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首页> 外文期刊>Brain pathology >Vasopressin Synthesis by the Magnocellular Neurons is Different in the Supraoptic Nucleus and in the Paraventricular Nucleus in Human and Experimental Septic Shock
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Vasopressin Synthesis by the Magnocellular Neurons is Different in the Supraoptic Nucleus and in the Paraventricular Nucleus in Human and Experimental Septic Shock

机译:人和实验性败血性休克中视上核和室旁核中核细胞神经元的加压素合成是不同的

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摘要

Impaired arginine vasopressin (AVP) synthesis and release by the neurohypophyseal system, which includes the neurohypophysis and magnocellular neurons of the paraventricular and supraoptic nuclei, have been postulated in septic shock, but changes in this system have never been assessed in human septic shock, and only partially experimentally. We investigated AVP synthesis and release by the neurohypophyseal system in 9 patients who died from septic shock and 10 controls, and in 20 rats with fecal peritonitis-induced sepsis and 8 sham-operation controls. Ten rats died spontaneously from septic shock, and the others were sacrificed. In patients with septic shock, as in rats that died spontaneously following sepsis induction, AVP immunohistochemical expression was decreased in the neurohypophysis and supraoptic magnocellular neurons, whereas it was increased in the paraventricular magnocellular neurons. No significant change was observed in AVP messenger RiboNucleic Acid (mRNA) expression assessed by in situ hybridization in either paraventricular or supraoptic magnocellular cells. This study shows that both in human and experimental septic shock, AVP posttranscriptional synthesis and transport are differently modified in the magnocellular neurons of the supraoptic and paraventricular nuclei. This may account for the inappropriate AVP release in septic shock and suggests that distinct pathogenic mechanisms operate in these nuclei.
机译:败血性休克中假定了神经下垂系统(包括脑室旁和视上核的神经下垂体和大细胞神经元)的精氨酸加压素(AVP)合成和释放受损,但尚未在人类感染性休克中评估该系统的变化,并且仅部分实验。我们调查了9名死于败血性休克的患者和10名对照以及20例因粪便性腹膜炎引起的脓毒症的大鼠和8名假手术对照的神经下垂系统的AVP合成和释放。十只大鼠因败血性休克自发死亡,另两只被处死。在败血性休克患者中,如在脓毒症诱导后自然死亡的大鼠中,神经垂体和视上巨细胞神经元中AVP免疫组织化学表达降低,而脑室旁大细胞神经元中AVP免疫组织化学表达升高。在室旁或视上巨细胞细胞中通过原位杂交评估的AVP信使核糖核酸(mRNA)表达未见明显变化。这项研究表明,在人和实验性败血性休克中,视光上和脑室旁核的大细胞神经元的转录后合成和转运均发生了不同的修饰。这可能解释了败血性休克中不适当的AVP释放,并表明在这些核中起作用的是不同的致病机制。

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