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In the present study we observed dynamically and systemically the changes of plasma somatostatin and glucagon in the peripheral and portal vein, and the changes of pancreatic immunopathology in the course of development of cirrhosis induced by CCl_4 and after portacaval shunt (PCS) in the cirrhotic rats as well as investigated their causes and correlationship. The results showed that hyperglucagonemia was caused by spontaneous portosystemic shunting and surgically induced portacaval anastomosis. Moreover, there was much higher level of glucagon in the portal vein with corresponding increase of A cells in PCS rats than those in the controls, indicating that another cause for elevation of glucagon was hypersecretion of pancreatic A cells. Our data demonstrated that both deterioration of liver function and portosystemic shunting might not be responsible for the elevated level of somatostatin in the cirrhotic rats with PCS. However, there was a closed positive correlation between plasma glucagon and somatostatin. Thus it was concluded that hyperglucagonemia stimulated the release of somatostatin. In view of the fact the elevated level of glucagon was much higher than that of somatostatin, there was probably a relative lack of somatostatin in cirrhosis with portal hypertension. 相似文献
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颅骨软骨粘液样纤维瘤较少见。现将我院20多年来遇到的1例报道如下: 周××、男、3岁。住院号:154761。患儿于1976年7月,偶然发现右耳后有一黄豆大小肿块,不痛、不痒,质硬,不活动。半年后肿块增至核桃大小。于1977年1月在外院切除,诊断为“纤维肉瘤”。术后1个月于手术处又 相似文献
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椎管腔内畸胎瘤极为少见,我院于1966及1981年共收治2例,现报告如下。 [例1] 葛××,男性,25岁,院号61605。患者于1956年春出现左下肢酸痛,麻木、无力。卧床休息后好转,半年后腰部酸痛,逐日加重,动则加剧,以致不能行走,伴大小便失控。自幼至18岁有遗尿史。于1966年10月4日住院。检查:左下肢肌萎缩,远端明显,大腿肌力4级左右,小腿伸趾肌力1~2级,肌张力低,膝和跟腱反射消失,股及小腿外侧痛温觉及右大腿内侧痛温觉减退。肛门反射消失,提睾反射存在。左腰背部肌痉挛,无叩痛,活动略受限,脑脊液色清,压力105mmH_2O,蛋白含量204 相似文献
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在动物实验的基础上,我院自1979年10月开始在临床上应用上海试产的GF—1型管状吻合器,在结直肠手术中,尤其对直肠中、上段癌,有其独到之处。本文就以应用管状吻合器(以下简称吻合器)于结直肠癌12个病例的临床结果和有关实验研究加以报道。 相似文献
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在人体的一定部位施加磁场治疗多种疾病的医疗方法称为磁疗。有关应用磁疗于软组织损伤,近年来已有不少报道,疗效显著且肯定,但对其治疗作用机理研究尚未多见,为此我科作了稀土钴永磁片对家兔耳部 相似文献
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In order to pinpoint the site causing increased intrahepatic vascular resistance, we observed the relationship between hepatic pathologic changes and free portal pressurre (FPP) during the development of CCl_4-induced liver cirrhosis of rat. The results suggested that the degeneration necrosis and regeneration of liver cells, and consequent stenosis, or obliteration of sinusoidal spaces caused by the swelling and disarrangement of the liver cell plates led to the occurence of portal hypertension, The possibility of pre-or post-sinusoidal obstruction was excluded by the manifestation of the pathologic lesions. It is the authors' belief that the exact site of the increased intrahepatic vascular resistance was most likely at the level of hepatic sinusoids. Furthermore, there was certain positive correlation between plasma glucagon concentration and FPP, indicating that glucagon was also involved in the pathogenesis of portal hypertension. 相似文献