensation method on weight calibration.The impacts on temperature change for the electronic balance measurement are analyzed,which proposes a method to eliminate these factors.

The purpose of the present study was to examine the effects of oxidative stress on ventricular arrhythmias in rabbits with adriamycin-induced cardiomyopathy and the relationship between oxidative stress and ventricular arrhythmia. Forty Japanese white rabbits were randomly divided into four groups (n=10 in each): control group, metoprolol (a selective β1 receptor blocker) group, carvedilol (a nonselective β blocker/α-1 blocker) group and adriamycin group. Models of adriamycin-induced cardiomyopathy were established by intravenously injecting adriamycin hydrochloride (1 mg/kg) to rabbits via the auri-edge vein twice a week for 8 weeks in the adriamycin, metoprolol and carvedilol groups. Rabbits in the control group were given equal volume of saline through the auri-edge vein. Rabbits in the metoprolol and carvedilol groups were then intragastrically administrated metoprolol (5 mg/kg/d) and carvedilol (5 mg/kg/d) respectively for 2 months, while those in the adriamycin and control groups were treated with equal volume of saline in the same manner as in the metroprolol and carvedilol groups. Left ventricular end diastolic diameter (LVEDd) and left ventricular ejection fraction (LVEF) were measured by echocardiography. Plasma levels of N-terminal pro B-type natriuretic peptide (NT-proBNP), malondialdehyde (MAD) and superoxide dismutase (SOD) were detected. The left ventricular wedge preparations were perfused with Tyrode's solution. The transmural electrocardiogram, transmural action potentials from epicardium (Epi) and endocardium (Endo), transmural repolarization dispersion (TDR) were recorded, and the incidences of triggered activity and ventricular arrhythmias were obtained at rapid cycle lengths. The results showed that TDR and the serum MDA and NT-proBNP levels were increased, and LVEF and the serum SOD level decreased in the adriamycin group compared with the control group. The incidences of triggered activity and ventricular arrhythmia were significantly higher in the adriamycin group than those in the control group (P<0.05). In the carvedilol group as compared with the adriamycin group, the serum SOD level and the LVEF were substantially increased; the TDR, and the serum MDA and NT-proBNP levels were significantly decreased; the incidences of triggered activity and ventricular arrhythmia were obviously reduced (P<0.05). There were no significant differences in the levels of MDA and SOD, LVEF, TDR and the incidences of triggered activity and ventricular arrhythmia between the adriamycin group and the metoprolol group. It was concluded that carvedilol may inhibit triggered activity and ventricular arrhythmias in rabbit with adriamycin-induced cardiomyopathy, which is related to the decrease in oxygen free radials.

The purpose of the present study was to examine the effects of oxidative stress on ventricular arrhythmias in rabbits with adriamycin-induced cardiomyopathy and the relationship between oxidative stress and ventricular arrhythmia. Forty Japanese white rabbits were randomly divided into four groups (n=10 in each): control group, metoprolol (a selective β1 receptor blocker) group, carvedilol (a nonselective β blocker/α-1 blocker) group and adriamycin group. Models of adriamycin-induced cardiomyopathy were established by intravenously injecting adriamycin hydrochloride (1 mg/kg) to rabbits via the auri-edge vein twice a week for 8 weeks in the adriamycin, metoprolol and carvedilol groups. Rabbits in the control group were given equal volume of saline through the auri-edge vein. Rabbits in the metoprolol and carvedilol groups were then intragastrically administrated metoprolol (5 mg/kg/d) and carvedilol (5 mg/kg/d) respectively for 2 months, while those in the adriamycin and control groups were treated with equal volume of saline in the same manner as in the metroprolol and carvedilol groups. Left ventricular end diastolic diameter (LVEDd) and left ventricular ejection fraction (LVEF) were measured by echocardiography. Plasma levels of N-terminal pro B-type natriuretic peptide (NT-proBNP), malondialdehyde (MAD) and superoxide dismutase (SOD) were detected. The left ventricular wedge preparations were perfused with Tyrode's solution. The transmural electrocardiogram, transmural action potentials from epicardium (Epi) and endocardium (Endo), transmural repolarization dispersion (TDR) were recorded, and the incidences of triggered activity and ventricular arrhythmias were obtained at rapid cycle lengths. The results showed that TDR and the serum MDA and NT-proBNP levels were increased, and LVEF and the serum SOD level decreased in the adriamycin group compared with the control group. The incidences of triggered activity and ventricular arrhythmia were significantly higher in the adriamycin group than those in the control group (P<0.05). In the carvedilol group as compared with the adriamycin group, the serum SOD level and the LVEF were substantially increased; the TDR, and the serum MDA and NT-proBNP levels were significantly decreased; the incidences of triggered activity and ventricular arrhythmia were obviously reduced (P<0.05). There were no significant differences in the levels of MDA and SOD, LVEF, TDR and the incidences of triggered activity and ventricular arrhythmia between the adriamycin group and the metoprolol group. It was concluded that carvedilol may inhibit triggered activity and ventricular arrhythmias in rabbit with adriamycin-induced cardiomyopathy, which is related to the decrease in oxygen free radials.
Animals ; Anti-Arrhythmia Agents ; administration & dosage ; Antibiotics, Antineoplastic ; Carbazoles ; administration & dosage ; Cardiomyopathies ; chemically induced ; physiopathology ; prevention & control ; Doxorubicin ; Heart Rate ; drug effects ; Male ; Metoprolol ; administration & dosage ; Oxidative Stress ; drug effects ; Propanolamines ; administration & dosage ; Rabbits ; Treatment Outcome ; Ventricular Fibrillation ; chemically induced ; physiopathology ; prevention & control

Objective:To investigate the infarct size and its related factors in patients with anterior choroidal artery (AchA) territory infarction.Methods:From April 2016 to April 2018, consecutive patients with acute AchA territory infarction hospitalized in the Department of Neurology, the Affiliated Shuyang Hospital of Xuzhou Medical University were enrolled retrospectively. The National Institutes of Health Stroke Scale (NIHSS) was used to assess the severity of the disease at baseline, and the Diffusion-Weighted Imaging (DWI) was used to determine the side, location, size, and morphology of the infarct lesions. The patients were divided into small infarction group (<20 mm) and large infarction group (≥20 mm). Multivariate logistic regression analysis was used to determine the independent risk factors for infarct size. Results:A total of 100 consecutive patients with acute AchA territory infarction were enrolled, including 86 (86.0%) in small infarction group, 14 (14.0%) in large infarction group. Based on the NIHSS score, there were 89 patients with mild stroke, 9 with moderate stroke, and 2 with severe stroke. According to DWI, 69 patients (69.0%) had long cord-like infarcts and 31 (31.0%) had other shapes of infarcts. The baseline NIHSS score (7.0 [2.0-10.5] vs. 3.0 [2.0-4.0]; Z=2.353, P=0.019) and the proportion of patients with severe stroke (14.3% vs. 0%; P=0.018), the infarcts in posterior part of periventricular area (85.7% vs. 57.0%; χ2=4.180, P=0.041) and medial globus pallidus (21.4% vs. 4.7%; χ2=5.206, P=0.023), and cord-like infarction (92.9% vs. 65.1%; χ2=4.332, P=0.037) in patients of the large infarction group were significantly higher than those of the small infarction group; leukocyte count (7.7±1.7×10 9/L vs. 6.6±1.8×10 9/L; t=2.214, P=0.036) and platelet count (234.5±39.5×10 9/L vs. 198.0±49.4×10 9/L; t=2.618, P=0.010) were significantly higher than those of the small infarction group; the proportion of patients with sensory impairment was significantly higher than that of the small infarction group (50.0% vs. 24.4%; χ2=3.908, P=0.048). Multivariate logistic regression analysis showed that platelet count (odds ratio 1.018, 95% confidence interval 1.000-1.621; P=0.044) and stroke severity (odds ratio 18.245, 95% confidence interval 1.534-217.052; P=0.022) were significantly and positively correlated with the infarct size. Conclusion:The related factors of the infarct size in patients with AchA territory infarction included sensory impairment, baseline NIHSS score, stroke severity, morphology and location of infarct lesions, and leukocyte and platelet counts, of which platelet count and stroke severity were independently positively correlated with the infarct size.