EDRF released from microvascular endothelial cells dilates arterioles in vivo.
EDRF released from microvascular endothelial cells dilates arterioles in vivo.
复制标题
微血管内皮细胞释放的 EDRF 可扩张体内小动脉。
DOI：
10.1152/ajpheart.1991.261.1.h128
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发表时间：
1991
期刊：
影响因子：
--
通讯作者：
Kaley,G
中科院分区：
文献类型：
--
作者：
Koller,A;Seyedi,N;Gerritsen,ME;Kaley,G
采用Cytodex 3微载体珠粒对大鼠附睾脂肪垫的微血管内皮细胞进行体外培养。用图像剪切视频显微镜测量戊巴比妥麻醉大鼠克雷布斯弥漫肌的小动脉直径（平均对照直径20.9±0.9微米）。建立两条浸润液线（每条1.5 ml/min）；其中一种仅含有微载体珠柱（无细胞在线；NC），另一种含有1ml的微载体珠柱（通过细胞；TC）。首先用吲哚美辛（吲哚美辛，28微米）治疗肌肉制剂和mec。吲哚治疗阻断小动脉扩张至A23187（1微米）和花生四烯酸（AA； 0.25微米）给药至NC线。然而，当A23187（而不是AA）通过含有吲哚处理的微球上mes的TC线注入时，观察到微动脉直径增加4.0 +/- 0.6微米。引入ng -单甲基- l-精氨酸（L-NMMA； 200微米）可消除a23187引起的扩张。通过NC线给予肌肌阿托品（2微米），抑制了对乙酰胆碱（ACh； 2.7微米）的扩张反应。然而，将乙酰胆碱通过TC细胞系输注到阿托品处理过的肌突肌上，引起小动脉直径增加5.8 +/- 1.3微米，这一反应被先前给药的L-NMMA阻断。腺苷（0.5微米）或硝普钠（0.5微米）通过NC或TC线诱导的小动脉扩张不受L-NMMA的影响。（摘要删节250字）
Microvascular endothelial cells (MECs) from rat epididymal fat pad were isolated and cultured in vitro on Cytodex 3 microcarrier beads. In Krebs-suffused cremaster muscle of pentobarbital-anesthetized rats arteriolar diameters (mean control diam 20.9 +/- 0.9 micron) were measured using image shearing video microscopy. Two lines of suffusate (1.5 ml/min each) were established; one contained a column of microcarrier beads only (no cells in line; NC) the other contained a 1-ml column of MECs grown on beads (through cells; TC). The muscle preparation and the MECs were first treated with indomethacin (Indo; 28 microM). Indo treatment blocked arteriolar dilation to A23187 (1 microM) and arachidonic acid (AA; 0.25 microM) administered into the NC line. A 4.0 +/- 0.6 micron increase in arteriolar diameter was observed, however, when A23187 (but not AA) was infused through the TC line containing Indotreated MECs on beads. The A23187-elicited dilation was abolished by the introduction of NG-monomethyl-L-arginine (L-NMMA; 200 microM) into the TC line. Administration of atropine (2 microM) onto the cremaster muscle via the NC line inhibited the dilations in response to acetylcholine (ACh; 2.7 microM) given through the NC line. Infusion of ACh through the TC line onto the atropine-treated cremaster muscle, however, elicited a 5.8 +/- 1.3 micron increase in arteriolar diameter, a response that was blocked by prior administration of L-NMMA into the TC line. Arteriolar dilation induced by adenosine (0.5 microM) or sodium nitroprusside (0.5 microM) applied via the NC or TC line was unaffected by L-NMMA.(ABSTRACT TRUNCATED AT 250 WORDS)