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The buried waveguide optical splitter is fabricated by Tl+–Na+ ion-exchange technology on BK7 glass substrates, and the refractive index distribution in branch district is analyzed by the interference method technology. The shape of the same refractive index distribution of the six successive different points in branch district is changed little by little from a semicircle to a half ellipse gradually, and finally separates into two semicircles. We also compare the experiment data by the interference method with the mathematical solution by two-dimensional diffusion equation. And the refractive index distribution is the ‘improved’ Gauss function.

UNLABELLED To evaluate the effect of gender on the pharmacokinetics of vecuronium, we studied 30 patients (15 male and 15 female) undergoing elective plastic surgery with anticipated surgical blood loss of

To determine the differences between men and women in the dose-response curve and the time-course of effect of vecuronium, we studied 60 adult patients (30 male and 30 female), ASA I, age 18-51 yr, undergoing elective plastic surgery. Anaesthesia was maintained with nitrous oxide 60% in oxygen; thiopentone and incremental doses of fentanyl were given as required. Neuromuscular function was assessed mechanomyographically using the train-of-four (TOF) stimulation at the wrist every 12 s. The percentage depression of T1 was used as the study variable. The dose-response relationship of vecuronium was determined by a cumulative dose-response technique. The dose-response curve in men was shifted in a parallel fashion to the right, indicating a decrease in the sensitivity to vecuronium-induced neuromuscular block, compared with women. The ED50, ED90 and ED95 of vecuronium were 23.9 (4.7), 45.4 (11.2) and 55.7 (14.3) micrograms kg-1 in men and 18.4 (3.7), 33.5 (7.8) and 39.8 (9.6) micrograms kg-1 in women respectively. There were statistically significant differences in these values between the two groups (P0.01 in each instance). After a total dose of vecuronium 80 micrograms kg-1, neuromuscular block was significantly longer in women than in men. The duration of peak effect, clinical duration, and the total duration were 18.7 (7.1), 26.6 (8.8) and 50.6 (16.0) min respectively in men and 26.0 (7.2), 37.1 (11.2) and 65.9 (20.7) min in women. They differed significantly between men and women (P0.005 in each case).

We have assessed the influence of different surgical procedures on the incidence, severity and duration of early postoperative hypoxaemia in 312 healthy infants and children undergoing elective palatoplasty. Group 1 patients underwent von Langenbeck palatoplasty (n = 149), group 2 patients underwent push-back palatoplasty (n = 124) and group 3 patients underwent combined push-back palatoplasty and superior pharyngeal flap surgery (n = 39). Arterial oxygen saturation (SpO2) was recorded while patients were breathing air shortly after arrival in the recovery room (0 min), and at 5, 10, 15, 20, 30, 40, 50, 60, 120 and 180 min thereafter. Patients who underwent more complex surgical techniques for palatoplasty had lower postoperative SpO2 values, slower recovery of SpO2 and a higher incidence of hypoxaemia during the early postoperative period. There were significant differences in postoperative SpO2, values and the incidence of hypoxaemia. The incidences of hypoxaemia and severe hypoxaemia were 27% and 1%, respectively, in group 1, 37% and 12% in group 2, and 36% and 33% in group 3. Hypoxaemia occurred most commonly in the first 15 min in children after von Langenbeck palatoplasty, in the first 40 min after push-back palatoplasty and in the 120 min after combined push-back palatoplasty and superior pharyngeal flap surgery. There were significant associations between low SpO2 values, incidence of hypoxaemia on admission to the recovery room and recovery scores.

To evaluate the influence of sevoflurane on the dose-response relationship and on the time-course of the effect of rocuronium, 60 adult patients undergoing elective plastic surgery were randomly allocated to either the control or the sevoflurane group. Anaesthesia was maintained with 60% nitrous oxide in oxygen and thiopentone in the control group and with 60% nitrous oxide in oxygen and an end-tidal concentration of 1.75% sevoflurane in the sevoflurane group. Neuromuscular function was assessed mechanomyographically with train-of-four stimulation at the wrist every 12s and the percentage depression of the first twitch of the train-of-four was used as the study parameter. The dose-response relationship of rocuronium in the two groups was determined by the cumulative dose-response technique. The dose-response curve of rocuronium in the sevoflurane group was shifted to the left compared to the control group, indicating a potentiation of rocuronium-induced neuromuscular block. The effective doses of rocuronium required to produce 50%, 90% and 95% twitch depression in the sevoflurane group were decreased by 30.5%, 26.7% and 25.2%, respectively, compared to the control group. Following the administration of a total dose of rocuronium of 400 micrograms.kg-1, the duration of action of, and the recovery from, rocuronium were both significantly prolonged by sevoflurane. There were significant differences in the duration of peak effect, clinical duration, recovery index and the total duration of action between the control and the sevoflurane groups.

To evaluate the effect of acute isovolaemic haemodilution on the pharmacokinetics of vecuronium, we studied 13 patients undergoing haemodilution during surgery and 13 control patients. General anaesthesia was induced with thiopentone 4-6 mg kg-1 and fentanyl 2-4 micrograms kg-1, and maintained with enflurane and 60% nitrous oxide in oxygen. The haemodilution patients underwent major elective plastic surgery with an anticipated surgical loss of more than 600 ml. Haemodilution was achieved by drainage of venous blood and i.v. infusion of lactated Ringer's solution and 6% dextran, during which the packed cell volume and haemoglobin concentration decreased from 45% to 28.1% and from 14.7 g dl-1 to 9.1 g dl-1, respectively. After administration of a bolus of vecuronium 100 micrograms kg-1, an improved fluorimetric assay was used to measure the plasma concentrations of vecuronium for 5 h. The results showed that the disposition kinetics of vecuronium were best described mathematically by a three-compartment open model in the two groups. The mean volume of the central compartment and volume of distribution at steady state were 42.3 (SD 11.8) ml kg-1 and 168.4 (31.5) ml kg-1, respectively, in control patients, and significantly greater (55.2 (13.4) ml kg-1 and 225.9 (53.3) ml kg-1) in the haemodilution patients (P0.05). The elimination half-life was 50.3 (11.5) min in control patients and significantly greater (68.2 (15.1) min) in the haemodilution patients (P0.05). The half-lives of fast distribution and distribution, mean residual time, area under the plasma concentration curve and plasma clearance were unchanged in patients who underwent haemodilution compared with the control group.

To determine differences from dose-response and time-course of rocuronium between male and female patients, 60 adult patients (30 male and 30 female), ASA grade I, aged 17-52 yr, undergoing elective plastic surgery were studied. Anesthesia was maintained with 60% nitrous oxide in oxygen, thiopental, and incremental doses of fentanyl as required. Neuromuscular function was assessed mechanomyographically with train-of-four (TOF) stimulation at the wrist every 12 s, and the percentage depression of the T1 response was used as the study variable. The dose-response relationship of rocuronium was determined by a cumulative dose-response technique. The results showed that the dose-response curve of rocuronium in the men was shifted to the right, indicating a decrease in the sensitivity to rocuronium-induced neuromuscular block versus the women. The 50%, 90%, and 95% effective doses of rocuronium were 178.4 +/- 53.7, 358.7 +/- 101.3, and 386.2 +/- 113.4 micro g/kg, respectively, in male patients, and 128.8 +/- 42.5, 252.8 +/- 51.7, and 274.4 +/- 59.4 micro g/kg in female patients. After an intravenous administration of total dose of 400 micro g/kg rocuronium, neuromuscular block was significantly longer in the men than in the women. The duration of peak effect, clinical duration, and total duration were 6.5 +/- 3.0,12.5 +/- 4.9, and 33.6 +/- 8.7 min, respectively, in male patients, and 11.8 +/- 2.7, 18.5 +/- 5.3, and 46.8 +/- 9.6 min in female patients. We conclude that women were approximately 30% more sensitive to rocuronium compared with men. Implications: The authors found that women were 30% more sensitive to rocuronium than men. This suggests that the routine dose of rocuronium should be reduced in women compared with men. (Anesth Analg 1997;85:667-71)

Both ischemic preconditioning (IPC) and limb remote ischemic postconditioning (LRIPOC) have been shown to possess significantly different cardioprotective effects against the myocardial ischemia reperfusion injury (IRI), but no study has compared the anti-inflammatory effects of IPC and LRIPOC during myocardial IRI process. We hypothesized that IPC and LRIPOC would produce different anti-inflammatory effects in an in vivo rat model with myocardial IRI.Eighty rats were randomly allocated into four equal groups: sham group, IRI group, IPC group and LRIPOC group. In 10 rats randomly selected from each group, serum levels of TNF-α, HMGB1, ICAM1, IL-1, IL-6 and IL-10 were assessed, and infarct size was determined. In another 10 rats of each group, myocardial levels of TNF-α, HMGB1, ICAM1, IL-1, IL-6 and IL-10 in both ischemic and non-ischemic regions were measured.The infarct size was significantly lower in IPC and LRIPOC groups than in IRI group. The serum and myocardial levels of pro-inflammatory cytokines including TNF-α, HMGB1, ICAM1, IL-1 and IL-6 during reperfusion were significantly reduced in IPC and LRIPOC groups compared to IRI group. As compared to the IPC group, infarct size, serum level of TNF-α at 60 minutes of reperfusion, serum levels of HMGB1 and ICAM1 at 120 minutes of reperfusion, myocardial levels of TNF-α, ICAM1, IL-1 and IL-6 in the ischemic region, myocardial levels of ICAM1, IL-1 and IL-6 in the non-ischemic region were significantly increased in the LRIPOC group.In the rats with myocardial IRI, IPC produces more powerful inhibitory effects on local myocardial and systemic inflammatory responses than LRIPOC. This may be partly attributed to more potent cardioprotection produced by IPC.

To determine the influence of age on postoperative hypoxemia, we studied postoperative hypoxemia in 1152 patients, from infants to adults, ASA physical status I, undergoing elective plastic surgery. Subjects were divided into four groups on the basis of age: Group 1, infants aged 1 yr or less (n = 108); Group 2, children aged 1-3 yr (n = 240); Group 3, children aged 3-14 yr (n = 482); and Group 4, adults aged 14-58 yr (n = 322). Arterial oxygen saturation (Spo2) levels were recorded while patients were breathing room air in the postanesthesia recovery room shortly after arrival (0 min), and 5, 10, 15, 20, 30, 40, 50, 60, 120, and 180 min thereafter. Younger patients showed lower Spo2 levels and a higher incidence of hypoxemia during the early postoperative period. The incidences of hypoxemia (Spo2 = 86%-90%) and severe hypoxemia (Spo2 < or = 85%) in the recovery room were 30.6% and 16.7%, respectively, in Group 1, 20.0% and 10.0% in Group 2, 14.1% and 3.3% in Group 3, and 7.8% and 0.6% in Group 4. Hypoxemia occurred most commonly within 1 h after anesthesia, particularly during the first 40 min in infants and during the first 15 min in older children and adults. A significant correlation was found by linear regression analysis between low Spo2 levels on admission to the recovery room and children's age. Thereafter, Spo2 levels and the incidence of hypoxemia during the early postoperative period were related only to infants' recovery scores.

The objective of this study was to evaluate the gestational results obtained with vitrified-thawed human cleavage-stage embryo by two different thaw protocols. Embryo development was observed to cleavage-stage and embryos were cryopreserved by vitrification on day 3 after oocyte retrieval. 51 cycles were thawed using vitrification warming kit with decreasing concentrations of sucrose in 3 dilutions ( 1.0, 0.5 and 0 mol per L respectively) as group 1, 56 cycles were thawed with decreasing concentrations of sucrose in 5 dilutions ( 0.8, 0.6, 0.33, 0.2 and 0 mol per L respectively) as group 2. Embryo survival (50 percent intact blastomeres), complete embryo survival (100 percent intact blastomeres), pregnancy and implantation rates were compared, and development rates the day after thawing were also compared. Multivariate analysis showed a significant difference in embryo immediate morphological survival rate, complete survival and clinical pregnancies rate between the two groups respectively (87.0 vs. 98.6 percent, p=0.000; 71.0 vs 82.0 percent embryo subsequent development rates, mean number of transferred embryos was similar between the two groups. (61.4 vs. 61.3 percent, p=0.502; 2.2 +/ 0.5 vs. 2.4 +/- 0.6, p=0.113). In addition, no differences in implantation rate were observed between two groups (17.7 vs. 25.6 percent, P=0.138). No difference in the multiple pregnancy rates was found among the two groups also.

Inflammation is one of important mechanisms for myocardial ischemia reperfusion injury (IRI). Ischemia postconditioning (IPOC) can protect the heart against IRI by inhibiting inflammation, but its cardioprotection is weaker than that of ischemia preconditioning. Recently, the α7 subunit-containing nicotinic acetylcholine receptor (α7nAChR) agonist has shown anti-inflammatory effects in many diseases related to inflammation. This randomized controlled experiment was designed to evaluate whether combined postconditioning with IPOC and the α7nAChR agonist could produce an enhanced cardioprotection in a rat in vivo model of acute myocardial IRI.Fifty Sprague-Dawley rats were randomly divided into five equal groups: sham group, control group, IPOC group, α7nAChR agonist postconditioning group (APOC group) and combined postconditioning with IPOC and α7nAChR agonist group (combined group). Hemodynamic parameters were recorded during the periods of ischemia and reperfusion. Serum concentrations of troponin I (TnI), tumor necrosis factor α (TNF-α) and high-mobility group box 1 (HMGB-1) at 180 minutes after reperfusion were assayed in all groups. At the end of the experiment, the infarct size was assessed from excised hearts by Evans blue and triphenyl tetrazolium chloride staining.As compared to the sham group, the infarct size in the other four groups was significantly increased, serum levels of TnI, TNF-α and HMGB1 in the control group and TNF-α, HMGB1 in the IPOC group were significantly increased. The infarct size and serum concentrations of TNF-α, HMGB1 and TnI in the IPOC, APOC and combined groups were significantly lower than those in the control group. As compared to the IPOC group, the infarct size in the combined group was significantly decreased, serum concentrations of TnI, TNF-α and HMGB1 in the APOC and combined groups were significantly reduced. Although the infarct size was significantly smaller in the combined group than in the APOC group, serum levels of TNF-α and HMGB1 were significantly higher in the combined group than in the APOC group.In a rat in vivo model of acute myocardial IRI, combined postconditioning with IPOC and the α7nAChR agonist can produce enhanced protection against myocardial IRI by increasing the anti-inflammatory effect.

A general review was made of studies involving: (1) The experimental evidence of remote ischemic preconditioning (RIPC) and relative clinical studies, (2) The experimental and clinical evidences of remote ischemic postconditioning (RIPOC), (3) The potential mechanistic pathways underlying their protective effects.The data used in this review were mainly from manuscripts listed in PubMed that were published in English from 1986 to 2010. The search terms were "myocardial ischemia reperfusion injury", "ischemia preconditioning", "ischemia postconditioning", "remote preconditioning" and "remote postconditioning".(1) Clinical and experimental evidence that both RIPC and RIPOC produce preservation of ischemia reperfusion injury (IRI) of myocardium and other organs, (2) Studies related to the potential mechanisms, by which remote ischemic conditioning protects myocardium against IRI.Both RIPC and RIOPC have been shown to attenuate myocardial IRI in laboratory animals. Also, their cardioprotective effects have appeared in some clinical studies. Except the external, the detailed internal mechanisms of remote ischemic conditioning have been generally described. Through these descriptions better protocols can be developed to provide improved cardioprotective procedures.Remote ischemic conditioning is an endogenous cardioprotective mechanism from outside the heart that protects against myocardial IRI and represents a general form of inter-organ protection. Remote ischemic conditioning may have an immense impact on clinical practice in the near future.

To assess the effects of ischemic postconditioning, remote ischemic postconditioning and naloxone postconditioning on focal cerebral ischemia-reperfusion injury in rats.A total of 110 adult SD rats were randomly divided into 5 groups (n = 22 each). The focal cerebral ischemia-reperfusion injury was induced by a 90-minute occlusion of right middle cerebral artery (MCA) and a 24-hour reperfusion sequentially. Group 1 was of ischemia-reperfusion control; Group 2 ischemic postconditioning induced by three 30-second cycles of MCA occlusion followed by a 30-second reperfusion; Group 3 remote ischemic postconditioning performed via a transient occlusion of right femoral artery at 5 min before the initiation of reperfusion; Group 4 naloxone postconditioning with naloxone 10 mg/kg intraperitoneally injected at the initiation of reperfusion; Group 5 combined ischemic, remote ischemicnaloxone postconditioning performed simultaneously in accordance with the methods used in Groups 2, 34. The neurologic deficit scores (NDS) were obtained at 2 h24 h post-reperfusion. At 24 h post-reperfusion, the anesthetized rat was sacrificed by decapitation and the brain rapidly extracted to assess the size of cerebral infarct (n = 10), detect the cerebral expression of microtubule-associated protein-2 (MAP2) (n = 6), measure the plasma volume of cerebral tissues and quantify the diameter and segment length of cerebral microvessel (n = 6).There were no significant differences in the heart rate (HR) and mean arterial pressure (MAP) among the above five groups at all observed time points (P0.05). At 24 h post-reperfusion, the percentage of ischemic cerebral infarct size was 43% ± 6%, 31% ± 4%, 32% ± 5%, 28% ± 6%21% ± 7% in ipsilateral hemisphere area (i.e., cerebral infarct severity) in Groups 1-5 respectively. Compared with Group 1, the levels of NDS and cerebral infarct severity significantly decreased at ischemic side in Groups 2-5 (P0.05). And the cerebral expression of MAP2, plasma volume of cerebral tissues, diameter and segment length of cerebral microvessel significantly increased at the ischemic side (all P0.05). However, there were no significant differences in the above-mentioned parameters at ischemic side among Groups 2, 3 and 4 (all P0.05). The parameters of NDS, cerebral infarct severity, cerebral expression of MAP2 and plasma volume of cerebral tissues in the ischemic side significantly increased in Group 5 compared with Groups 1, 2, 3 and 4 (all P0.05). The diameter and segment length of cerebral microvessel at ischemic side were not different among Groups 2, 3, 4 and 5 (all P0.05).In focal cerebral ischemia-reperfusion rats, ischemic, remote ischemic and naloxone postconditioning may produce significant neuroprotective effects of reduced cerebral infarct severity and improved neurologic dysfunctions. A combination of three postconditioning approaches enhances the above neuroprotective effects.

To the Editor, In a randomized controlled trial in morbidly obese patients undergoing bariatric surgery, Wong et al. compared the Boussignac continuous positive airway pressure (CPAP) mask with a venturi mask and showed that the Boussignac CPAP mask can improve early postoperative oxygenation as measured by the PaO2/FIO2 ratio. These results make a valuable contribution to the treatment of postoperative respiratory insufficiency following bariatric surgery, which is a major concern for morbidly obese patients. However, in our view, there are two issues related to this study that warrant cautious interpretation of the results. First, the patient position during the early postoperative period is not clearly documented. Considering the potentially deleterious effects of supine positioning on pulmonary function in morbidly obese patients, these patients are more optimally managed in a non-supine position. During the first 48 postoperative hours after abdominal surgery, it has been shown that arterial oxygenation in morbidly obese patients is better maintained in the semi-recumbent position rather than in the supine position. Furthermore, morbidly obese patients placed in a reverse Trendelenburg position have improved pulmonary compliance and increased functional residual capacity, which improves oxygenation relative to the supine position. In our view, an important variable to consider is whether Wong et al. maintained identical positioning in all patients when evaluating the effects of the two respiratory treatments on postoperative pulmonary function. Second, although pain scores were reported to have been similar in the two groups at all time points, the article did not specify the postoperative analgesic protocol used in the two groups. This makes it difficult to assess whether all patients were ensured adequate postoperative analgesia. Following bariatric surgery, pain is recognized as being the most frequent postoperative problem, even for surgery that is performed laparoscopically. Inadequate postoperative analgesia results in splinting with rapid and shallow breathing. Furthermore, in morbidly obese patients, intensity of postoperative pain influences the extent of postoperative atelectasis 24 hr after tracheal extubation. Thus, ensuring optimal analgesia for morbidly obese patients in the postoperative period is of great importance, not only for patient comfort but also for improvement of pulmonary function and a reduction in the risk of respiratory complications. We recognize that providing optimal postoperative pain relief for morbidly obese patients remains a major challenge for modern anesthetic practice. For example, use of opioids is often inevitable to achieve satisfactory postoperative pain control, especially when regional anesthetic techniques are either difficult or impossible for anatomical reasons. Morbidly obese patients are at a very high risk for postoperative exacerbation of respiratory depression, with further depression with the administration of opioids. For this reason, standardization of the postoperative analgesic protocol should be an important element of the study design when evaluating effects of different treatments on He Ping Liu and Fu Shan Xue contributed equally to this work.

To the Editor, In a randomized controlled clinical trial, Park et al. showed that using triamcinolone acetonide paste over an endotracheal tube can reduce the incidence and severity of postoperative sore throat (POST) compared with using chlorhexidine gluconate jelly. Their findings have potential implications for prevention of POST, one of the common side effects associated with tracheal intubation. In our view, however, there are several aspects of this study that need to be clarified before adoption into routine practice. First, the article did not specify the manufacturers and ingredients of either the 0.1% chlorhexidine gluconate jelly or the 0.1% triamcinolone acetonide paste used in this study. It has been shown that chemical additives in some endotracheal tube lubricants, including local anesthetics, can irritate airway mucosa, potentially causing airway mucosal damage and ultimately leading to an increased incidence and severity of POST. The article did not clearly explain whether the 0.1% triamcinolone acetonide paste was a special preparation for airway mucosal use, hence, we suggest cautious interpretation of these findings. Second, POST is a result of airway mucosal injury with ensuing inflammation caused by the combined effects of airway instrumentation (i.e., laryngoscopy, endotracheal tube insertion, and airway suctioning) or the irritating effects of a foreign object (i.e., endotracheal tube, or cuff). The incidence and severity of POST are associated with many factors, including patient sex and age, tube size, surgical site, external laryngeal manipulation, intubating stylet during laryngoscopy and intubation, use of nitrous oxide during anesthesia, intracuff pressure during surgery, airway suctioning, duration of intubation, and postoperative analgesic protocols. To differentiate the effect of one factor related to POST, the other factors need to be standardized in the study design. The authors are to be commended for having tried to control for the majority of these factors. However, in this study, three factors do not appear to have been addressed adequately, i.e., use of the intubating stylet, external laryngeal manipulation, and oropharyngeal suctioning. It is logical to assume that use of the intubating stylet will predispose to airway trauma, especially when it is used blindly and with excessive force. Moreover, pharyngeal trauma caused by aggressive oropharyngeal suctioning has also been shown to be a contributing factor related to POST. In contrast, application of external laryngeal manipulation to facilitate visualization of the glottis during laryngoscopy may help to avoid damage around the glottis caused by forcible intubation, resulting in a decreased risk of laryngeal damage. Addressing these factors would further clarify the transparency of this study. Finally, one must consider the use of chlorhexidine gluconate jelly for comparison with triamcinolone acetonide paste. In previous studies, the authors have commented on the absence of a significant difference in the incidence of POST between unlubricated and lubricated tracheal tubes using chlorhexidine gluconate-containing jelly as a lubricant. Nevertheless, in these studies, we noted that the endotracheal tubes were actually lubricated with water-soluble jelly and Fu Shan Xue and He Ping Liu contributed equally to this work.

To the Editor, We congratulate Truong et al. on their successful airway management using retromolar fibreoptic orotracheal intubation in a patient with severe trismus undergoing nasal surgery. We too have employed this technique in three adult patients during the past five years. The first case involved a 52-yr-old woman who suffered from a severely limited mouth opening (interincisor distance = 7 mm) due to previous radiotherapy for oral cancer. On this admission, she underwent nasal metastatic tumour excision and temporomandibular joint arthroplasty. The second case involved a 21-yr-old male with chronic temporomandibular joint ankylosis (interincisor distance = 5 mm), mandibular hypoplasia, and left nasal passage stenosis. He was scheduled for temporomandibular joint arthroplasty and surgery of the left nasal passage. The third case involved a 32-yr-old male with decerebrate rigidity secondary to brain trauma. He had severe trismus (interincisor distance = 0 mm), a basal skull fracture, and cerebrospinal fluid rhinorrhea, and he required orotracheal intubation for airway management because his legally responsible relative refused tracheotomy. In all three cases, retromolar fibreoptic orotracheal intubation was an effective choice to secure an airway for patients with concomitant severe trismus and contraindications to nasotracheal intubation. We offer several observations from our experience to facilitate use of retromolar fibreoptic intubation

To the Editor, The Airtraq optical laryngoscope (Airtraq) (Prodol Meditec S.A., Vizcaya, Spain) is a relatively new disposable tracheal intubation device with an anatomically shaped blade that has two parallel channels, the optical channel and the guiding channel, which accommodates the endotracheal tube (ETT). The Airtraq incorporates a guiding channel to the right of the viewing axis to solve the challenge of passing the ETT through the glottis. However, delivering the ETT through the gap between the end of the guiding channel tube to the glottis may not be straightforward. The guiding channel tube and viewing axis are somewhat incongruent, because the direction of ETT advancement from the guiding channel is defined by the configuration of the guiding channel tube and the ETT angulation. When attempting to advance the ETT through the laryngeal aperture with the Airtraq during tracheal intubation, it has been reported that a posterior tube tip location can be problematic, especially for pediatric patients. On the basis of our cumulated experience with the Airtraq, which includes more than 500 pediatric patients to date, another possible difficulty in advancing the ETT through the glottis, especially in infants and young children with smaller airways, is a left tube tip location. This potential problem arises because the Airtraq is designed with the guiding channel at the right of the viewing axis, and a left-oriented slope at the right side of the distal opening of the guiding channel is devised to direct the tube tip into the glottis in the midline (Figure, Panel A). This design results in ETT advancement from the guiding channel towards the left. Consequently, during advancement of the ETT, the tube tip may move across the midline (Figure, Panel B) towards either the left vocal cord or the left laryngeal vestibule rather than align the ETT towards the midline of the glottis (Figure, Panel C). Whenever this problem arises, our practice has been to withdraw the ETT by approximately 0.5 cm and to exercise one of four available options: 1) slightly rotate the Airtraq in a clockwise direction; 2) advance the Airtraq downwards; 3) gently apply leftwards laryngeal pressure with external laryngeal manipulation, then re-attempt ETT advancement; and 4) in the very rare occasions the above measures fail, withdraw the ETT from the guiding channel and introduce a pediatric bougie into the visualized glottis via the guiding channel. The ETT is then railroaded along the bougie through the larynx, and the Airtraq is used to monitor the progress of the ETT advancement. Over the previous two years, we have used these maneuvers quite successfully to facilitate advancing the ETT into the glottis with the Airtraq device in pediatric patients with uncomplicated and difficult airways alike.

A general review was made of studies involving: (1) the concept and mechanism of the cholinergic anti-inflammatory pathway (CAP), (2) the important role of inflammatory response in myocardial ischemia reperfusion (I/R) injury and (3) the evidence and mechanisms by which CAP may provide protection against myocardial I/R injury.The data used in this review were mainly from manuscripts listed in PubMed that were published in English from 1987 to 2009. The search terms were "vagal nerve stimulation", "myocardial ischemia reperfusion injury", "nicotine acetylcholine receptor" and "inflammation".(1) Clinical and experimental evidence that the inflammatory response induced by reperfusion enhances myocardial I/R injury. (2) Clinical and laboratory evidence that the CAP inhibits the inflammation and provides protection against myocardial I/R injury.The myocardial I/R injury is really an inflammatory process characterized by recruitment of neutrophils into the ischemic myocardium and excessive production of pro-inflammatory cytokines. Because the CAP can modulate the inflammatory response by decreasing the production and release of pro-inflammatory cytokines, it can provide protection against myocardial I/R injury.The CAP can inhibit the inflammatory response induced by reperfusion and protect against myocardial I/R injury. It represents an exciting opportunity to develop new and novel therapeutics to attenuate the myocardial I/R injury.

To the Editor, The Airtraq optical laryngoscope (Airtraq) (Prodol Meditec S.A., Vizcaya, Spain) is a new disposable tracheal intubation device with an anatomically-shaped blade that contains two parallel channels, the optical channel and the guiding channel, which accommodates the endotracheal tube (ETT). The image is transmitted to a proximal viewfinder, and the distal viewing lens allows visualization of the larynx and advancement of the ETT. In addition, the Airtraq has a warming element at the blade tip. According to the manufacturer’s manual, the Airtraq light should be turned on at least 30 sec before use to allow heating of the viewing lens and to prevent fogging. Despite the Airtraq’s anti-fog mechanism, we have observed that visualization of the laryngeal inlet can be obscured by fogging on the viewing lens, especially when tracheal intubation time is prolonged in patients with difficult airways. To resolve this issue, and in view of previous experience with another optical laryngoscope (Truview laryngoscope, Truphatek International Ltd, Netanya, Israel) and the fibreoptic laryngoscopes, we tested the effectiveness of using highflow oxygen to eliminate fogging during laryngoscopy and tracheal intubation using the Airtraq. After receiving local ethics committee approval and written informed consent, we recruited 321 children (aged three months to 17 yr) and 283 adults (aged 18-75 yr) into the study. All of the patients were American Society of Anesthesiologists’ physical status I-II patients who were scheduled for elective plastic surgery in our hospital from March 2009 to June 2010. All procedures called for general anesthesia requiring tracheal intubation. Exclusion criteria included patients with a limited mouth opening that precluded insertion of the Airtraq and refusal to participate in the study. All intubations were performed by anesthesiologists who had been trained in the use of an Airtraq in a short-term airway management program and who had performed tracheal intubations using this device in more than 20 patients prior to this study. Induction and maintenance of anesthesia were not standardized but were left to the discretion of the staff anesthesiologist to use either a propofol or sevofluranebased technique with or without neuromuscular blockade. Before orotracheal intubation, an appropriately-sized ETT was loaded into the guiding channel of the Airtraq, and the ETT tip was positioned at the right side of the viewing lens. When performing nasotracheal intubation, the ETT was inserted via the pre-selected nostril until its tip passed through the posterior naris. The Airtraq was then passed into the patient’s airway over the tongue in the midline. Once the Airtraq blade tip was positioned in the vallecula with the glottis in the centre of the viewfinder, the ETT was passed by the glottis and advanced downwards into the trachea. Obscured vision during laryngoscopy and intubation was defined as fogging on the viewing lens that impeded continuous observation for airway structures and ETT advancement. Whenever this problem occurred, an assistant immediately attached the anesthesia circuit to the ETT. By intermittently pushing the oxygen flush valve of an anesthesia machine, a high oxygen flow was transported via the ETT to the distal end of the Airtraq to eliminate the fogging (Figure). The efficiency of de-fogging was assessed using a three-point scale (inefficient = no Fu Shan Xue, Jian-Hua Liu contributed equally to this work.

There are few studies to assess whether propofol attenuates myocardial ischemia-reperfusion injury via a mechanism related to nitric oxide (NO) route, so we designed this randomized blinded experiment to observe the changes of NO contents, nitric oxide synthase (NOS) activity, NOS contents in the myocardium, and cardiac function in ischemic reperfused isolated rat hearts, and to assess the relation between myocardial NO system and cardioprotection of propofol.The hearts of 30 Sprague-Dawley male rats were removed, mounted on a Langendorff apparatus, and randomly assigned to one of three groups (n = 10 each group) to be treated with the following treatments in a blinded manner: Group 1, control group, after perfusion with pure Krebs Henseleit bicarbonate (K-HBB) buffer solution for 15 minutes, hearts were subjected to 20 minutes global ischemia followed by 60 minutes reperfusion with pure K-HBB buffer; Group 2, after perfusion with K-HBB buffer solution containing propofol (10 microg/ml) for 15 minutes, the hearts underwent 20 minutes global ischemia followed by 60 minutes reperfusion with the same K-HBB buffer solution; Group 3, after perfusion with K-HBB buffer solution containing propofol (10 microg/ml) and L-NAME (100 micromol/L) for 15 minutes, the hearts underwent 20 minutes global ischemia followed by 60 minutes reperfusion with the same K-HBB buffer solution. The cardiac function was continuously monitored throughout the experiment. The coronary flow was also measured. An ISO-NO electrode was placed into the right atrium close to the coronary sinus to continuously measure NO concentration in the coronary effluent. The tissue samples from apex of hearts in Groups 1 and 2 were obtained to measure the NOS activity by spectrophotometry and the NOS contents by immunohistochemistry, respectively.The cardiac function was significantly inhibited after ischemia and then gradually improved with reperfusion in all three groups. As compared with Group 1, the cardiac function variables and coronary flow at all the observed points were significantly improved in Group 2. The cardiac function variables and coronary flow were better in Group 3 than in Group 1, but were inferior in Group 3 than in Group 2. Both NO contents and NOS activity in the myocardium were significantly higher in Group 2 than in Group 1. However, NOS contents in the myocardium did not significantly differ between Groups 1 and 2.In isolated rat hearts, propofol can improve cardiac functional recovery after ischemia-reperfusion by upregulating NOS activity in the myocardium. The NO system may play an important role in the preservation of myocardial ischemia-reperfusion injury produced by propofol.