ABSTRACT
Dexmedetomidine is a suitable sedative for awake fiberoptic intubation in patients with obstructive sleep apnea (OSA). However, previous studies have shown that dexmedetomidine delays recovery from propofol-remifentanil anesthesia. This study aimed to determine whether doxapram may hasten the recovery following dexmedotomidine-propofol-remifentanil anesthesia. Sixty patients scheduled for uvulopalatopharyngoplasty with total intravenous anesthesia were randomized to two groups according to the medicine given at the end of surgery. These were the doxapram (1 mg/kg) and control (normal saline) groups (n=30 per group). The primary outcome was the time to eye opening on verbal command. The time to return to spontaneous breathing, to hand squeezing in response to verbal command, to extubation of the trachea, and the heart rate (HR), bispectral index (BIS) values, respiratory rate (RR) and pulse oximetry values were also recorded and compared. The time to return to spontaneous breathing (5.2±2.9 vs. 11.7±3.4 min, P<0.001), eye opening (9.3±4.7 vs. 15.9±6.3 min, P<0.001), hand squeeze to command (11.8±6.5 vs. 17.6±7.7 min, P=0.0026) and extubation (14.2±7.8 vs. 19.2±9.6 min, P=0.0308) were significantly shorter in the doxapram group compared with the control group. BIS scores (at 3-14 min), RR (at 4-10 min) and HR (at 2-13 min) were significantly higher in the doxapram group compared with those in the control group (P<0.05). Doxapram hastens the recovery from dexmedetomidine-propofol-remifentanil anesthesia in patients undergoing uvulopalatopharyngoplasty, and may benefit patients with OSA.
ABSTRACT
HMGB1 is a necessary and critical mediator of acute lung injury and can act as a chemoattractant and anti-apoptosis factor in injury or repair in diseases. In this study we sought to determine whether HMGB1 is involved in the remodeling of pulmonary artery and investigate the mechanism. A rat model of pulmonary artery remodeling was successful induced with LPS infusion and the increasing of pulmonary arteries media was obviously inhibited in rats treated with thrice inject of HMGB1 neutralizing antibody. The percent of areas of tunica media to total artery wall was (0.53 ± 0.15), (0.81 ± 0.10) and (0.59 ± 0.11) in control, LPS and antibody group respectively (p<0.05). Meanwhile, treatment with HMGB1 neutralizing antibody not only decreased the level of HMGB1 mRNA and protein significantly, but inhibited the expression of PCAN and Bcl-2 as well. On the contrary, Bax, a gen which represented the apoptosis, revealed an absolutely reversed trend to Bcl-2 in pulmonary arteries. Experiments in vitro showed that HMGB1 could stimulate the proliferation of hPASMC in MTT test and increase the number of migrated cells in a concentration-dependent manner in chemotaxis assay using modified Boyden chambers. In conclusion, data from this study support the concept that HMGB1 is involved in the remodeling of pulmonary artery by enhancing proliferation and migration of smooth muscle cell. Inhibiting HMGB1 may be a new target to deal with the remodeling of pulmonary artery.