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本工作观察麻醉兔用氟哌啶醇阻断肾多巴胺受体对血量扩张（ＶＥ）和脑室高张盐溶液注射（ＩＣＨＮａ）引起促钠排泄反应的影响。在ＶＥ实验中。对照组与氟哌啶醇组排销量增加峰值分别为６５．６±１５．０与１９．０±５．５μｍｏｌ／ｍｉｎ（Ｐ＜０．０２）；在ＩＣＨＮａ实验中，对照组与氟哌啶醇组排钠量增加峰值分别为２８．９±４．６与２９．０±５．８μｍｏｌ／ｍｉｎ（Ｐ＞０．０５），在肾多巴胺受体完好兔实验中，ＶＥ＋ＩＣＨＮａｇ；起的促钠排泄大于ＶＥ（Ｐ＜０．０１）或ＩＣＨＮａ（Ｐ＜０．０１）引起的反应。肾多巴胺受体阻断也可显著减弱ＶＥ＋ＩＣＨＮａ引起促钠排泄反应。结果表明：肾多巴胺受体阻断显著减弱ＶＥ以及ＶＥ＋ＩＣＨＮａ引起促钠排泄，对ＩＣＨＮａ的反应无效；在正常兔ＶＥ＋ＩＣＨＮａ引起促钠排泄显著大于各单一刺激的反应。
This study was designed to observe the effect of haloperidol on anesthetized rabbits in blocking renal sodium dopamine receptor-induced vasodilatation induced by sodium dilation (VE) and intraventricular hypertensive saline injection (ICHNa). In VE experiments. In the control group and the haloperidol group, the peak increase of the sales volume was 65.6 ± 15.0 and 19.0 ± 5.5 μmol / min, respectively (P <0.02); in the ICHNa test, In alcohol group, the peak value of sodium excretion was 28.9 ± 4.6 and 29.0 ± 5.8μmol / min, respectively (P> 0.05). In the experiment of renal dopamine receptor intact rabbit, VE + ICHNag Excretion was greater than that of VE (P <0.01) or ICHNa (P <0.01). Blockade of renal dopamine receptors also significantly attenuated the sodium-promoting urinary excretion response of VE + ICHNa. The results showed that renal dopamine receptor blockade significantly attenuated the pro-sodium excretion induced by VE and VE + ICHNa, but failed to respond to ICHNa. Sodium-induced excretion of VE + ICHNa in normal rabbits was significantly greater than that of single stimulation.