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ABSTRACT: Background: Foreign body aspiration is a common life-threatening event in young children. Tracheobronchial foreign body removal is usually performed by rigid tracheobronchoscopy under general anesthesia. Anesthetic and ventilation techniques vary greatly among anesthesiologists and institutions. In the present retrospective study, we report our anesthetic experience over 5 years. We describe complications and outcomes and analyze the clinical characteristics of anesthesia and ventilation. Methods: We retrospectively reviewed relevant clinical findings of 586 pediatric patients treated with rigid tracheobronchoscopy under general anesthesia. All procedures were performed under inhaled sevoflurane anesthesia combined with remifentanil infusion, with spontaneous respiration assisted by high-frequency jet ventilation (HFJV) and topical airway anesthesia. Results: Among 586 patients, the foreign body was successfully removed by rigid tracheobronchoscopy in 558 patients, and no foreign body was found in 28 patients. Laryngospasm was observed during the procedure in five patients. Hypoxemia was observed in 15 patients (2.6%). No severe complications or deaths occurred. The mean operation time was 22 min and the average hospital stay was 2 days. Conclusion: Inhaled sevoflurane anesthesia combined with remifentanil infusion, with spontaneous respiration assisted by HFJV and topical airway anesthesia, is safe and effective for tracheobronchial foreign body removal.
Pediatric Anesthesia 05/2012; · 2.10 Impact Factor
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ABSTRACT: It has been reported that sevoflurane preconditioning can induce neuroprotection, the mechanisms of which, however, are poorly elucidated. We designed the present study to examine the hypothesis that sevoflurane preconditioning could reduce cerebral ischemia- reperfusion injury through up-regulating antioxidant enzyme activities before ischemic injury by generating reactive oxygen species (ROS).
In preconditioning groups, adult male Sprague-Dawley rats were pretreated with 1 hour sevoflurane exposure at a dose of 1%, 2%, or 4% for 5 consecutive days. At 24 hours after the last exposure, all rats were subjected to focal brain ischemia induced by middle cerebral artery occlusion for 120 minutes followed by 72-hour reperfusion. The role of ROS in ischemic tolerance was assessed by administration of the free radical scavenger dimethylthiourea and antioxidant N-acetylcysteine before each preconditioning. Brain ischemic injury was evaluated by neurologic behavior scores and brain infarct volume calculation. Antioxidant enzyme activities (superoxide dismutase, catalase, and glutathione peroxidase [GSH-px]) of brain tissue and blood serum were tested at 24 hours after the last sevoflurane preconditioning.
Sevoflurane preconditioning reduced infarct size and improved neurobehavioral outcome in a dose-dependent manner. The neuroprotective effects of sevoflurane preconditioning were abolished by dimethylthiourea and N-acetylcysteine. The activities of catalase and glutathione peroxidase (GSH-px) in the brain tissue were elevated by sevoflurane preconditioning before ischemic injury. The up-regulated activity of GSH-px in serum negatively correlated with brain infarct volume percentage.
Sevoflurane preconditioning induces cerebral ischemic tolerance in a dose- response manner through ROS release and consequent up-regulation of antioxidant enzyme activity before ischemic injury in rats. Serum GSH-px activity could be developed as a marker to assess the effectiveness of sevoflurane preconditioning before ischemia.
Anesthesia and analgesia 03/2011; 112(4):931-7. · 3.08 Impact Factor
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ABSTRACT: Remote ischemic preconditioning (RIPC) may protect the spinal cord from ischemic injury. This randomized clinical trial was designed to assess whether a large clinical trial testing the effect of RIPC on neurologic outcome in patients undergoing spine surgery is warranted. This trial was registered with ClinicalTrials.gov, number NCT00778323.
Forty adult cervical spondylotic myelopathy patients undergoing elective decompression surgery were randomly assigned to either the RIPC group (n=20) or the control group (n=20). Limb RIPC consisted of three 5-minutes cycles of upper right limb ischemia with intervening 5-minute periods of reperfusion. Neuron-specific enolase and S-100B levels were measured in serum at set time points. Median nerve somatosensory-evoked potentials (SEPs) were also recorded. Neurologic recovery rate was evaluated using a Japanese Orthopaedic Association scale.
RIPC significantly reduced serum S-100B release at 6 hours and 1 day after surgery, and reduced neuron-specific enolase release at 6 hours, and then at 1, 3, and 5 days after surgery. No differences were observed in SEP measurements or the incidence of SEP changes during surgery between the control and RIPC groups. Recovery rate at 7 days, and at 1 and 3 months after surgery was higher in the RIPC group than in the control group (P<0.05).
Our results for markers of neuronal ischemic injury and rate of recovery suggest that a clinical trial with sufficient statistical power to detect an effect of RIPC on the incidence of neurologic complications (paresis, palsy, etc) due to spinal cord ischemia-reperfusion injury after spine surgery is warranted [corrected].
Journal of neurosurgical anesthesiology 12/2009; 22(1):46-52. · 2.41 Impact Factor
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ABSTRACT: The protective effect of sevoflurane preconditioning against spinal cord ischemia/reperfusion (I/R) is unclear. We designed this study to investigate whether sevoflurane preconditioning could induce rapid ischemic tolerance to the spinal cord in a rabbit model of transient spinal cord ischemia and how the role of extracellular signal-regulated kinase (ERK) is involved.
To test whether preconditioning with sevoflurane induces rapid ischemic tolerance, New Zealand White male rabbits were randomly assigned to three groups. Animals in the Sev group received preconditioning with 3.7% sevoflurane (1.0 minimum alveolar anesthetic concentration) in 96% oxygen for 30 min, whereas animals in the O(2) group serving as controls inhaled only 96% oxygen for 30 min. The Sham group received the same anesthesia and surgical preparation but no preconditioning or spinal cord I/R. To evaluate the role of ERK activation in sevoflurane preconditioning, rabbits were randomly assigned to four groups. U0126, an ERK inhibitor, was administered IV 20 min before the beginning of preconditioning in the U0126 + O(2) and U0126 + Sev groups. Dimethylsulfoxide was administered IV at the same time in the vehicle + O(2) and vehicle + Sev groups. At 1 h after preconditioning, the animals were subjected to spinal cord I/R induced by infrarenal aorta occlusion. All animals were assessed at 48 h after reperfusion with modified Tarlov criteria, and the spinal cord segments (L5) were harvested for histopathological examination, TUNEL staining, and Western blot of phosphor-ERK1/2.
The animals in the Sev group had higher neurological scores and more normal motor neurons than those in the O(2) group (P < 0.01 for each comparison). Compared with vehicle + Sev group, the U0126 + Sev group had worse neurological outcomes, fewer viable neurons, more apoptotic neurons, and significantly decreased ERK1/2 phosphorylation (P <or= 0.01 for each comparison). There were no significant differences in the outcomes among vehicle + O(2), U0126 + O(2), and U0126 + Sev groups.
This study demonstrates that sevoflurane preconditioning induces rapid tolerance to spinal cord I/R in rabbits, and the tolerance is possibly mediated through the activation of ERK. These data suggest that sevoflurane preconditioning might provide a new practical method for protecting perioperative spinal cord I/R.
Anesthesia and analgesia 10/2009; 109(4):1263-72. · 3.08 Impact Factor
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ABSTRACT: The purpose of this study was to explore the therapeutic time window and mechanism of tetramethylpyrazine on transient focal cerebral ischemia/reperfusion injury. Middle cerebral artery occlusion was conducted in male Sprague-Dawley rats and 20mg/kg tetramethylpyrazine was injected intraperitoneally at different time points. Neurological deficit scores and brain infarction volumes were measured 72 h after reperfusion started. The expression of thioredoxin and thioredoxin reductase were examined at 6h and at 24h after reperfusion. Our results included the findings of a significant reduction in neurological deficit scores and infarction volume in the treatment group as compared to the control group. Ischemia/reperfusion injury resulted in a decrease in the expression of thioredoxin, while tetramethylpyrazine administration greatly elevated the expression of thioredoxin-1/thioredoxin-2 mRNA and thioredoxin reductase-1/thioredoxin reductase-2 mRNA. These findings suggest that administration of tetramethylpyrazine, within a 4h time period post-transient focal stroke, may reduce cerebral ischemic reperfusion damage. Moreover, the neuroprotective effect of tetramethylpyrazine may be mediated, in part, by an increase in genetic transcription of thioredoxin.
Neuroscience Letters 10/2008; 449(1):24-7. · 2.11 Impact Factor
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ABSTRACT: To evaluate the neuroprotective effect of tetramethylpyrazine (TMP) against focal cerebral ischemic injury in rats with diffusion-weighted magnetic resonance imaging (DWMRI).
Rat models of focal cerebral ischemic injury were established in 16 male SD rats. They were randomly divided into the TMP group and the control group, eight in each group, and pretreated with TMP and normal saline respectively before modeling. Change of infarcted cerebral focus was observed with DWMRI at 1, 2, 6, 12 and 24 hrs after infarction, and the infarction volume (IV) at 24 hrs after modeling was estimated by triphenyltetrazolium chloride (TTC) stain.
The IV in all time points observed in the TMP group with DWMRI was significantly smaller than that in the control group (P<0.01). Compared with that at 1 hr after infarction, in the control group at 2, 6, 12 and 24 hrs after modeling, the IV enlarged by 13.3%, 29.7%, 50.3% and 57.3% respectively, while that in the TMP group 9.9%, 21.3%, 37.1% and 40.5% respectively. The cerebral IV estimated by TTC stain 24 hrs after modeling was larger than that estimated by DWMRI.
TMP pretreatment before modeling was effective in protecting brain against cerebral ischemic damage in rats. DWMRI dynamic scanning observation has important significance in observing the cerebral ischemic developing process and evaluating the effectiveness of brain protective measures.
Zhongguo Zhong xi yi jie he za zhi Zhongguo Zhongxiyi jiehe zazhi = Chinese journal of integrated traditional and Western medicine / Zhongguo Zhong xi yi jie he xue hui, Zhongguo Zhong yi yan jiu yuan zhu ban 03/2005; 25(2):134-7.
