Hemodynamic responses to leukotriene receptor stimulation in conscious rats.
Hemodynamic responses to leukotriene receptor stimulation in conscious rats.
复制标题
清醒大鼠对白三烯受体刺激的血流动力学反应。
DOI：
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发表时间：
1990
影响因子：
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通讯作者：
M. Gellai
中科院分区：
文献类型：
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作者：
D. Allen;M. Gellai
我们评估了白三烯（LTs） C4和D4对清醒大鼠全身和肾脏血流动力学的影响。静脉注射LTC4或LTD4（0.5-10微克/千克）引起心输出量（CO）、肾血流量（RBF）和心率（HR）的剂量依赖性降低。血流改变伴随着全身和肾血管阻力（SVR和RVR）和平均动脉血压（MAP）的增加。未观察到继发性降压作用。HR反应是双相的，心动过速取代最初短暂的心动过缓。RBF和CO的变化并非同时发生；当CO浓度仅下降9.1 +/- 3.6% （P < 0.05）且RBF在3-4 min内完全恢复时，RBF下降幅度最大（47.6 +/- 9.5%,P < 0.05），而CO浓度仍下降26.3 +/- 3.5% （P < 0.001）。注射5和10微克/千克剂量的LTC4或LTD4后，红细胞压积（HCT）增加，恢复到基础水平的时间过程（30-60分钟）与CO相似。持续静脉注射选择性LT受体拮抗剂SK&F 104353，剂量依赖性地抑制LTD4注射后的即时血流动力学变化。SK&F 104353还能减弱血管通透性的增加和CO的持续下降，表明LTs的心脏和血管作用是通过刺激LTs受体介导的。
We evaluated the effects of leukotrienes (LTs) C4 and D4 on systemic and renal hemodynamics in conscious rats. Intravenous injections of LTC4 or LTD4 (0.5-10 micrograms/kg) caused dose-dependent decreases in cardiac output (CO), renal blood flow (RBF), and heart rate (HR). Flow alterations were accompanied by increased systemic and renal vascular resistances (SVR and RVR) and mean arterial blood pressure (MAP). No secondary hypotensive effect was observed. The HR response was biphasic, with tachycardia replacing the initial brief bradycardia. The changes in RBF and CO were not concurrent; the maximum RBF decrease (47.6 +/- 9.5%, P less than 0.05) occurred when CO was down only by 9.1 +/- 3.6% (P less than 0.05) and RBF had fully recovered in 3-4 min, while CO was still down by 26.3 +/- 3.5% (P less than 0.001). Hematocrit (HCT) increased after the injection of 5 and 10 micrograms/kg doses of LTC4 or LTD4, and its time course of recovery to basal level (30-60 min) paralleled that of CO. Sustained intravenous infusion of the selective LT receptor antagonist, SK&F 104353, dose-dependently inhibited the immediate hemodynamic changes after LTD4 injections. SK&F 104353 also attenuated the increase in vascular permeability and the prolonged decrease in CO, suggesting that the observed cardiac and vascular effects of LTs were mediated by stimulation of LT receptors.