Nalbuphine reduces the incidence of emergence agitation in children undergoing Adenotonsillectomy: A prospective, randomized, double-blind, multicenter study.

OBJECTIVE: To evaluate the effect of nalbuphine on emergence agitation (EA) in children undergoing adenotonsillectomy. DESIGN: Multicenter, prospective, double-blind, randomized controlled trial. SETTING: The First People's Hospital of Foshan and three other participating institutions in China, from April 2020 to December 2021. PATIENTS: Eight hundred patients, 3-9 years of age, American Society of Anesthesiologists (ASA) classification I or II, undergoing elective adenotonsillectomy were included. INTERVENTIONS: Nalbuphine (0.1 mg/kg) or saline was administered intravenously. MEASUREMENTS: The incidence of EA; the pediatric anesthesia emergence delirium (PAED) scale; and the faces, legs, activity, cry, and consolability (FLACC) scales. Extubation time, duration of post-anesthesia care unit (PACU) stay, anesthesia nurses' and parents' satisfaction, and other side effects. MAIN RESULTS: The incidence of EA in the nalbuphine group was lower than that in the saline group 30 min after extubation (10.28% vs. 28.39%, P = 0.000). In addition, the FLACC scores in the nalbuphine group were lower than those in the saline group 30 min after extubation (P < 0.05). Furthermore, the proportion of moderate-to-severe pain cases (FLACC scores >3) was significantly lower in the nalbuphine group than in the saline group (33.58% vs. 60.05%, P = 0.000). Adjusting the imbalance of postoperative pain intensity, the risk of EA was still lower in the nalbuphine group at 0 min (OR, 0.39; 95% CI, 0.26-0.60; P = 0.000), (OR, odds ratio; CI, confidence interval), 10 min (OR, 0.39; 95% CI, 0.19-0.79; P = 0.01), and 20 min (OR, 0.27; 95% CI, 0.08-0.99; P = 0.046) than in the saline group. There were no significant differences in extubation time, duration of PACU stay, nausea and vomiting, or respiratory depression between the two groups (P > 0.05). CONCLUSION: Nalbuphine reduced the incidence of EA in children after adenotonsillectomy under general anesthesia, which may be involved in both analgesic and non-analgesic pathways.

[Endothelial dysfunction and target organ damage in hypertensive patients complicating with or without metabolic syndrome].

OBJECTIVE: To investigate the impacts of metabolic syndrome (MS) on endothelial function and target organ damage in hypertensive patients. METHODS: Patients with essential hypertension (EH) were divided into two groups: hypertension and metabolic syndrome (EH + MS, n = 61), hypertension without metabolic syndrome (EH + nonMS, n = 95) and 31 healthy subjects served as normal control (NC). The change of brachial artery vascular diameter, blood flow volume and vascular resistance after reactive hyperemia were measured by color Doppler ultrasonography. RESULTS: (1) Triglyceride (TG), fasting blood glucose (FBG), body mass index (BMI) were higher in EH + MS group than that in EH + nonMS group (P < 0.05). (2) Endothelium-dependent Dilatation (FMD%) and rate of flow volume of reactive hyperemia were significantly lower in EH + MS group than that in EH + nonMS and NC group [(7.08 +/- 3.21)% vs. (8.18 +/- 1.74)% and (10.41 +/- 4.52)%, P < 0.05 and 0.01 respectively; (154.19 +/- 78.94)% vs. (196.44 +/- 64.22)% and (221.81 +/- 89.64)%, P < 0.05 and 0.01 respectively], while these parameters were similar between EH + nonMS and NC groups (P > 0.05). (3) The high sequence of forearm dilatation capability was also significantly reduced in EH + MS group compared to other groups. (4) The incidences of carotid atherosclerotic plaque and left ventricular hypertrophy (LVH) were significantly increased in EH + MS group compared to EH + nonMS group and NC group. (5) FMD was correlated with age, gender, smoking, SBP, DBP, TG, Fib respectively (P < 0.05). Intima-media thickness (IMT) of carotid artery was positively related with age, smoking, SBP, DBP, BMI, TG, Fib respectively. The left ventricular mass index (LVMI) was positively related with age, smoking, SBP, DBP, BMI, TG respectively. FMD was negatively related with IMT and LVMI respectively (P < 0.01). CONCLUSION: Metabolic syndrome further aggravated endothelial dysfunction and target organ damage in patients with essential hypertension.

Distinct regulation of expressed calcium channels 2.3 in Xenopus oocytes by direct or indirect activation of protein kinase C.

Protein kinase C (PKC)-dependent regulation of voltage-gated Ca (Ca(v); with alpha(1)beta1Balpha2/delta subunits) channel 2.3 was investigated using phorbol 12-myristate 13-acetate (PMA), or by M(1) muscarinic receptor activation in Xenopus oocytes. The inward Ca(2+)-current with Ba(2+) (I(Ba)) as the charge carrier was potentiated by PMA or acetyl-beta-methylcholine (MCh). The inactivating [I(inact)] and non-inactivating [I(noninact)] components of I(Ba) and the time constant of inactivation tau(inact) were all increased by MCh or PMA. This may be a PKC-dependent action since the effect of MCh and PMA was blocked by Ro-31-8425 or beta-pseudosubstrate. MCh effect was blocked by atropine, guanosine-5'-O-(2-thiodiphosphate) trilithium (GDPbetaS) or U-73122. The effect of MCh but not PMA was blocked by the inhibition of inositol-1,4,5-trisphosphate (IP3) receptors, intracellular Ca(2+) ([Ca(2+)](i)) or the translocation of conventional PKC (cPKC) with heparin, BAPTA and betaC2.4, respectively. While a lower concentration (25 nM) of Ro-31-8425 blocked MCh, a higher concentration (500 nM) of Ro-31-8425 was required to block PMA action. This differential susceptibility of MCh and PMA to heparin, BAPTA, betaC2.4 or Ro-31-8425 is suggestive of the involvement of Ca(2+)-dependent cPKC in MCh action, whereas cPKC and Ca(2+)-independent novel PKC (nPKC) in PMA action. PMA led to additional increase in I(Ba) that was already potentiated by preadministered MCh (1 or 10 microM), leading to the suggestion that differential phosphorylation sites for cPKC and nPKC may be present in the alpha(1)2.3 subunit of Ca(v) 2.3 channels.