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      Analysis of treatment effect of urinary kallidinogenase combined with edaravone on massive cerebral infarction

      research-article
      1 , 2
      Biomedical Reports
      D.A. Spandidos
      massive cerebral infarction, urinary kallidinogenase, edaravone, clinical effect

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          Abstract

          The aim of the study was to investigate the clinical effect of urinary kallidinogenase combined with edaravone in the treatment of massive cerebral infarction. A total of 58 patients with massive cerebral infarction were admitted to hospital between January 2013 and January 2014. There were 34 male and 24 female patients. The patients were randomly divided into the observation and control groups (n=29 cases per group). The patients in the control group received edaravone treatment, while patients in the observation group were treated with urinary kallidinogenase and edaravone. The clinical effects of the two groups were then compared. The results showed that the National Institutes of Health Stroke Scale score and serum C-reactive protein level of the patients in the two groups were significantly decreased following treatment. The decreased degree in the observation group was significantly smaller than that in the control group. The difference was statistically significant [(11.03±3.75) vs. (16.58±7.43) scores, P<0.05; (9.88±4.82) vs. (11.98±4.69) mmol/l, P<0.05]. The serum levels of vascular endothelial growth factor were significantly increased in patients of the two groups after treatment. The increased degree in the observation group was significantly higher than that in the control group. The difference was statistically significant [(268.51±77.34) vs. (188.82±57.33) ng/l, P<0.05]. The total effective rate of the observation group was significantly higher than that of the control group and the difference was statistically significant (89.66 vs. 62.07%, P<0.05). In conclusion, urinary kallidinogenase combined with edaravone treatment has a certain clinical curative effect on massive cerebral infarction.

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          Most cited references19

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          The Efficacy of Edaravone (Radicut), a Free Radical Scavenger, for Cardiovascular Disease

          Edaravone was originally developed as a potent free radical scavenger, and has been widely used to treat acute ischemic stroke in Japan since 2001. Free radicals play an important role in the pathogenesis of a variety of diseases, such as cardiovascular diseases and stroke. Therefore, free radicals may be targets for therapeutic intervention in these diseases. Edaravone shows protective effects on ischemic insults and inflammation in the heart, vessel, and brain in experimental studies. As well as scavenging free radicals, edaravone has anti-apoptotic, anti-necrotic, and anti-cytokine effects in cardiovascular diseases and stroke. Edaravone has preventive effects on myocardial injury following ischemia and reperfusion in patients with acute myocardial infarction. Edaravone may represent a new therapeutic intervention for endothelial dysfunction in the setting of atherosclerosis, heart failure, diabetes, or hypertension, because these diseases result from oxidative stress and/or cytokine-induced apoptosis. This review evaluates the potential of edaravone for treatment of cardiovascular disease, and covers clinical and experimental studies conducted between 1984 and 2013. We propose that edaravone, which scavenges free radicals, may offer a novel option for treatment of cardiovascular diseases. However, additional clinical studies are necessary to verify the efficacy of edaravone.
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            Cerebral infarction: incidence and risk factors after diagnostic and interventional cardiac catheterization--prospective evaluation at diffusion-weighted MR imaging.

            To prospectively evaluate incidence of clinically silent and clinically apparent embolic cerebral infarction following diagnostic and interventional coronary angiography and associated risk factors. Written informed consent was obtained from all patients, and the study was approved by the research ethics committee of University of Heidelberg, Germany. Fifty-two patients, including 37 men (mean age, 66.1 years +/- 11.9 [standard deviation]) and 15 women (mean age, 65.3 years +/- 10.3), undergoing elective cardiac catheterization were examined 3-26 hours (mean, 15.3 hours +/- 6) before and 12-48 hours (mean, 25.9 hours +/- 10.4) after cardiac catheterization. Magnetic resonance imaging protocol included isotropic and anisotropic diffusion-weighted single-shot echo-planar sequences. T2-weighted turbo spin-echo and T1-weighted spin-echo sequences also were performed. Apparent diffusion coefficient maps were calculated to exclude false-positive reading results on diffusion-weighted images because of T2 shine-through effect. Images were assessed by two experienced radiologists blinded to clinical data. Cardiac catheterization was performed by 11 experienced cardiologists to exclude operator-related risk. A neurologic examination according to the National Institutes of Health Stroke Scale and Barthel index was performed by a senior cardiologist before acquisition of each image. Sixteen clinical and angiographic variables were analyzed with univariate analysis for ability to predict occurrence of cerebral infarction. No embolic cerebral lesions could be detected at diffusion-weighted imaging before catheterization. After coronary angiography, seven (15%) of 48 patients demonstrated nine focal cerebral infarcts affecting anterior and posterior circulation. Patients remained asymptomatic. Of all tested variables, only duration of the procedure was identified as an independent predictor of occurrence of cerebral infarction (P < .05). In this prospective study, asymptomatic cerebral infarction following cardiac catheterization occurred in 15% of patients in whom duration of the procedure was significantly longer than in those without infarction (P = .017). (c) RSNA, 2005.
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              Neuroprotection against cerebral ischemia/reperfusion injury by intravenous administration of liposomal fasudil.

              Fasudil, a Rho-kinase inhibitor, is a promising neuroprotectant against ischemic stroke; however, its low bioavailability is an obstacle to be overcome. Our previous study revealed that the liposomal drug delivery system is a hopeful strategy to increase the therapeutic efficacy of neuroprotectants. In the present study, the usefulness of intravenously administered liposomal fasudil for cerebral ischemia/reperfusion (I/R) injury treatment was examined in transient middle cerebral artery occlusion (t-MCAO) rats. The results showed that PEGylated liposomes of approximately 100nm in diameter accumulated more extensively in the I/R region compared with those of over 200nm. Confocal images showed that fluorescence-labeled liposomal fasudil was widely distributed in the I/R region, and was not noticeably taken up by microglia, which are well-known resident macrophages in the brain, and neuronal cells. These data indicated that liposomal fasudil mainly exerted its pharmacological activity by releasing fasudil from the liposomes in the I/R region. Moreover, liposomal fasudil effectively suppressed neutrophil invasion and brain cell damage in the t-MCAO rats, resulting in amelioration of their motor function deficits. These findings demonstrated both the importance of particle size for neuroprotectant delivery and the effectiveness of liposomal fasudil for the treatment of cerebral I/R injury.
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                Author and article information

                Journal
                Biomed Rep
                Biomed Rep
                BR
                Biomedical Reports
                D.A. Spandidos
                2049-9434
                2049-9442
                August 2016
                26 May 2016
                26 May 2016
                : 5
                : 2
                : 155-158
                Affiliations
                [1 ]Department of Neurology, East People's Hospital, Xuzhou, Jiangsu 221000, P.R. China
                [2 ]Department of Cardiology, Xuzhou City Center Hospital, Xuzhou, Jiangsu 221009, P.R. China
                Author notes
                Correspondence to: Dr Mou Jing, Department of Cardiology, Xuzhou City Center Hospital, 199 South Jiefang Road, Xuzhou, Jiangsu 221009, P.R. China, E-mail: siyuanmujing@ 123456126.com
                Article
                BR-0-0-692
                10.3892/br.2016.692
                4950744
                27446533
                51f7fcdb-6593-4852-9330-2ef35e8e1787
                Copyright: © Ke et al.

                This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

                History
                : 10 February 2016
                : 23 May 2016
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                massive cerebral infarction,urinary kallidinogenase,edaravone,clinical effect

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