Akademik Veri Yönetim Sistemi
Turk Anesteziyoloji ve Reanimasyon, cilt.29, sa.6, ss.245-250, 2001 (Scopus)
This study was aimed to compare the effects of sevoflurane propofol and isoflurane on RAAS. Fifteen New Zealand male rabbits were randomly allocated into three groups to receive either propofol (n=5) or isoflurane (n=5) or sevoflurane (n=5). After venous cannulation of the ear, 0.9 % NaCl was infused at a rate of 2 mL/kg/h. Heart rate and invazive arterial blood pressure were also monitored. Spontaneous breathing was maintained during the whole anaesthesia period, which lasted 45 mn in each group. Monitoring was terminated at 60 mn. Mean arterial blood pressure (MAP) and heart rate (HR) were recorded at 0, 15, 30, 45 and 60 mn. Arterial blood samples were obtained for Na+, Htc, arterial blood gas and pH measurements at times 0 and 60 mn. Blood samples were obtained for plasma renin (PR) and plasma aldosterone (PAL) level measurements at 0, 30 and 60 mn. MAP decrease at 15 mn showed a statistically significant difference between the propofol group and other two groups. Mean PaO2 values differed significantly between the groups, only minor change were observed in HR, Hct, Na+, PaCO2. Thus aldosterone and renin levels. This increase in PAL and PR levels tended to increase. According to these findings we concluded that RAAS is activated to control the hypotension caused by propofol and sevoflurane like halothane, enflurane and isoflurane and this activation is parallel to the degree of hypotension.