期刊简介

               本刊是中国科学技术协会主管、中国病理生理学会主办、暨南大学承办的国家级综合性病理生理学高级学术刊物。杂志刊登有关病理生理学理论研究(包括实验研究和临床研究)方面的论著、专题综述、教学研究、科研仪器和药品评价介绍等,注重介绍疾病发病机制和临床病理生理学研究。适合医药院校教学科研人员、研究生、临床医务工作者和高年级医学生阅读。                

首页>中国病理生理杂志
  • 杂志名称:中国病理生理杂志
  • 主管单位:中国科学技术协会
  • 主办单位:中国病理生理学会
  • 国际刊号:1000-4718
  • 国内刊号:44-1187/R
  • 出版周期:月刊
期刊荣誉:2008和2011年分别被评为第一届和第二届中国精品科技期刊;2008~2011年连续4次荣获“百种中国杰出学术期刊”奖;2011年被评为RCCSE(武汉大学中国科学评价研究中心)中国权威期刊;2010年荣获广东省期刊评选最高奖——品牌期刊奖;2011年荣获广东省优秀科技期刊一等奖。期刊收录:万方收录(中), JST 日本科学技术振兴机构数据库(日), 北大核心期刊(中国人文社会科学核心期刊), CA 化学文摘(美), 上海图书馆馆藏, 维普收录(中), 统计源核心期刊(中国科技论文核心期刊), 知网收录(中), CSCD 中国科学引文数据库来源期刊(含扩展版), 国家图书馆馆藏
中国病理生理杂志2001年第08期

关键词:in vitro, response curve, endotoxic shock, pulmonary hypertension, adenosine diphosphate, sodium nitroprusside, pulmonary artery, possible role
摘要:In order to investigate the possible role of ONOO- in regulatory disorder of pulmonary arterial tension in endotoxic shock, the responses of rabbit pulmonary arterial rings (PARs) preincubated with ONOO- to endothelial dependent and receptor dependent relaxants acetylcholine (ACh) and adenosine diphosphate (ADP), endothelial dependent and receptor independent relaxant A23187, endothelial independent relaxant sodium nitroprusside (SNP) and α1-adrenoceptor agonist phenylephrine (PE) were observed in vitro in accumulative manner. Results were as follow: (1) Relaxations of PARs to ACh, A23187 and ADP were markedly impaired with shift of accumulative dose response curve of each agonist to the right. Inhibition of endothelial dependent and receptor dependent or independent relaxation by ONOO- was dose dependent. (2) ONOO- incubation inhibited SNP-induced relaxation in a dose dependent manner. Accumulative dose response curve of SNP was right shift to some degree depending on the doses of ONOO-. (3) Contractile response of PARs to PE varied with the different doses of ONOO-. In PARs preincubated with 0.5 mmol/L ONOO-, contractile reponse was significantly enhanced with shift of PE accumulative dose response curve to the left, while in PARs preincubated with 1.0 mmol/L or 2.0 mmol/L ONOO-, it was markedly reduced with right shift of PE accumulative dose response curve. (4) Vehicle of ONOO- had no effect on responses to every agonist, whereas decomposed ONOO- had minimal effect on the response to PE and ADP. In contrast, relaxation of PARs to ACh, A23187 and SNP were enhanced. These results suggested that direct effect of ONOO- on pulmonary artery may be a key factor contributing to regulatory disorder of pulmonary arterial tension induced by LPS and pulmonary hypertension in the early stage of endotoxic shock.