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Objective To investigate the efficacy of precise ultrasound-guided stellate ganglion block(UG-SGB)combined with ozonated autohemotherapy in the treatment of sudden hearing loss.Methods Fifty-seven patients with sudden hearing loss,27 males and 30 females,aged 19-82 years,BMI 20-29 kg/m2,ASA physical status Ⅰ or Ⅱ,were randomly divided into drugs combined with UG-SGB and ozonated autohemotherapy treatment group(group U,n=29)and drugs group(group D,n=28)accord-ing to the random number table.All patients were given drug therapy.In addition to the treatment above,pa-tients in group U also received precise ultrasound-guided stellate ganglion block once on affected side com-bined with ozonated autohemotherapy once daily for 10 consecutive days.Patients in group D received drug therapy only.The average hearing threshold of the two groups was compared before treatment(T0),at dis-charge(T1),1 month(T2),3 months(T3),and 6 months after discharge(T4).The hearing improve-ment of the two groups was also compared at T1-T4 on the basis of T0.Moreover,tinnitus rate of the two groups was recorded T0-T4.In addition,adverse reactions such as toxicosis of local anaesthetics,pneumo-thorax were recorded.Results Compared with T0,the average hearing threshold was reduced significantly in both groups at T1-T4(P＜0.05),the incidence of tinnitus was reduced significantly at T1-T4 in both groups(P＜0.05).Compared with T,,the average hearing threshold was reduced significantly in group U at T2-T4(P＜0.05).The average hearing threshold of group U was lower than that in group D at T1-T4(P＜0.05).The hearing improvement in group U was better than that in group D at T2-T4(P＜0.05).The proportion of complete hearing recovery in group U was increased significantly than that in group D at T2-T4(P＜0.05)The proportion of effective hearing improvement in group U was decreased than that in group D at T3-T4(P＜0.05).No obvious adverse reaction was recorded,such as toxicosis of local anaesthetics,pneumothorax.Conclusion Precise ultrasound-guided stellate ganglion block combined with ozonated auto-hemotherapy based on drug treatment significantly improves the average hearing threshold of patients with sudden hearing loss in acute stage and improve their hearing.
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Objective To evaluate the effect of emulsified isoflurane post-conditioning on the mitochondrial function during lung ischemia-reperfusion (I/R) in rats in an in vitro experiment.Methods Twenty-four SPF healthy male Sprague-Dawley rats,weighing 250-300 g,were used in the study.After the animals were anesthetized,the lungs were removed,connected to the perfusion system and then divided into 4 groups (n=6 each) using a random number table:control group (group C),group I/R,emulsified isoflurane post-conditioning group (group EI) and intralipid post-conditioning group (group IL).After 20 min of equilibration,the lungs were continuously perfused for 105 min in group C,and the lungs were subjected to 45 min ischemia followed by 60 min reperfusion to establish the model of lung I/R injury in the other three groups.During the reperfusion period,the common perfusate was used in group I/R,the perfusate containing 1.68 mmol/L emulsified isoflurane was used in group EI,and the equal volume of perfusate containing 30％ intralipid was used in group IL.At the end of the equilibration (T0),immediately after beginning of reperfusion (T1) and at 30 and 60 min of reperfusion (T2.3),the arterial oxygen partial pressure (PaO2),airway resistance,pulmonary compliance and tidal volume (VT) were recorded.The right upper lobe of the lung was removed at T3 for determination of wet to dry weight ratio (W/D ratio).The right middle lobe of the lung was removed at T3 for pathologic examination with light microscope.The contents of reactive oxygen species (ROS),NAD+ and ATP in lung tissues were detected.Results Compared with group C,the PaO2,pulmonary compliance and Vr were significantly decreased,and the airway resistance was increased at T1-3,and the W/D ratio and ROS content were increased,and NAD+ and ATP contents were decreased at T3 in I/R,EI and IL groups (P＜0.05).Compared with I/R and IL groups,the PaO2,pulmonary compliance and VT were significantly increased,and the airway resistance was decreased at T2.3,and the W/D ratio and ROS content were decreased,and NAD+ and ATP contents were increased at T3 in group EI (P＜0.05).The pathologic changes of lungs were significantly attenuated in group EI as compared with group I/R.Conclusion The mechanism by which emulsified isoflurane post-conditioning attenuates lung I/R injury is related to decrease in mitochondrial dysfunction in rats in an in vitro experiment.
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Objective To evaluate the role of α2 adrenergic receptors in dexmedetomidine-induced inhibition of lipid peroxidation during lung ischemia-reperfusion (I/R) injury in rats.Methods Thirty-two isolated rat lungs in which the model of isolated lung perfusion was successfully established,were divided into 4 groups (n=8 each) using a random number table:control group (C group),I/R group,dexmedetomidine group (D group) and dexmedetomidine plus yohimbine group (DY group).The isolated lungs were subjected to 60 min of ischemia and apnea followed by 75 min of reperfusion and ventilation to establish the model of isolated lung I/R injury.From the beginning of reperfusion,2.3 ng/ml dexmedetomidine was added to the perfusion fluid in D group,and 2.3 ng/ml dexmedetomidine and 0.4 μg/ml yohimbine (an α2 adrenergic receptor blocker) were added to the perfusion fluid in DY group.Lung specimens were obtained immediately after the end of reperfusion for determination of the wet/dry weight ratio (W/D ratio),superoxide dismutase (SOD) activity (by using modified pyrogallol autoxidation method) and malondialdehyde (MDA) content (by thiobarbituric acid method) and for examination of the pathological changes (using haematoxylin and eosin staining).Results Compared with C group,the W/D ratio and MDA content were significantly increased,and the SOD activity was decreased in I/R,D and DY groups (P＜0.05).Compared with I/R group,the W/D ratio and MDA content were significantly decreased,and the SOD activity was increased in D group (P＜0.05).Compared with DY group,the W/D ratio and MDA content were significantly decreased,and the SOD activity was increased in group D (P＜0.05).The pathological changes of lung tissues were significantly attenuated in D group as compared with I/R and DY groups.Conclusion The mechanism by which dexmedetomidine inhibits lipid peroxidation is related to activating α2 adrenergic receptors during lung I/R injury in rats.