Ultrasound-guided internal branch of superior laryngeal nerve block on postoperative sore throat: A randomized controlled trial.

IntroductionUltrasound-guided internal branch of the upper laryngeal nerve block (USG-guided iSLN block) have been used to decrease the perioperative stress response of intubation. It is more likely to be successful than blindly administered superior laryngeal nerve blocks with fewer complications. Here, we evaluated the efficacy of USG-guided iSLN block to treat postoperative sore throat (postoperative sore throat, POST) after extubation.Methods100 patients, aged from 18 to 60 years old, ASA I~II who underwent general anesthesia and suffered from the moderate to severe postoperative sore throat after extubation were randomized into two groups(50 cases per group). Patients in group S received USG-guided iSLN block bilaterally (60mg of 2% lidocaine, 1.5ml each side), whereas those in group I received inhalation with 100 mg of 2% lidocaine and 1mg of budesonide suspension diluted with normal saline (oxygen flow 8 L /min, inhalation for 15 minutes). The primary outcome were VAS scores in both groups before treatment (T0), 10 min (T1), 30 min(T2), 1h(T3), 2 h(T4), 4h(T5), 8h(T6), 24h(T7), and 48h(T8) after treatment. The secondary outcome were satisfaction scores after treatment, MAP, HR, and SPO2 fromT0 to T8. The adverse reactions such as postoperative chocking or aspiration, cough, hoarseness, dyspnea were also observed in both groups.ResultsPatients in group S had significantly lower VAS score than that in group I at points of T1 ~ T6 (P ConclusionCompared with inhalation, USG-guided iSLN block may effectively relieve the postoperative sore throat after extubation under general anesthesia and provided an ideal treatment for POST in clinical work

Dexmedetomidine reduces isoflurane-induced neuroapoptosis partly by preserving PI3K/Akt pathway in the hippocampus of neonatal rats.

Prolonged exposure to volatile anesthetics, such as isoflurane and sevoflurane, causes neurodegeneration in the developing animal brains. Recent studies showed that dexmedetomidine, a selective α2-adrenergic agonist, reduced isoflurane-induced cognitive impairment and neuroapoptosis. However, the mechanisms for the effect are not completely clear. Thus, we investigated whether exposure to isoflurane or sevoflurane at an equivalent dose for anesthesia during brain development causes different degrees of neuroapoptosis and whether this neuroapoptosis is reduced by dexmedetomidine via effects on PI3K/Akt pathway that can regulate cell survival. Seven-day-old (P7) neonatal Sprague-Dawley rats were randomly exposed to 0.75% isoflurane, 1.2% sevoflurane or air for 6 h. Activated caspase-3 was detected by immunohistochemistry and Western blotting. Phospho-Akt, phospho-Bad, Akt, Bad and Bcl-xL proteins were detected by Western blotting in the hippocampus at the end of exposure. Also, P7 rats were pretreated with various concentrations of dexmedetomidine alone or together with PI3K inhibitor LY294002, and then exposed to 0.75% isoflurane. Terminal deoxyribonucleotide transferase-mediated dUTP nick end labeling (TUNEL) and activated caspase-3 were used to detect neuronal apoptosis in their hippocampus. Isoflurane, not sevoflurane at the equivalent dose, induced significant neuroapoptosis, decreased the levels of phospho-Akt and phospho-Bad proteins, increased the expression of Bad protein and reduced the ratio of Bcl-xL/Bad in the hippocampus. Dexmedetomidine pretreatment dose-dependently inhibited isoflurane-induced neuroapoptosis and restored protein expression of phospho-Akt and Bad as well as the Bcl-xL/Bad ratio induced by isoflurane. Pretreatment with single dose of 75 µg/kg dexmedetomidine provided a protective effect similar to that with three doses of 25 µg/kg dexmedetomidine. Moreover, LY294002, partly inhibited neuroprotection of dexmedetomidine. Our results suggest that dexmedetomidine pretreatment provides neuroprotection against isoflurane-induced neuroapoptosis in the hippocampus of neonatal rats by preserving PI3K/Akt pathway activity

Sevoflurane Preconditioning Reduces Intestinal Ischemia-Reperfusion Injury: Role of Protein Kinase C and Mitochondrial ATP-Sensitive Potassium Channel

<div><p>Ischemic preconditioning (IPC) has been considered to be a potential therapy to reduce ischemia-reperfusion injury (IRI) since the 1980s. Our previous study indicated that sevoflurane preconditioning (SPC) also reduced intestinal IRI in rats. However, whether the protective effect of SPC is similar to IPC and the mechanisms of SPC are unclear. Thus, we compared the efficacy of SPC and IPC against intestinal IRI and the role of protein kinase C (PKC) and mitochondrial ATP-sensitive potassium channel (mK_ATP) in SPC. A rat model of intestinal IRI was used in this study. The superior mesenteric artery (SMA) was clamped for 60 min followed by 120 min of reperfusion. Rats with IPC underwent three cycles of SMA occlusion for 5 min and reperfusion for 5 min before intestinal ischemia. Rats with SPC inhaled sevoflurane at 0.5 minimum alveolar concentration (MAC) for 30 min before the intestinal ischemic insult. Additionally, the PKC inhibitor Chelerythrine (CHE) or mK_ATP inhibitor 5-Hydroxydecanoic (5-HD) was injected intraperitoneally before sevoflurane inhalation. Both SPC and IPC ameliorated intestinal IRI-induced histopathological changes, decreased Chiu’s scores, reduced terminal deoxyribonucleotide transferase-mediated dUTP nick end labeling (TUNEL) positive cells in the epithelium, and inhibited the expression of malondialdehyde (MDA) and tumor necrosis factor-α (TNF-α). These protective effects of SPC were similar to those of IPC. Pretreatment with PKC or mK_ATP inhibitor abolished SPC—induced protective effects by increasing Chiu’s scores, down-regulated the expression of Bcl-2 and activated caspase-3. Our results suggest that pretreatment with 0.5 MAC sevoflurane is as effective as IPC against intestinal IRI. The activation of PKC and mK_ATP may be involved in the protective mechanisms of SPC.</p></div

Both SPC and IPC inhibited the increase in IRI-induced TUNEL positive cells in the intestine of rats.

<p>(A) Representative images of TUNEL fluorescent staining in the intestinal mucosa (×200) (scan bar = 100 μm). Green staining indicates TUNEL-positive cells, blue staining indicates nuclear. (B) Quantification of TUNEL positive cells in the intestinal mucosal. Data are expressed as the mean ± SD, n = 9. Results were compared using one-way ANOVA with Bonferroni’s posttest. *** <i>P < 0</i>.<i>001</i> vs. Sham, ^&&&<i>P</i> < 0.001 vs. SPC-Sham. ^▲▲▲<i>P</i> < 0.001 vs. IPC-Sham, ^###<i>P < 0</i>.<i>001</i> vs. IRI. IPC = ischemic preconditioning; IRI = ischemia-reperfusion injury; SPC = sevoflurane preconditioning.</p

CHE and 5-HD reversed the inhibition of SPC on intestinal apoptosis induced by intestinal IRI in rats.

<p>(A) Representative immunohistochemical images of cleaved caspase-3 in the intestinal mucosa (×400), caspase-3 positive cells are stained dark brown under light microscopy shown by the arrows; (B) Representative western blots of cleaved caspase-3 and Bcl-2; (C) The quantitative analysis of Bcl-2 and caspase-3. Data are expressed as the mean ± SD, n = 9. Results were compared using one-way ANOVA with Bonferroni’s posttest. * <i>P < 0</i>.<i>05</i>, ** <i>P < 0</i>.<i>01</i>, *** <i>P < 0</i>.<i>001</i> vs. the Sham; ^###<i>P < 0</i>.<i>001</i> vs. IRI; ^$<i>P < 0</i>.<i>05</i>, ^$$<i>P < 0</i>.<i>01</i>, ^$$$<i>P < 0</i>.<i>001</i> vs. SPC. 5-HD = 5-Hydroxydecanoic; CHE = Chelerythrine; IRI = ischemia-reperfusion injury; SPC = sevoflurane preconditioning.</p

Both SPC and IPC attenuated the increased plasma MDA and TNF-α induced by IRI, but did not significantly change the level of SOD.

<p>(A) Quantification of the plasma MDA level; (B) Quantification of the plasma SOD level; (C) Quantification of the plasma TNF-α level. Data are expressed as the mean ± SD, n = 9. Results were compared using one-way ANOVA with Bonferroni’s posttest. ** <i>P < 0</i>.<i>01</i>, *** <i>P < 0</i>.<i>001</i> vs. Sham; ^&<i>P</i> < <i>0</i>.<i>05</i>, ^&&<i>P</i> < <i>0</i>.<i>01</i>, ^&&&<i>P</i> < 0.001 vs. SPC-Sham; ^▲▲<i>P</i> < <i>0</i>.<i>01</i>, ^▲▲▲<i>P</i> < 0.001, vs. IPC-Sham; ^##<i>P < 0</i>.<i>01</i>, ^###<i>P < 0</i>.<i>001</i> vs. IRI. IPC = ischemic preconditioning; IRI = ischemia-reperfusion injury; SPC = sevoflurane preconditioning.</p

The protocol of the experiment one and two.

<p>Sham: involving isolation of SMA without occlusion; IRI: performed SMA occlusion for 60 min followed by reperfusion for 120 min without any interventions; SPC-sham: Rats were pretreated with 0.5 MAC sevoflurane for 30 min before sham operation; IPC-sham: Rats underwent intestinal IPC without 60 min ischemia; SPC: Rats were pretreated with 0.5 MAC sevoflurane for 30 min before 60 min ischemia; IPC: Rats underwent intestinal IPC prior to 60 min ischemia; SPC + CHE: Rats received intraperitoneal injection of the PKC inhibitor Chelerythrine (5 mg/kg) 15 min before SPC; SPC + 5-HD: Rats received intraperitoneal injection of the mK_ATP inhibitor 5-Hydroxydecanoic (10 mg/kg) 15 min before SPC. 5-HD = 5-Hydroxydecanoic; CHE = Chelerythrine; IPC = ischemic preconditioning; IRI = ischemia-reperfusion injury; SPC = sevoflurane preconditioning; SMA = superior mesenteric artery. * = SMA occlusion for 5 min; # = reperfusion for 5 min.</p

CHE and 5-HD inhibited the protective effect of SPC against intestinal IRI.

<p>(A) Morphologic changes of intestinal mucosa under light microscopy (×200); (B) The evaluation of intestinal injury with Chiu’s scores. The Chiu’s score data are expressed as the mean ± SD, n = 9. Results were compared using one-way ANOVA with Bonferroni’s posttest. *** <i>P < 0</i>.<i>001</i> vs. Sham, ^###<i>P < 0</i>.<i>001</i> vs. IRI, ^$<i>P < 0</i>.<i>05</i>, ^$$$<i>P < 0</i>.<i>001</i> vs. SPC. 5-HD = 5-Hydroxydecanoic; CHE = Chelerythrine; IRI = ischemia-reperfusion injury; SPC = sevoflurane preconditioning.</p

Both SPC and IPC inhibited intestinal IRI.

<p>(A-F) Histopathological changes of intestinal mucosa under light microscopy (×200); (G) The evaluation of intestinal injury with Chiu’s scores. In the sham (A) and SPC- sham (B) groups, there were no injuries to the villi and glands, whereas mildly injured villi and glands were observed in the IPC-sham group (C). However, severe intestinal glands injury, mucosa villi disintegration or edema, increased gap of epithelial cells and severe hemorrhage were observed in the IRI group (D). In the SPC (E) and IPC (F) groups, the damageto intestinal villi and glands was much slighter than that in the IRI group. The Chiu’s score data are expressed as the mean ± SD, n = 9. Results were compared using one-way ANOVA with Bonferroni’s posttest. *** <i>P < 0</i>.<i>001</i> vs. the Sham group, * <i>P < 0</i>.<i>05</i> vs. the Sham group, ^&&&<i>P</i> < 0.001 vs. SPC-Sham. ^▲▲▲<i>P</i> < 0.001 vs. IPC-Sham, ^###<i>P</i> < 0.001 vs. the IRI group. IPC = ischemic preconditioning; IRI = ischemia-reperfusion injury; SPC = sevoflurane preconditioning.</p