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外源性前列环素不会使动脉压力感受器敏感化。

Exogenous prostacyclin does not sensitize arterial baroreceptors.

作者信息

Hirooka Y, Ando S, Imaizumi T, Suzuki S, Takeshita A

机构信息

Research Institute of Angiocardiology, Faculty of Medicine, Kyushu University, Fukuoka, Japan.

出版信息

Am J Physiol. 1991 Jun;260(6 Pt 2):H1760-6. doi: 10.1152/ajpheart.1991.260.6.H1760.

Abstract

It has been shown that prostacyclin (PGI2) sensitizes cardiac receptors. However, the effects of PGI2 on arterial baroreceptors are not well understood. In rabbits anesthetized with alpha-chloralose (n = 12), we examined reflex changes in multiunit efferent renal sympathetic nerve activity (RSNA) during hypotension caused by intravenous PGI2 (0.1, 0.2, 0.5, 1.0, 2.0 micrograms/kg), nitroglycerin (NG; 5, 10, 20, 50, 100 micrograms/kg), and sodium nitroprusside (SNP; 5, 10, 20, 50, 100 micrograms/kg) before and after bilateral vagotomy. Before vagotomy, RSNA increased during hypotension caused by NG or SNP (P less than 0.01) but did not significantly change during comparable hypotension caused by PGI2. After vagotomy, PGI2 increased RSNA as much as NG or SNP. In another group (n = 6), we examined the changes in aortic pressure (AoP), multiunit afferent aortic nerve activity (ANA), and the aortic diameter (AoD) during hypotension caused by intravenous PGI2, NG, and SNP. The relationship between changes in AoP and those in ANA did not differ during hypotension caused by the three drugs. The relationship between changes in AoP and those in AoD and that between changes in AoD and those in ANA also did not differ. Finally, we examined changes in AoP, ANA, and AoD during ramp increases or decreases of AoP caused by intravenous angiotensin II or NG under background infusion of saline, PGI2, or SNP (n = 6). The relationship among these variables did not differ during infusion of PGI2 and SNP. These results suggest that PGI2 stimulates cardiac receptors with vagal afferents but does not sensitize arterial baroreceptors.

摘要

已表明前列环素(PGI2)可使心脏受体敏感化。然而,PGI2对动脉压力感受器的作用尚未完全了解。在使用α-氯醛糖麻醉的兔子(n = 12)中,我们检查了静脉注射PGI2(0.1、0.2、0.5、1.0、2.0微克/千克)、硝酸甘油(NG;5、10、20、50、100微克/千克)和硝普钠(SNP;5、10、20、50、100微克/千克)引起低血压期间多单位传出肾交感神经活动(RSNA)的反射变化,实验在双侧迷走神经切断术前和术后进行。在迷走神经切断术前,NG或SNP引起低血压时RSNA增加(P < 0.01),但PGI2引起的类似低血压期间RSNA无显著变化。迷走神经切断术后,PGI2使RSNA增加的程度与NG或SNP相同。在另一组(n = 6)中,我们检查了静脉注射PGI2、NG和SNP引起低血压期间主动脉压力(AoP)、多单位传入主动脉神经活动(ANA)和主动脉直径(AoD)的变化。三种药物引起低血压期间,AoP变化与ANA变化之间的关系无差异。AoP变化与AoD变化之间的关系以及AoD变化与ANA变化之间的关系也无差异。最后,我们在生理盐水、PGI2或SNP背景输注下,检查了静脉注射血管紧张素II或NG引起AoP斜坡上升或下降期间AoP、ANA和AoD的变化(n = 6)。在PGI2和SNP输注期间,这些变量之间的关系无差异。这些结果表明,PGI2通过迷走传入神经刺激心脏受体,但不使动脉压力感受器敏感化。

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