{"title":"体外与体内脂多糖对大鼠胸主动脉反应性影响的比较。","authors":"K Takakura, Y Goto, S Kigoshi, I Muramatsu","doi":"","DOIUrl":null,"url":null,"abstract":"<p><p>Effects of treatment in vivo and in vitro with lipopolysaccharide (LPS) on the responsiveness of rat thoracic aorta were examined. The endothelium-denuded aortic strips isolated 6 hr after intraperitoneal (i.p.) administration of LPS (20 mg/kg), which could produce hemodynamic changes, relaxed in response to L-arginine. The same amplitude of relaxation was produced by L-arginine in the aortic strips incubated with a lower dose of LPS (1 microgram/ml) in vitro for 6 hr. Both relaxing responses were inhibited by NG-nitro-L-arginine (L-NOARG). The contractile responses to phenylephrine and KCl were reduced by LPS treatment in vivo or in vitro, but the extent of inhibition was greater in vivo than in vitro. Further, the attenuation of contractile responses was completely reversed by L-NOARG in the strips treated in vitro, whereas the reversal by L-NOARG was incomplete in the strips treated with LPS in vivo. Endothelium-dependent relaxation induced by acetylcholine was attenuated by LPS in vivo but not in vitro. These results suggest that the hyporesponsiveness of rat thoracic aorta after treatment in vitro with LPS, which can produce hemodynamic changes, may be related to an enhanced NO production in the smooth muscle cells, while not only the NO pathway but also additional factors may be involved in the vascular hyporesponsiveness of the sepsis rats.</p>","PeriodicalId":10280,"journal":{"name":"Circulatory shock","volume":"42 3","pages":"141-6"},"PeriodicalIF":0.0000,"publicationDate":"1994-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Comparison between the effects of treatment in vitro and in vivo with lipopolysaccharide on responsiveness of rat thoracic aorta.\",\"authors\":\"K Takakura, Y Goto, S Kigoshi, I Muramatsu\",\"doi\":\"\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Effects of treatment in vivo and in vitro with lipopolysaccharide (LPS) on the responsiveness of rat thoracic aorta were examined. The endothelium-denuded aortic strips isolated 6 hr after intraperitoneal (i.p.) administration of LPS (20 mg/kg), which could produce hemodynamic changes, relaxed in response to L-arginine. The same amplitude of relaxation was produced by L-arginine in the aortic strips incubated with a lower dose of LPS (1 microgram/ml) in vitro for 6 hr. Both relaxing responses were inhibited by NG-nitro-L-arginine (L-NOARG). The contractile responses to phenylephrine and KCl were reduced by LPS treatment in vivo or in vitro, but the extent of inhibition was greater in vivo than in vitro. Further, the attenuation of contractile responses was completely reversed by L-NOARG in the strips treated in vitro, whereas the reversal by L-NOARG was incomplete in the strips treated with LPS in vivo. Endothelium-dependent relaxation induced by acetylcholine was attenuated by LPS in vivo but not in vitro. These results suggest that the hyporesponsiveness of rat thoracic aorta after treatment in vitro with LPS, which can produce hemodynamic changes, may be related to an enhanced NO production in the smooth muscle cells, while not only the NO pathway but also additional factors may be involved in the vascular hyporesponsiveness of the sepsis rats.</p>\",\"PeriodicalId\":10280,\"journal\":{\"name\":\"Circulatory shock\",\"volume\":\"42 3\",\"pages\":\"141-6\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"1994-03-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Circulatory shock\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Circulatory shock","FirstCategoryId":"1085","ListUrlMain":"","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
摘要
研究了体内和体外脂多糖(LPS)对大鼠胸主动脉反应性的影响。腹腔注射LPS (20 mg/kg) 6小时后分离的内皮剥离主动脉条带,可产生血流动力学改变,l -精氨酸对血流动力学反应松弛。l -精氨酸与低剂量LPS(1微克/毫升)体外培养6小时后,主动脉条带产生相同幅度的松弛。ng -硝基- l -精氨酸(L-NOARG)抑制了这两种放松反应。体内和体外LPS处理均能降低对苯肾上腺素和KCl的收缩反应,但体内抑制程度大于体外抑制程度。此外,L-NOARG在体外处理的条带中完全逆转了收缩反应的衰减,而L-NOARG在体内处理的条带中则不完全逆转。LPS在体内可减弱乙酰胆碱诱导的内皮依赖性松弛,但在体外无减弱作用。上述结果提示,体外LPS处理后大鼠胸主动脉反应性降低,血流动力学发生改变,可能与平滑肌细胞NO生成增强有关,脓毒症大鼠血管反应性降低不仅与NO通路有关,还可能与其他因素有关。
Comparison between the effects of treatment in vitro and in vivo with lipopolysaccharide on responsiveness of rat thoracic aorta.
Effects of treatment in vivo and in vitro with lipopolysaccharide (LPS) on the responsiveness of rat thoracic aorta were examined. The endothelium-denuded aortic strips isolated 6 hr after intraperitoneal (i.p.) administration of LPS (20 mg/kg), which could produce hemodynamic changes, relaxed in response to L-arginine. The same amplitude of relaxation was produced by L-arginine in the aortic strips incubated with a lower dose of LPS (1 microgram/ml) in vitro for 6 hr. Both relaxing responses were inhibited by NG-nitro-L-arginine (L-NOARG). The contractile responses to phenylephrine and KCl were reduced by LPS treatment in vivo or in vitro, but the extent of inhibition was greater in vivo than in vitro. Further, the attenuation of contractile responses was completely reversed by L-NOARG in the strips treated in vitro, whereas the reversal by L-NOARG was incomplete in the strips treated with LPS in vivo. Endothelium-dependent relaxation induced by acetylcholine was attenuated by LPS in vivo but not in vitro. These results suggest that the hyporesponsiveness of rat thoracic aorta after treatment in vitro with LPS, which can produce hemodynamic changes, may be related to an enhanced NO production in the smooth muscle cells, while not only the NO pathway but also additional factors may be involved in the vascular hyporesponsiveness of the sepsis rats.