Sevoflurane Pretreatment Research Articles

Protective effects of sevoflurane preconditioning on cerebral ischemia-reperfusion injury in rats

To investigate if sevoflurane preconditioning attenuate neuronal apoptosis induced by ischemia-reperfusion. Thirty-six male SD rats weighing 250 - 300 g were randomly divided into three groups (n = 12 each): control group (group C), ischemia-reperfusion group (group IR) (rats were established cerebral artery clamped and reperfusion model), sevoflurane preconditioning group (group S) (rats were established cerebral artery clamped and reperfusion model after 1 h 2.4% sevoflurane preconditioning). Apoptosis neurons were observed by Hematoxylin and Eosin (HE) staining and transmission electron microscope, TdT mediated Dutp nick end labeling (TUNEL) method was used to count apoptosis neurons density, fresh ischemic brain tissue was taken out, while Caspase-3 zymogen and 20 000 segment were checked by Western blot. apoptosis neurons in group IR were more than ones in group S under HE staining and light microscope and transmission electron microscope, and apoptosis neurons density (cell number/0.1 mm(2)) by TUNEL staining: group C, 13.0 +/- 1.4; group IR, 189.8 +/- 6.8; group S, 110.5 +/- 4.3, the relative gray values of the contents of procaspase-3 and its 20 000 cleavage fragment were 16.72 +/- 3.0, 76.1 +/- 3.4, 51.2 +/- 3.1 and 8.2 +/- 2.3, 59.0 +/- 6.3, 31.2 +/- 5.4 respectively. Sevoflurane pretreatment can protect neuron on ischemia-reperfusion injury by attenuating neuronal apoptosis in rats.

Sevoflurane preconditioning reverses impairment of hippocampal long-term potentiation induced by myocardial ischaemia–reperfusion injury

We sought to test whether a transient myocardial ischaemia can induce impairment of hippocampal long-term potentiation (LTP) and whether sevoflurane preconditioning can provide robust protective effects on this neurological impairment. Wistar rats were subjected to a transient coronary artery occlusion for 30 min. Sevoflurane preconditioning was performed by exposure to 1.0 minimum alveolar concentration of sevoflurane for 1 h and washout for 30 min before myocardial ischaemia. Hippocampal LTP was evaluated during a 7-day observation period. The expressions of haem oxygenase-1 mRNA, tumour necrosis factor-alpha mRNA and interleukin-1beta mRNA in the hippocampus were analysed by quantitative reverse transcription-PCR. LTP was significantly inhibited 1 and 3 days after the transient myocardial ischaemia in the control group when compared with the animals subjected to a sham operation without coronary occlusion, and the LTP recovered to a normal magnitude 7 days later. Sevoflurane preconditioning remarkably reversed the transient inhibition of LTP observed at 1 and 3 days after myocardial ischaemia. Compared with the sham animals, the expressions of haem oxygenase-1 mRNA, tumour necrosis factor-alpha mRNA and interleukin-1beta mRNA in the hippocampus of the control rats were significantly increased during the early stage after myocardial ischaemia (1-3 days), and the increases of these cytokines were attenuated by sevoflurane pretreatment. Sevoflurane preconditioning induced neuroprotection against impairment of hippocampal LTP resulting from myocardial ischaemia and reperfusion.

Anti-inflammatory and antinecrotic effects of the volatile anesthetic sevoflurane in kidney proximal tubule cells

Renal ischemia-reperfusion (IR) injury is a major clinical problem without effective therapy. We recently reported that volatile anesthetics protect against renal IR injury, in part, via their anti-inflammatory properties. In this study, we demonstrate the anti-inflammatory and antinecrotic effects of sevoflurane in cultured kidney proximal tubule cells and probed the mechanisms of sevoflurane-induced renal cellular protection. To mimic inflammation, human kidney proximal tubule (HK-2) cells were treated with tumor necrosis factor-alpha (TNF-alpha; 25 ng/ml) in the presence or absence of sevoflurane. In addition, we studied the effects of sevoflurane pretreatment on hydrogen peroxide (H2O2)-induced necrotic cell death in HK-2 or porcine proximal tubule (LLC-PK1) cells. We demonstrate that sevoflurane suppressed proinflammatory effects of TNF-alpha evidenced by attenuated upregulation of proinflammatory cytokine mRNA (TNF-alpha, MCP-1) and ICAM-1 protein and reduced nuclear translocation of the proinflammatory transcription factors NF-kappaB and AP-1. Sevoflurane reduced necrotic cell death induced with H2O2 in HK-2 cells as well as in LLC-PK1 cells. Sevoflurane treatment resulted in phosphorylation of prosurvival kinases, ERK and Akt, and increased de novo HSP-70 protein synthesis without affecting the synthesis of HSP-27 or HSP-32. We conclude that sevoflurane has direct anti-inflammatory and antinecrotic effects in vitro in a renal cell type particularly sensitive to injury following IR injury. These mechanisms may, in part, account for volatile anesthetics' protective effects against renal IR injury.

Sevoflurane Pretreatment Inhibits Endotoxin-Induced Shock in Rats

We examined the effects of sevoflurane pretreatment on mortality and inflammatory responses during endotoxin-induced shock. Rats were allocated randomly to 1 of 4 groups (n = 12 per group): an endotoxemia group, receiving IV Escherichia coli endotoxin (15 mg/kg over 2 min); a saline control group, receiving 0.9% saline (1.0 mL/kg); a sevoflurane-only group, receiving 2.4% sevoflurane for 30 min immediately before injection of 0.9% saline; and a sevoflurane pretreatment group, receiving 2.4% sevoflurane for 30 min immediately before injection of endotoxin. Hemodynamic variables, arterial blood gases, and plasma concentrations of tumor necrosis factor-alpha and interleukin-6 were measured. The 8-h mortality rate was determined. Systolic arterial blood pressure and acid-base balance improved with sevoflurane pretreatment before induction of endotoxemia. Mortality rates 8 h after endotoxin injection were 83%, 8%, 0%, and 25% for the endotoxemia, saline control, sevoflurane-only, and sevoflurane pretreatment groups, respectively. Plasma cytokine concentrations were significantly larger in the endotoxemia group than in the other groups. Sevoflurane pretreatment inhibited inflammatory responses and decreased mortality in rats exposed to endotoxin. Sevoflurane pretreatment decreased mortality rate, severity of hypotension, and acidosis, and inhibited cytokine responses in rats injected with endotoxin, suggesting that sevoflurane may be an anesthetic of choice in endotoxemic states.

Room 309, 10/18/2000 2: 00 PM - 3: 30 PM (PD) Sevoflurane Pre-treatment Improves Function and Reduces Formation of Peroxynitrite after Global Ischemia in Isolated Hearts

Room 309, 10/18/2000 2: 00 PM - 3: 30 PM (PD) Sevoflurane Pre-treatment Improves Function and Reduces Formation of Peroxynitrite after Global Ischemia in Isolated Hearts

Sevoflurane reduces myocardial infarct size and decreases the time threshold for ischemic preconditioning in dogs.

Recent evidence indicates that volatile anesthetics exert protective effects during myocardial ischemia and reperfusion. The authors tested the hypothesis that sevoflurane decreases myocardial infarct size by activating adenosine triphosphate-sensitive potassium (K(ATP)) channels and reduces the time threshold of ischemic preconditioning necessary to protect against infarction. Barbiturate-anesthetized dogs (n = 75) were instrumented for measurement of aortic and left ventricular pressures and maximum rate of increase of left ventricular pressure and were subjected to a 60-min left anterior descending (LAD) coronary artery occlusion followed by 3-h reperfusion. In four separate groups, dogs received vehicle or the K(ATP) channel antagonist glyburide (0.1 mg/kg intravenously), and 1 minimum alveolar concentration sevoflurane (administered until immediately before coronary artery occlusion) in the presence or absence of glyburide. In three additional experimental groups, sevoflurane was discontinued 30 min (memory) before the 60-min LAD occlusion or a 2-min LAD occlusion as an ischemic preconditioning stimulus was used with or without subsequent sevoflurane (with memory) pretreatment. Regional myocardial perfusion and infarct size were measured with radioactive microspheres and triphenyltetrazolium staining, respectively. Vehicle (23 +/- 1% of the area at risk; mean +/- SEM) and glyburide (23 +/- 2%) alone produced equivalent effects on myocardial infarct size. Sevoflurane significantly (P < 0.05) decreased infarct size (13 +/- 2%). This beneficial effect was abolished by glyburide (21 +/- 3%). Neither the 2-min LAD occlusion nor sevoflurane followed by 30 min of memory were protective alone, but together, sevoflurane enhanced the effects of the brief ischemic stimulus and profoundly reduced infarct size (9 +/- 2%). Sevoflurane reduces myocardial infarct size by activating K(ATP) channels and reduces the time threshold for ischemic preconditioning independent of hemodynamic effects in vivo.