Cecanho Rodrigo, De Luca Laurival Antonio, Ranali José
Dentistry School São Leopoldo Mandic, Campinas, Brazil.
Anesth Prog. 2006 Winter;53(4):119-25. doi: 10.2344/0003-3006(2006)53[119:CEOF]2.0.CO;2.
Cardiovascular effects of felypressin (FEL) were studied in Wistar rats. Heart rate and mean arterial pressure measurements were taken in awake rats treated with vasopressin (AVP), FEL, or epinephrine (EPI). Each group received either an intravenous (IV) or an intracerebroventricular V1 receptor antagonist, saline, area postrema removal, or sham surgery. Analysis of variance and Student-Newman-Keuls (P < .05) were applied. Felypressin and AVP induced a pressor effect, and bradycardia was inhibited by IV V1 antagonist. Intracerebroventricular V1 antagonist and area postrema removal enhanced their pressor effects. Epinephrine induced a higher pressor effect and a similar bradycardia that was not affected by the treatments. It was concluded that FEL depends on V1 receptors to induce pressor and bradycardic effects, and that it produces a high relationship between bradycardia and mean arterial pressure variation depending on area postrema and central V1 receptors. These effects are potentially less harmful to the cardiovascular system than the effects of EPI.
在Wistar大鼠中研究了去甲金霉素(FEL)的心血管效应。对用血管加压素(AVP)、去甲金霉素或肾上腺素(EPI)治疗的清醒大鼠进行心率和平均动脉压测量。每组接受静脉内(IV)或脑室内V1受体拮抗剂、生理盐水、最后区切除或假手术。应用方差分析和Student-Newman-Keuls检验(P <.05)。去甲金霉素和AVP诱导升压效应,静脉内V1拮抗剂可抑制心动过缓。脑室内V1拮抗剂和最后区切除增强了它们的升压效应。肾上腺素诱导更高的升压效应和类似的心动过缓,且不受这些治疗的影响。得出的结论是,去甲金霉素依赖V1受体诱导升压和心动过缓效应,并且它在心动过缓和平均动脉压变化之间产生高度相关性,这取决于最后区和中枢V1受体。这些效应可能比EPI对心血管系统的危害小。