艾司洛尔联合胺碘酮治疗心室电风暴160例临床分析

目的：探讨和分析盐酸艾司洛尔与胺碘酮联合使用在治疗心室电风暴患者的效果。方法整群选取该院在2011年9月-2014年6月期间所收治的329例心室电风暴患者,遵照随机与知情自愿原则,分为观察组(160例)和对照组(169例)。给予药物胺碘酮治疗,对观察组患者采用盐酸艾司洛尔与胺碘酮联合治疗方案,疗程结束后,认真观察和对比两组患者所取得治疗的效果。结果观察组患者总有效率为95.0%,明显高于对照组的70.4%,该两组患者总有效率对比,差异有统计学意义(P<0.01);治疗后观察组患者收缩压与心率分别为(104.0±15.0)mmHg、(84.0±13.0)次/min全部低于对照组,该两组患者治疗后的收缩压与心率对比,差异有统计学意义(P<0.05)。结论采用盐酸艾司洛尔联合药物胺碘酮共同治疗心室电风暴患者的临床效果满意,能够提高心室风暴患者的治愈率,具有临床推广价值。     

Anomalous collateral from the coronary artery to the affected lung in a case of congenital absence of the left pulmonary artery: effect on coronary circulation

A case of congenital absence of the left pulmonary artery, in which perfusion of the affected lung was accomplished via an arterial shunt from the circumflex coronary artery, is discussed. Data from myocardial perfusion scintigraphy showed that myocardial perfusion was unaffected by the existence of the shunt, largely because the flow through the shunt occurred mainly during systole.     

Acute effect of esmolol intravenously on coronary microcirculation in patients with idiopathic dilated cardiomyopathy

Although coronary flow reserve (CFR) impairment was correlated with the prognosis of patients with idiopathic dilated cardiomyopathy (IDC) and microvascular ischemia was implicated in the progress of the disease, little is known about the effect of the established therapy with beta blockers on coronary microcirculation. The purpose of this study was to assess the effect of beta(1) blockade on coronary blood flow and CFR in patients with IDC. Fourteen patients with IDC and 10 control subjects underwent time-averaged peak coronary flow velocity (APCFV) measurements (centimeters per second) in the proximal left anterior descending coronary artery at baseline and at maximal hyperemia before and after beta(1) blockade with intravenous esmolol. CFR was defined as APCFV at maximal hyperemia/APCFV at baseline. Although there were no significant differences in APCFV at baseline between patients with IDC and controls, patients with IDC had significantly lower APCFV at maximal hyperemia than controls (54.2 +/- 12.0 vs 75.1 +/- 18.6, p <0.05) and decreased CFR (2.39 +/- 0.38 vs 3.50 +/- 0.54, respectively, p <0.05). After beta(1) blockade, a significant decrease in APCFV at baseline (19.5 +/- 3.7 vs 22.9 +/- 5.0, p <0.05) and enhancement of APCFV at maximal hyperemia (59.5 +/- 13.3 vs 54.2 +/- 12.0, p <0.05) were observed in patients with IDC, but not in control subjects, leading to significant improvement in CFR (3.06 +/- 0.40 vs 2.39 +/- 0.38, p <0.05). In conclusion, patients with IDC had alterations in coronary blood flow and decreased CFR that improved after beta(1) blockade. These alterations in microvascular function, which are partially reversed by beta blockade, may be 1 of the underlying mechanisms that contribute to the improved prognosis of patients with IDC under such therapy.     

Evaluation of the chronic toxicity and oncogenicity of N,N-diethyl-m- toluamide (DEET)

Chronic toxicity and/or oncogenicity studies were conducted in rats, mice, and dogs with the insect repellent DEET. DEET was mixed in the diet and administered to CD rats for two years at concentrations that corresponded to dosage levels of 10, 30 or 100 mg/kg/day for males and 30, 100, or 400 mg/kg/day for females; to CD-1 mice for 18 months at dosage levels of 250, 500, or 1000 mg/kg/day; and to dogs for one year, via gelatin capsules, at dosage levels of 30, 100, or 400 mg/kg/day. In the rodent studies, each group consisted of 60 animals of each sex, and two concurrent independent control groups, each containing 60 animals/sex were included in each study. Each group in the dog study consisted of four male and four female dogs and one control group was included in the study. Treatment-related effects were observed at the highest dose level in all three studies. For rats, the effects included decreases in body weight and food consumption and an increase in serum cholesterol in females only. In mice, the effects observed were decreases in body weight and food consumption in both sexes. The effects observed in dogs included increased incidences of emesis and ptyalism, and levels of transient reduction in hemoglobin and hematocrit, increased alkaline phosphatase (males only), decreased cholesterol, and increased potassium. One male dog in the high-dose group also exhibited ataxia, tremors, abnormal head movements, and/or convulsions on several occasions during the study. The highest no- observed-effect levels (NO-ELs) for rats, mice and dogs were determined to be 100, 500, and 100 mg/kg/day, respectively. No specific target organ toxicity or oncogenicity was observed in any of the studies.      

Evaluation of the systematic set-up errors using electronic portal image device in the radiotherapy procedures

Objective： The aim of this work was to quantify the extent of set-up errors to conduct a quality assurance （QA） aspect of treatment delivery, verification of the treatment field＇s position on different days using electronic portal. Methods： This study was carried out on 12 patients, treated for pelvis tumor; and total of 240 images obtained by electronic portal image device （EPID） were analyzed. The EPIs acquire using EPID attached to the Siemens linear accelerator. The anatomy match- ing software （Theraview） was used and displacement in two dimensions were noted for each treatment field to study patient setup errors. Results： The percentages of mean deviations less than 5 mm in X direction were 65% ＆ 92%, from 5-10 mm were 31% ＆ 19% and more than 10 mm were 11% ＆ 9% forNP and lateral direction respectively. The percentages of mean deviations less than 5 mm in Y direction were 65% ＆ 63%, from 5-10 mm were 33% ＆ 28% and more than 10 mm were 22% ＆ 29%. The mean deviations in 2D-vector errors were 〈 5 mm in 47% and 46%, 5-10 mm in 36% and 37% and 〉 10 mm in 37% and 37% of images in the NP and lateral direction respectively. Conclusion： The results revealed that the ranges of set up errors are immobilization method to improve reproducibility. The observed variations were not within the limits..     

A murine monoclonal antibody that blocks fibrinogen binding to normal platelets also inhibits fibrinogen interactions with chymotrypsin- treated platelets

We recently described a monoclonal antibody, 10E5 , that completely blocks adenosine diphosphate (ADP) induced fibrinogen binding to platelets and aggregation induced by ADP, epinephrine, and thrombin. Multiple lines of evidence indicate that 10E5 binds to platelet membrane glycoproteins IIb and/or IIIa. Because it has been reported that platelets treated with chymotrypsin aggregate when fibrinogen is added, we tested the effect of 10E5 antibody on chymotrypsin-induced fibrinogen binding and platelet aggregation. Aspirin-treated human platelets were washed in modified Tyrode's buffer (pH 7.5), incubated for 5 minutes at 22 degrees C with 300 micrograms/mL chymotrypsin, and washed again. The amount of 10E5 antibody bound to these platelets (37,232 +/- 2,928 molecules/platelet; mean +/- SEM, N=9) was similar to that bound to unstimulated control platelets (36,910 +/- 2,669) and did not differ significantly from the amount of antibody bound to ADP- treated platelets (P less than .01, N = 5). The amount of 10E5 bound to chymotrypsin-treated platelets correlated directly with the amount of fibrinogen bound to separate aliquots of the same platelet samples (r = .876, P less than .001). The 10E5 antibody caused virtually complete inhibition of both the binding of fibrinogen to chymotrypsin-treated platelets and the aggregation induced by exogenous fibrinogen. Immunoprecipitation studies of 125I-labeled chymotrypsin-treated platelets revealed that the 10E5 antibody bound proteins with molecular weights characteristic of glycoproteins IIb and IIIa. These data suggest that the fibrinogen receptor on chymotrypsin-treated platelets is identical to that on ADP-treated platelets and that this receptor is either near to, or on, the glycoprotein IIb/IIIa complex.