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Journal of Anesthesia 02/2011; 25(1):131-2; author reply 133-4. · 0.83 Impact Factor
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Anesthesiology 02/2011; 114(2):462-3. · 5.36 Impact Factor
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Canadian Anaesthetists? Society Journal 12/2010; 58(3):338-9. · 2.31 Impact Factor
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ABSTRACT: To compare cardioprotective and anti-inflammatory effects of ischemia preconditioning (IPC) and ischemia postconditioning (IPOC) in a rat myocardial ischemia-reperfusion injury (IRI) model.
Forty Sprague-Dawley rats were randomly divided equally into four groups. In the groups other than the sham group, the left anterior descending coronary artery was ligated for 30 min followed by a 180 min reperfusion in vivo. The control group was subjected to no additional intervention, the IPC group to three cycles of 5 min ischemia separated by 5 min reperfusion before the index ischemia and the IPOC group to three cycles of 10 s ischemia separated by 10 s reperfusion immediately after the end of the index ischemia. Hemodynamic changes during the ischemia and reperfusion were recorded. At 180 min of reperfusion, serum concentrations of troponin I (TnI), tumor necrosis factor α (TNF-α) and high-mobility group box 1 (HMGB-1) were assayed, and the infarction size was assessed by Evans blue and triphenyltetrazolium chloride staining.
Compared to the control group, infarct size and serum concentrations of TnI, TNF-α and HMGB1 at 180 min of reperfusion were significantly reduced in the IPC and IPOC groups. However, infarct size and serum concentrations of TNF-α and HMGB1 at 180 min of reperfusion were significantly increased in the IPOC group compared to the IPC group.
In the rats with myocardial IRI in vivo, both IPC and IPOC can produce significant cardioprotective and anti-inflammatory effects. However, cardioprotective and anti-inflammatory effects provided by IPOC are weaker than with IPC.
Agents and Actions 12/2010; 60(6):547-54. · 1.59 Impact Factor
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Pediatric Anesthesia 11/2010; 20(11):1058-9. · 2.10 Impact Factor
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The American journal of emergency medicine 10/2010; 29(1):126. · 1.54 Impact Factor
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The American journal of emergency medicine 10/2010; 29(1):123-4. · 1.54 Impact Factor
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The American journal of emergency medicine 10/2010; 29(1):120-1; author reply 121-2. · 1.54 Impact Factor
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The American journal of emergency medicine 10/2010; 29(1):126-7; author reply 128. · 1.54 Impact Factor
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ABSTRACT: 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.
Chinese medical journal 10/2010; 123(19):2720-6. · 0.86 Impact Factor
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Journal of Emergency Medicine 09/2010; · 1.31 Impact Factor
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Canadian Anaesthetists? Society Journal 09/2010; 57(12):1133-5. · 2.31 Impact Factor
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Anesthesiology 06/2010; 112(6):1536-7. · 5.36 Impact Factor
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Pediatric Anesthesia 06/2010; 20(6):575-6. · 2.10 Impact Factor
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ABSTRACT: To compare the hemodynamic responses to orotracheal intubation using a Shikani Optical Stylet (SOS) laryngoscope or a Macintosh direct laryngoscope (MDLS).
Totally 41 patients with American Society of Anesthesiologists ASA physical status -aged 20-60 years and scheduled for elective surgery under general anesthesia requiring orotracheal intubation, were randomly allocated to either the SOS group (n=21) or MDLS group (n=20). After an intravenous anesthetic induction the orotracheal intubation was performed using a SOS laryngoscope or a MDLS. Blood pressure and heart rate (HR) were recorded before and after anesthetic induction immediately after intubation, and 5 minutes after intubation. Rate pressure product RPP were calculated.
Blood pressures and RPP in both two groups significantly decreased after anesthetic induction (P<0.05) while blood pressures HR, and RPP significantly increased after orotracheal intubation (P<0.05). HR in both groups after intubation were significantly higher than the pre-induction level (P<0.05)and such an increase lasted for 3 min. HR immediately after intubation was also significantly higher in MDLS group than in SOS group (P<0.05); however, such difference was not observed in other time points (P>0.05). In the MDLS group when compared with the occurrence time required for the maximum values of systolic blood pressure (SBP)the occurrence time required for the maximum values of HR after the start of intubation and success of intubation during the observation were significantly delayed (P<0.05). Compared with the MDLS group, the occurrence time required for the maximum values of SBP after the start of intubation and the success of intubation were significantly delayed in the SOS group (P<0.05). The incidences of SBP more than 130% of baseline value and RPP more than 22 000 were not significantly differently(P>0.05). Also, the intubation time was not significantly different (P>0.05).
The hemodynamic responses to orotracheal intubation is milder in SOS laryngoscope than in MDLS.
Zhongguo yi xue ke xue yuan xue bao. Acta Academiae Medicinae Sinicae 06/2010; 32(3):303-9.
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Pediatric Anesthesia 04/2010; 20(4):377-9. · 2.10 Impact Factor
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Pediatric Anesthesia 03/2010; 20(3):279-81. · 2.10 Impact Factor
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ABSTRACT: 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.
Chinese medical journal 12/2009; 122(24):3048-54. · 0.86 Impact Factor
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Pediatric Anesthesia 11/2009; 19(11):1135-6. · 2.10 Impact Factor
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Pediatric Anesthesia 10/2009; 19(9):918-9. · 2.10 Impact Factor
