Acute stress increases venomotor tone in conscious rats.
Acute stress increases venomotor tone in conscious rats.
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急性应激会增加清醒大鼠的静脉运动张力。
DOI：
10.1152/ajpheart.1996.271.4.h1375
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发表时间：
1996
期刊：
影响因子：
--
通讯作者：
Egland,MC
中科院分区：
文献类型：
--
作者：
Martin,DS;Appelt,C;Rodrigo,MC;Egland,MC
本研究验证了急性心理应激导致静脉收缩的假设。在雄性Sprague-Dawley大鼠的股动脉和静脉中植入留置导管，在右心房中植入球囊导管。监测清醒大鼠的平均动脉压（MAP）、静脉压、心率（HR）和平均循环充盈压（MCFP）。在用生理盐水、氯异松达明、酚妥拉明或哌唑嗪治疗之前和之后进行空气喷射应激。喷气应激导致MAP、HR和MCFP分别增加10 +/- 1 mmHg、31 +/- 4次/min和0.95 +/- 0.09 mmHg。无论是氯异松达明或酚妥拉明治疗是同样有效地消除压力引起的MAP，HR和MCFP的增加。哌唑嗪治疗取消了升压反应的喷气压力，但没有显着影响HR和MCFP的反应。与此相反，预处理与α 2-受体拮抗剂rauwolscine盐酸盐废除MAP和MCFP的反应，喷气应激，但不影响HR的反应。这些发现表明，静脉收缩是心血管对急性心理应激反应的重要组成部分。应激诱导的静脉收缩似乎主要通过α 2受体亚型介导。
This study tested the hypothesis that acute psychological stress causes venoconstriction. Male Sprague-Dawley rats were instrumented with indwelling catheters in a femoral artery and vein and a balloon-tipped catheter in the right atrium. Mean arterial pressure (MAP), venous pressure, heart rate (HR), and mean circulatory filling pressure (MCFP) were monitored in conscious rats. Air-jet stress was performed before and after treatment with saline, chlorisondamine, phentolamine, or prazosin. Air-jet stress caused MAP, HR, and MCFP to increase by 10 +/- 1 mmHg, 31 +/- 4 beats/min, and 0.95 +/- 0.09 mmHg, respectively. Treatment with either chlorisondamine or phentolamine was equally effective in abolishing the stress-induced increases in MAP, HR, and MCFP. Prazosin treatment abolished the pressor response to air-jet stress but did not significantly affect the HR and MCFP responses. In contrast, pretreatment with the alpha 2-receptor antagonist rauwolscine hydrochloride abolished both the MAP and MCFP responses to air-jet stress but did not affect the HR response. These findings indicate that venoconstriction is an important component of the cardiovascular response to acute psychological stress. Stress-induced venoconstriction appears to be mediated primarily via the alpha 2-receptor subtype.