2015Zhonghua mazuixue zazhiRequires access

Effect of sevoflurane on brain injury in pigs with hemorrhagic shock

Xi Liu, Bin Zou, Yingjie Sun, Tiezheng Zhang

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Abstract

Objective To evaluate the effect of sevoflurane on brain injury in pigs with hemorrhagic shock (HS). Methods Twenty-four adult male Bama miniature pigs, aged 6 months, weighing 22–25 kg, were equally and randomly divided into 3 groups using a random number table: sham operation group (group Sham), group HS, and sevoflurane group (S group). In group Sham, the bilateral femoral arteries and internal jugular vein were only punctured. The animals were anesthetized with iv propofol 3.0 mg/kg, tracheostomized and mechanically ventilated. The right femoral artery was cannulated for blood-letting.HS was induced by blood-letting (40% blood volume within 15 min), and it was then maintained for 1 h after the end of blood-letting to induce brain injury. In group S, 2% sevoflurane was inhaled for 30 min after successful establishment of the model. Immediately before establishment of the model (T0), and at 30, 60, 90, 120, 180 and 240 min after HS (T1-6), blood samples were collected from the internal jugular vein for determination of interleukin-1beta (IL-1β) and tumor necrosis factor-alpha (TNF-α) concentrations in serum (by enzyme-linked immunosorbent assay), and neuron-specific enolase (NSE) and S-100β protein concentrations in serum (using double antibody sandwich method). Results Compared with group Sham, the serum IL-1β, TNF-α, NSE and S-100β protein concentrations were significantly increased at T2-6 in HS and S groups (P<0.05). Compared with group HS, the serum IL-1β, TNF-α, NSE and S-100β protein concentrations were significantly decreased at T3-6 in group S (P<0.05). Conclusion Sevoflurane can mitigate brain injury in pigs with HS, and the mechanism is associated with inhibition of inflammatory responses. Key words: Anesthetics, inhalation; Shock, hemorrhagic; Brain injuries

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Objective To evaluate the effect of sevoflurane on brain injury in pigs with hemorrhagic shock (HS). Methods Twenty-four adult male Bama miniature pigs, aged 6 months, weighing 22–25 kg, were equally and randomly divided into 3 groups using a random number table: sham operation group (group Sham), group HS, and sevoflurane group (S group). In group Sham, the bilateral femoral arteries and internal jugular vein were only punctured. The animals were anesthetized with iv propofol 3.0 mg/kg, tracheostomized and mechanically ventilated. The right femoral artery was cannulated for blood-letting.HS was induced by blood-letting (40% blood volume within 15 min), and it was then maintained for 1 h after the end of blood-letting to induce brain injury. In group S, 2% sevoflurane was inhaled for 30 min after successful establishment of the model. Immediately before establishment of the model (T0), and at 30, 60, 90, 120, 180 and 240 min after HS (T1-6), blood samples were collected from the internal jugular vein for determination of interleukin-1beta (IL-1β) and tumor necrosis factor-alpha (TNF-α) concentrations in serum (by enzyme-linked immunosorbent assay), and neuron-specific enolase (NSE) and S-100β protein concentrations in serum (using double antibody sandwich method). Results Compared with group Sham, the serum IL-1β, TNF-α, NSE and S-100β protein concentrations were significantly increased at T2-6 in HS and S groups (P<0.05). Compared with group HS, the serum IL-1β, TNF-α, NSE and S-100β protein concentrations were significantly decreased at T3-6 in group S (P<0.05). Conclusion Sevoflurane can mitigate brain injury in pigs with HS, and the mechanism is associated with inhibition of inflammatory responses. Key words: Anesthetics, inhalation; Shock, hemorrhagic; Brain injuries

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Available abstract

Objective To evaluate the effect of sevoflurane on brain injury in pigs with hemorrhagic shock (HS). Methods Twenty-four adult male Bama miniature pigs, aged 6 months, weighing 22–25 kg, were equally and randomly divided into 3 groups using a random number table: sham operation group (group Sham), group HS, and sevoflurane group (S group). In group Sham, the bilateral femoral arteries and internal jugular vein were only punctured. The animals were anesthetized with iv propofol 3.0 mg/kg, tracheostomized and mechanically ventilated. The right femoral artery was cannulated for blood-letting.HS was induced by blood-letting (40% blood volume within 15 min), and it was then maintained for 1 h after the end of blood-letting to induce brain injury. In group S, 2% sevoflurane was inhaled for 30 min after successful establishment of the model. Immediately before establishment of the model (T0), and at 30, 60, 90, 120, 180 and 240 min after HS (T1-6), blood samples were collected from the internal jugular vein for determination of interleukin-1beta (IL-1β) and tumor necrosis factor-alpha (TNF-α) concentrations in serum (by enzyme-linked immunosorbent assay), and neuron-specific enolase (NSE) and S-100β protein concentrations in serum (using double antibody sandwich method). Results Compared with group Sham, the serum IL-1β, TNF-α, NSE and S-100β protein concentrations were significantly increased at T2-6 in HS and S groups (P<0.05). Compared with group HS, the serum IL-1β, TNF-α, NSE and S-100β protein concentrations were significantly decreased at T3-6 in group S (P<0.05). Conclusion Sevoflurane can mitigate brain injury in pigs with HS, and the mechanism is associated with inhibition of inflammatory responses. Key words: Anesthetics, inhalation; Shock, hemorrhagic; Brain injuries

Key concepts: Sevoflurane, Enolase, Anesthesia, Jugular vein, Medicine, Femoral vein, Femoral artery, Propofol

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