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重组人白细胞介素-1β对清醒大鼠的心血管效应

Cardiovascular effects of human recombinant interleukin-1 beta in conscious rats.

作者信息

Bataillard A, Sassard J

机构信息

Department of Physiology and Clinical Pharmacology, Faculty of Pharmacy, Centre National de la Recherche Scientifique Unité de Recherche Associée 1483, Lyon, France.

出版信息

Am J Physiol. 1994 Apr;266(4 Pt 2):R1148-53. doi: 10.1152/ajpregu.1994.266.4.R1148.

DOI:10.1152/ajpregu.1994.266.4.R1148
PMID:8184956
Abstract

Cardiovascular effects of human recombinant interleukin-1 beta (hrIL-1 beta) were investigated in normotensive rats using a computerized analysis of arterial blood pressure in conscious, unrestrained animals. Intravenous injection of hrIL-1 beta induced a rapid and short-lasting rise in blood pressure associated with a first slight tachycardia followed by a second sustained and pronounced increase in heart rate. These effects occurred in a dose-related manner. Pretreatment with a converting-enzyme inhibitor (perindopril) did not modify the hrIL-1 beta-induced increase in blood pressure. Blockade of beta 1-adrenoceptors (atenolol) prevented the tachycardia, but did not significantly affect the pressor response to hrIL-1 beta. On the contrary, the hrIL-1 beta-induced increase in blood pressure was inhibited by an alpha 1-adrenoceptor antagonist (prazosin), whereas the tachycardia was untouched. Finally, pretreatment with a cyclooxygenase inhibitor (indomethacin) completely abolished the cardiovascular response to hrIL-1 beta. These results suggest that the hrIL-1 beta-induced pressor response and associated tachycardia require the synthesis of prostaglandins and involve a sympathetic nervous system activation but do not depend on the renin-angiotensin system.

摘要

利用对清醒、自由活动动物的动脉血压进行计算机分析,在正常血压大鼠中研究了重组人白细胞介素-1β(hrIL-1β)的心血管效应。静脉注射hrIL-1β可引起血压迅速且短暂的升高,伴随首次轻微心动过速,随后心率出现第二次持续性显著增加。这些效应呈剂量相关方式出现。用转化酶抑制剂(培哚普利)预处理并未改变hrIL-1β诱导的血压升高。β1-肾上腺素能受体阻断剂(阿替洛尔)可预防心动过速,但对hrIL-1β的升压反应无显著影响。相反,α1-肾上腺素能受体拮抗剂(哌唑嗪)可抑制hrIL-1β诱导的血压升高,而心动过速不受影响。最后,用环氧化酶抑制剂(吲哚美辛)预处理可完全消除对hrIL-1β的心血管反应。这些结果表明,hrIL-1β诱导的升压反应和相关心动过速需要前列腺素的合成,涉及交感神经系统激活,但不依赖肾素-血管紧张素系统。

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