A new air- and moisture-stable pentagonal-bipyramidal DyIII single-ion magnet based on the HMPA ligand.

Based on the HMPA ligand, a new air- and moisture-stable pentagonal-bipyramidal DyIII single-ion magnet [Dy(HMPA)2(H2O)5]2·Br6·2HMPA·2H2O (1) was prepared and characterized. Single-crystal X-ray tests showed the two crystallographically independent DyIII ions located in a pentagonal-bipyramidal coordination sphere with strong axial HMPA ligands and weak equatorial water molecules relating to strong unaxial anisotropy. Direct-current and alternating-current magnetic susceptibilities were measured and showed that 1 exhibited slow relaxation of magnetization up to 36 K (1000 Hz) with an energy barrier of 556 K and blocking temperature of 7 K (defined by the peak temperature of zero-field cooling data). The application of a dc field and magnetic dilution were also carried out to explore the existing quantum tunelling of the magnetization process.

κ-Opioid receptors are involved in enhanced cardioprotection by combined fentanyl and limb remote ischemic postconditioning.

BACKGROUND: The combination of various interventions to obtain enhanced cardioprotection is always an important area of research focus. This randomized experiment was designed to assess whether combined fentanyl and limb remote ischemic postconditioning produced enhanced protection against myocardial ischemia/reperfusion injury in an in vivo rat model, and to determine if κ-opioid receptors were implicated in the cardioprotection of these interventions. METHODS: Seventy-two rats were exposed to a 30-min myocardial ischemia followed by a 180-min reperfusion. Half of the rats (36) were randomized into four different groups receiving control treatment, fentanyl postconditioning, limb remote ischemic postconditioning, and combined fentanyl and limb remote ischemic postconditioning. The remaining 36 rats were also randomized into four groups receiving the same interventions as the above groups following the intravenous administration of a κ-opioid receptor antagonist, nor-binaltorphimine, before myocardial ischemia. At the end of reperfusion, both serum cardiac troponin I and infarct size were determined. RESULTS: Both fentanyl postconditioning and limb remote ischemic postconditioning significantly decreased the infarct size and serum cardiac troponin I level, and combined fentanyl and limb remote ischemic postconditioning produced enhanced cardioprotection on the infarct size-sparing effect. The use of nor-binaltorphimin to block κ-opioid receptors eliminated cardioprotection by fentanyl postconditioning and enhanced cardioprotection by combined fentanyl and limb remote ischemic postconditioning, but did not change cardioprotection by limb remote ischemic postconditioning. CONCLUSIONS: Combined fentanyl and limb remote ischemic postconditioning produced enhanced protection against myocardial ischemia/reperfusion injury. κ-Opioid receptors are essential for cardioprotection by fentanyl postconditioning and enhanced cardioprotection by combined fentanyl and limb remote ischemic postconditioning; however, they do not play a pivotal role in cardioprotection by limb remote ischemic postconditioning.

[Effects of combined ischemic postconditioning, remote ischemic postconditioning and naloxone postconditioning on focal cerebral ischemia-reperfusion injury in rats].

OBJECTIVE: To assess the effects of ischemic postconditioning, remote ischemic postconditioning and naloxone postconditioning on focal cerebral ischemia-reperfusion injury in rats. METHODS: 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 ischemic & naloxone postconditioning performed simultaneously in accordance with the methods used in Groups 2, 3 & 4. The neurologic deficit scores (NDS) were obtained at 2 h & 24 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). RESULTS: 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 (P > 0.05). 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 (P < 0.05). 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 P < 0.05). However, there were no significant differences in the above-mentioned parameters at ischemic side among Groups 2, 3 and 4 (all P > 0.05). 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 P < 0.05). The diameter and segment length of cerebral microvessel at ischemic side were not different among Groups 2, 3, 4 and 5 (all P > 0.05). CONCLUSION: 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.

[Effect of remifentanil preconditioning on myocardial ischemia-reperfusion injury].

OBJECTIVE: To investigate the delayed cardioprotection induced by remifentanil in intact rat ischemia-reperfusion (I/R) models. METHODS: Totally 42 adult male Wistar rats weighing 200-300 g were randomly divided into 7 groups (n = 6 in each group): In Group I, rats were injected with normal saline via tail vein, performed with the regimen of 3 x 5-min intravenous (i.v.) infusion at a rate of 0.1 ml x kg(-1) min(-1) 24 h before I/R; In Group II, rats were treated according to the same experimental protocols as in Group I except receiving additional naloxone (0.1 mg/kg) 10 minutes before normal saline pretreatment; In Groups III, IV, V, and VI, rats were treated with remifentanil via tail vein, performed with the regime of 3 x 5-min i.v. infusion at a rate of 2 microg x kg(-1) x min(-1) 12 h, 24 h, 48 h, and 72 h before I/R; In Group VII, the rats were treated according to the same experimental protocols as in Group IV except that they received additional naloxone (0.1 mg/kg) 10 minutes before remifentanil pretreatment. Heart rate (HR), mean arterial pressure (MAP), and a lead II electrocardiogram were continuously monitored during IR process. To determine plasma concentration of creatine kinase myocardial isoenzyme-MB (CK-MB), arterial blood samples were obtained immediately before ischemia, and at the end of ischemia and reperfusion. After a 120-min reperfusion, heart was removed for the measurement of myocardial infarct size. Infarct size (IS) was expressed as percentage of the area at risk. RESULTS: HR, MAP, and rate-pressure product were not significantly different at each time points among all groups (P > 0.05). Compared with Group I, plasma concentrations of CK-MB at the end of ischemia and reperfusion and myocardial infarct size were significantly lower in Groups IV and V (P < 0.05). Compared with Group IV, plasma concentrations of CK-MB at the end of ischemia and reperfusion were significantly higher and myocardial infarct size was significantly larger in Group VII (P < 0.05). CONCLUSION: Remifentanil preconditioning induces delayed cardioprotection in intact rat ischemia-reperfusion model, which may be triggered via opioid receptors.

Median effective dose of remifentanil for awake laryngoscopy and intubation.

BACKGROUND: Awake intubation requires an anesthetic management that provides sufficient patient safety and comfort, adequate intubating conditions, and stable hemodynamics. In this prospective clinical study, our aim was to determine the median effective dose (ED(50)) of remifentanil in combination with midazolam and airway topical anesthesia for awake laryngoscopy and intubation. METHODS: Thirty-six female adult patients, scheduled for elective plastic surgery under general anesthesia requiring orotracheal intubation were included in this study. Ten minutes after intravenous administration of midazolam 0.1 mg/kg, patients were assigned to receive remifentanil in bolus, followed by a continuous infusion. The bolus dose and infusion rate of remifentanil were adjusted by a modified Dixon's up-and-down method. Patient's reaction score at laryngoscopy and an Observer's Assessment of Alertness/Sedation Scale (OAA/S) were used to determine whether the remifentanil dosage regimen was accepted. During laryngoscopy, 2% lidocaine was sprayed into the airway to provide the topical anesthesia. ED(50) of remifentanil was calculated by the modified Dixon up-and-down method, and the probit analysis was then used to confirm the results obtained from the modified Dixon's up-and-down method. In the patients who were scored as "accept", patient's OAA/S and reaction scores at different observed points, intubating condition score and patient's tolerance to the endotracheal tube after intubation were evaluated and recorded. Blood pressure and heart rate at different measuring points were also noted. RESULTS: ED(50) of remifentanil for awake laryngoscopy and intubation obtained by the modified Dixon's up-and-down method was (0.62 +/- 0.02) microg/kg. Using probit analysis, ED(50) and ED(95) of remifentanil were 0.63 microg/kg (95% CI, 0.54 - 0.70) and 0.83 microg/kg (95% CI, 0.73 - 2.59), respectively. Nineteen patients who were scored as "accept" had an OAA/S of > 15 and tolerated well laryngoscopy without significant discomfort or gagging. The mean intubating condition score was 1.8 +/- 0.8. The endotracheal tube was well tolerated. During awake laryngoscopy and intubation, blood pressure and heart rate were also kept stable. The postoperative follow up showed that no patient recalled discomfort and pain for airway manipulation. CONCLUSIONS: When combined with midazolam 0.1 mg/kg and airway topical anesthesia, ED(50) of remifentanil for successful awake laryngoscopy and intubation is 0.62 microg/kg in bolus followed by continuous infusion of 0.062 microg*kg(-1)*min(-1). This sedation and analgesia regimen can provide patient safety and comfort, ensure adequate intubating conditions, maintain hemodynamic stability, and prevent negative recall of the airway procedure.

Clinical assessment of awake endotracheal intubation using the lightwand technique alone in patients with difficult airways.

BACKGROUND: There is few study to determine whether the use of the lightwand technique alone could achieve effective, safe and successful awake endotracheal intubation (ETI), therefore we designed a prospective clinical study to systematically evaluate the feasibility, safety and efficacy of awake ETI using the lightwand alone in patients with difficult airways. METHODS: Seventy adult patients with difficult airways were enrolled in this study. After the desired sedation with fentanyl and midazolam, airway topical anesthesia was performed with 9 ml of 2% lidocaine, which were in order sprayed in three aliquots at 5 minutes intervals into the supraglottic (two doses) and laryngotracheal areas (one dose) using a combined unit of the lightwand and MADgic atomizer. After airway topical anesthesia, awake ETI was performed using a Lightwand. Subjective assessments by patients and operators using the visual analogue scores (VAS), and objective assessments by an independent investigator using patients' tolerance and reaction scores, coughing severity, intubating conditions and cardiovascular variables were taken as the observed parameters. RESULTS: Of 210 airway sprays, 197 (93.8%) were successfully completed on the first attempt. The total time for airway spray was (14.6 +/- 1.5) minutes. During airway topical anesthesia, the average patients' tolerance scores were 1.7 - 2.3. After airway topical anesthesia, the mean VAS for discomfort levels that the patients reported was 6.5. Also airway topical anesthesia procedure was rated as acceptable and no discomfort by 94.3% of patients. The lightwand-guided awake ETI was successfully completed on first attempt within 29 seconds in all patients. During awake ETI, patients' reaction and coughing scores were 1.9 and 1.6, respectively. All patients exhibited excellent or acceptable intubating conditions. Cardiovascular monitoring revealed that changes of systolic blood pressure and heart rate at each stage of airway manipulations were less than 20% of baseline values. The postoperative follow-up showed that 95.7% of patients had no recall or slight memories of all airway instrumentation. The incidence of postoperative mild airway complications was 38.6%. CONCLUSION: Alone use of the lightwand technique can achieve effective, safe and successful awake ETI in patients with difficult airways.

Comparison of bolus remifentanil versus bolus fentanyl for blunting cardiovascular intubation responses in children: a randomized, double-blind study.

BACKGROUND: The authors found no study to compare the efficacy of bolus dose fentanyl and remifentanil blunting the cardiovascular intubation response in children, so they designed this randomized, double-blind clinical study to assess the effects of remifentanil 2 microg/kg and fentanyl 2 microg/kg by bolus injection on the cardiovascular intubation response in healthy children. METHODS: One hundred and two children, the American Society of Anesthesiologists (ASA) physical status 1-2 and scheduled for elective plastic surgery under general anesthesia, were randomly divided into one of two groups to receive the following treatments in a double blind manner: remifentanil 2 microg/kg (Group R) and fentanyl 2 microg/kg (Group F) when anesthesia was induced with propofol and vecuronium. The orotracheal intubation was performed using a direct laryngoscope. Blood pressure (BP) and heart rate (HR) were recorded before anesthesia induction (baseline values), immediately before intubation, at intubation and every minute for 5 minutes after intubation. The percent changes of systolic blood pressure (SBP) and HR relative to baseline values and the rate pressure product (RPP) at every observing point were calculated. The incidences of SBP and HR percent changes >30% of baseline values and RPP >22,000 during the observation were recorded. RESULTS: There were no significant differences between groups in the demographic data, baseline values of BP and HR and the intubation time. As compared to baseline values, BP, HR and RPP at intubation and their maximum values during observation increased significantly in Group F, but they all decreased significantly in Group R. BP, HR and RPP at all observed points, and their maximum values during the observation, were significantly different between groups. There were also significant differences between groups in the percent change of SBP and HR relative to baseline values at all observed points and their maximum percent changes during the observation. The incidences of SBP and HR percent increased >30% of the baseline values and RPP >22,000 during the observation, were significantly higher in Group F than in Group R, but the incidences of SBP and HR percent decreased >30% of baseline values were significantly lower in Group F compared with Group R. CONCLUSIONS: When used as part of routine anesthesia induction with propofol and vecuronium in children, fentanyl 2 microg/kg by bolus injection fails to effectively depress the cardiovascular intubation response. Remifentanil 2 microg/kg by bolus injection can completely abolish the cardiovascular intubation response, but also cause more adverse complications of temporary significant cardiovascular depression.

Bolus dose remifentanil and sufentanil blunting cardiovascular intubation responses in children: a randomized, double-blind comparison.

BACKGROUND AND OBJECTIVE: The present randomized controlled study was designed to compare the efficacy of remifentanil 2 microg kg(-1) and sufentanil 0.2 microg kg(-1) by bolus injection on the cardiovascular response to intubation in healthy children. METHODS: One hundred and five children, ASA 1-2 and scheduled for elective plastic surgery under general anaesthesia, were randomly divided into one of two study groups to receive the following treatments in a double-blind manner: remifentanil 2 microg kg(-1) (group R) and sufentanil 0.2 microg kg(-1) (group S). Blood pressure and heart rate (HR) were recorded before anaesthesia induction (baseline values), immediately before intubation (postinduction values), at intubation and every minute for 5 min after intubation. The percentage changes in systolic blood pressure (SBP) and HR relative to baseline values were calculated. The incidences of SBP and HR percentage changes of more than 30% of baseline values during the observation were recorded. RESULTS: As compared with baseline values, blood pressure and HR at intubation and their maximum values during the observation increased significantly in group S, but decreased significantly in group R. Blood pressure and HR at intubation and their maximum values during the observation were significantly different between the groups. There were significant differences between the groups in the percentage changes of SBP and HR relative to baseline values and their maximum percentage changes during the observation. The incidences of SBP and HR percentage increases of more than 30% of baseline values were not significantly different between the groups, but the incidences of SBP and HR percentage decreases of more than 30% of baseline values were significantly higher in group R than in group S. CONCLUSION: In combination with propofol for anaesthesia induction in children, sufentanil 0.2 microg kg(-1) by bolus injection fails to depress the cardiovascular intubation response. Remifentanil 2 microg kg(-1) by bolus injection can completely abolish the cardiovascular intubation response, but causes more adverse cardiovascular depression.

Propofol improves cardiac functional recovery after ischemia-reperfusion by upregulating nitric oxide synthase activity in the isolated rat hearts.

BACKGROUND: 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. METHODS: 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. RESULTS: 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. CONCLUSIONS: 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.