阻塞性睡眠呼吸暂停低通气综合征患者腭帆张肌中半胱氨酸天冬氨酸蛋白酶3表达及意义

目的观察阻塞性睡眠呼吸暂停低通气综合征(OSAHS)患者腭帆张肌中半胱氨酸天冬氨酸蛋白酶3(Caspase-3)mRNA及蛋白表达水平,探讨OSAHS患者上气道扩张肌凋亡情况。方法选取30例OSAHS患者为实验组,1 0例排除OSAHS的慢性扁桃体炎患者为对照组。采用实时荧光定量RT-PCR和Western blot方法检测两组腭帆张肌中Caspase-3的mRNA及蛋白的表达水平。结果①实验组Caspase-3的mRNA及蛋白表达水平明显高于对照组,差异有显著性意义(t=6.71,P<0.05;t=12.63,P<0.05);②实验组Caspase-3蛋白表达水平与呼吸紊乱指数呈正相关(r=0.789,P<0.01)。结论 OSAHS患者腭帆张肌存在肌纤维凋亡现象,且随着病情加重,凋亡程度也加重。     

OSAHS患者腭帆张肌失神经现象研究

目的:观察OSAHS患者腭帆张肌中神经细胞黏附分子(NCAM)mRNA及蛋白的表达水平,探讨OSAHS患者腭帆扩张肌失神经变化的情况。方法:选取30例OSAHS患者为实验组,10例排除OSAHS的慢性扁桃体炎患者为对照组。采用实时荧光定量RT-PCR和Western blot方法检测患者腭帆张肌中NCAM mRNA及蛋白的表达水平。结果:①实验组NCAM mRNA及蛋白的表达水平均明显高于对照组,差异有统计学意义(均P<0.05);②实验组NCAM蛋白的表达水平与AHI呈正相关(r=0.803,P<0.01)。结论:OSAHS患者腭帆张肌肌纤维存在失神经变化现象,且随着病情加重,失神经的程度也加重。     

阻塞性睡眠呼吸暂停低通气综合征腭帆张肌失神经变化

目的通过研究阻塞性睡眠呼吸暂停低通气综合征（OSAHS）患者腭帆张肌中钙蛋白酶-1（calpain 1）和神经细胞黏附分子（neural cell adhesion molecule,NCAM）的表达以及运动终板形态改变,探讨OSAHS患者上气道扩张肌失神经变化。方法选取30例OSAHS患者作为实验组,10例排除OSAHS的慢性扁桃体炎患者作为对照组。通过乙酰胆碱脂酶（acetylchelin esterase,AchE）染色法显示运动终板形态变化,免疫组化Elivison二步法检测腭帆张肌中calpain 1和NCAM的表达。结果①OSAHS组运动终板数量明显减少甚至消失：②calpain-1和NCAM的表达水平明显高于对照组,差异有显著性意义（P〈0．05）;③calpain1和NCAM的表达水平均与呼吸紊乱指数呈正相关（r=0．811,P=O．000：r=0．692,P=0．000）。结论OSAHS患者上气道扩张肌存在失神经支配病变,且病情越重失神经的程度也越严重。     

睡眠状态下阻塞性睡眠呼吸暂停低通气综合征患者上气道扩张肌肌电活性的变化

目的：观察睡眠状态下阻塞性睡眠呼吸暂停低通气综合征（OSAHS）患者上气道扩张肌肌电活性的变化,探讨其在OSAHS中的作用及意义。方法：对中、重度OSAHS患者69例（OSAHS组）及健康志愿者20例（对照组）于诱导睡眠后分别行颏舌肌、腭帆张肌和腭帆提肌等上气道扩张肌肌电图的检测并与诱导睡眠前比较。结果：（1）清醒状态下OSAHS组上气道扩张肌肌电水平较对照组高（均P〈0．01）;②与清醒状态比较,睡眠状态下OSAHS组上气道扩张肌肌电水平显著下降（均P〈0．01）;③从清醒状态到睡眠状态,OSAHS组上气道扩张肌肌电水平下降幅度明显大于对照组（均P〈0．01）。结论：OSAHS患者清醒状态下上气道扩张肌肌电活性代偿性升高及睡眠状态下失代偿是该病发生的重要病理生理机制。     

阻塞性睡眠呼吸暂停低通气综合征腭帆张肌病理形态学研究

目的 通过研究阻塞性睡眠呼吸暂停低通气综合征(OSAHS)患者腭帆张肌病理形态学改变,探讨腭帆张肌病理变化与失神经支配的关系。方法 经PSG检查确诊OSAHS患者30例,通过HE、Masson、胆碱脂酶（AchE）染色及透射电镜进行腭帆张肌形态学观察和图像分析,并与10例慢性扁桃体炎患者作比较。结果 OSAHS患者腭帆张肌的病理变化为肌纤维细胞萎缩,截面积减少,胶原纤维细胞增加,胶原纤维截面积增加,肌肉截面积/胶原截面积比率下降;肌纤维结构紊乱,肌丝溶解,部分Z线呈锯齿状排列,甚至消失,肌原纤维排列紊乱,肌浆网扩张,线粒体聚集,有髓鞘神经纤维水肿,髓鞘部分松解,鞘膜断裂呈葱皮样改变,出现裂隙,见大量异常颗粒沉积;运动终板数量明显减少甚至消失。结论 OSAHS患者腭帆张肌中运动终板及周围神经发生了明显形态学变化,病变程度与肌肉病理变化呈正相关,OSAHS的发生发展可能与腭帆张肌失神经支配有关。     

腭帆间隙解剖学研究与腭咽成形术

目的 研究软腭解剖学,探讨腭咽成形术中病变组织的切除及正常结构的保护,指导手术方式的改良。方法 测量阻塞性睡眠呼吸暂停低通气综合征(obstructive sleep apneahypopnea syndrome,OSAHS) 患者软腭解剖参数71例,非OSAHS成人软腭解剖参数30例;于手术中解剖OSAHS患者部分软腭组织71例,观察OSAHS患者软腭的形态学变化、脂肪及肌肉的分布;取尸体软腭标本6例,行轴位及矢状位连续切片观察。结果 OSAHS患者软腭较正常人明显增长,是形成气道狭窄的重要解剖学基础;软腭粘膜于游离缘折返处、悬雍垂肌与腭帆张肌及腭帆提肌交界处粘膜下组织疏松,是OSAHS患者脂肪沉积的主要部位,有重要的临床意义,将其命名为腭帆间隙。结论 腭帆间隙因OSAHS患者脂肪沉积而扩大,该间隙脂肪组织切除不仅可缩短软腭、扩大咽腔,同时可提高软腭张力,并对软腭功能无明显影响。     

腭帆间隙解剖学研究与腭咽成形术

目的研究软腭解剖学，探讨腭咽成形术中病变组织的切除及正常结构的保护，指导手术方式的改良。方法测量阻塞性睡眠呼吸暂停低通气综合征(obstructive sleep apnea hypopnea syndrome，OSAHS)患者软腭解剖参数71例，非OSAHS成人软腭解剖参数30例；于手术中解剖OSAHS患者部分软腭组织71例，观察OSAHS患者软腭的形态学变化、脂肪及肌肉的分布；取尸体软腭标本6例，行轴位及矢状位连续切片观察。结果OSAHS患者软腭较正常人明显增长，是形成气道狭窄的重要解剖学基础；软腭粘膜于游离缘折返处、悬雍垂肌与腭帆张肌及腭帆提肌交界处粘膜下组织疏松，是OSAHS患者脂肪沉积的主要部位，有重要的临床意义，将其命名为腭帆间隙。结论腭帆间隙因OSAHS患者脂肪沉积而扩大，该间隙脂肪组织切除不仅可缩短软腭、扩大咽腔，同时可提高软腭张力，并对软腭功能无明显影响。     

阻塞性睡眠呼吸暂停低通气综合征患者腭咽肌的病理变化

目的 研究阻塞性睡眠呼吸暂停低通气综合征(obstructive sleep apnea hypopnea syndrome,OSAHS)患者腭咽肌病理变化,探索腭咽肌在OSAHS发病机制中的作用.方法 30例行悬雍垂腭咽成形术的OSAHS患者为实验组(病情中度患者13例,重度患者17例),10例无OSAHS行扁桃体摘除术为对照组.利用电镜对两组患者腭咽肌行超微结构观察,并行免疫组化染色,观察腭咽肌的肌钙蛋白Ⅰ(troponin Ⅰ-SS)含量的改变.结果 透射电镜下可见30例OSAHS患者中29例腭咽肌的标本有不同程度的病理改变,如肌纤维萎缩,细胞核固缩,线粒体增多、固缩,肌纤维明带增宽等;对照组10例中2例仅有轻度的肌纤维萎缩或水肿.免疫组化观察:实验组30例标本有7例肌钙蛋白Ⅰ抗体表达阳性,1例表达强阳性,22例表达弱阳性;而对照组10例标本肌钙蛋白Ⅰ均显示阳性或强阳性表达.计算机图像分析实验组平均((-x)±s,下同)阴性灰度值为146.30±10.72,对照组平均阴性灰度值为107.50±4.81,二者差异有统计学意义(P＜0.05).但13例病情中度患者腭咽肌标本阴性灰度值平均为143.12,17例重度患者标本阴性灰度值平均为148.80,二者差异无统计学意义(P＞O.05).结论 OSAHS患者腭咽肌萎缩等不同程度的病理变化可能是引起患者上呼吸道异常塌陷的重要发病机制之一.     

局部应用糖皮质激素对鼻息肉组织中蛋白激酶C和Bcl-2及Bax蛋白表达的影响

目的:探讨局部应用糖皮质激素对鼻息肉组织中蛋白激酶C(PKC)、抑制凋亡基因Bcl-2和促进凋亡基因Bax蛋白表达的影响及意义.方法:应用免疫组织化学方法检测PKC、Bcl-2和Bax蛋白在16例鼻息肉患者(鼻息肉组)中的表达,并在鼻腔局部应用糖皮质激素治疗4周后观察其表达的变化;以同期手术的6例鼻中隔偏曲患者的下鼻甲黏膜组织作对照组.结果:糖皮质激素治疗前,鼻息肉组中PKC主要表达在嗜酸粒细胞(Eos)、血管内皮细胞及腺体细胞, Bcl-2及Bax蛋白主要表达于鼻黏膜腺体细胞、上皮层及Eos;与对照组相比,PKC、Bcl-2表达有明显差异(P<0.01),鼻息肉组PKC、Bcl-2在使用激素后,表达明显减低;Bax蛋白在使用激素后,表达明显增加.结论:鼻息肉组中PKC及细胞凋亡相关基因表达异常可能与鼻息肉的发生、发展有一定关系,糖皮质激素可能通过抑制鼻息肉组织中PKC的表达,调节相关凋亡基因的表达,减少Eos的浸润,达到治疗鼻息肉的效果.     

阻塞性睡眠呼吸暂停低通气综合征软腭肌肌纤维亚型构成变化的研究

目的:研究阻塞性睡眠呼吸暂停低通气综合征(OSAHS)患者相关的腭肌肌纤维亚型、胶原纤维mRNA表达情况及其病理形态学上的变化.方法:对12例OSAHS患者(实验组)及8例正常人(对照组)使用实时定量PCR方法检测其软腭肌各重链亚型肌纤维及胶原纤维mRNA的表达量.并利用肌肉ATP酶染色技术鉴别软腭肌3种肌纤维亚型Ⅰ型、ⅡA型与ⅡB型,计算各型肌纤维的数目.结果:实验组ⅡA亚型肌纤维mRNA表达明显增多(P<0.01).而Ⅰ型肌纤维在PH4.3染色条件下实验组数目低于对照组(P<0.05).结论:与对照组比较,实验组收缩速度快、收缩力大但持久性差的ⅡA型肌纤维mRNA表达相对增多,ATP酶染色显示收缩速度慢、持久性好的Ⅰ型肌纤维细胞减少.     

A new aspect on the development of chronic middle ear diseases in patients with cleft palate

BACKGROUND: The prevalence of chronic middle ear disease in patients after surgery for cleft palate is about 50%. Aim of the present study was to analyse its morphological and physiological causes to prevent chronic atelectatic otitis media or cholesteatoma. METHODS: 15 adult patients with cleft palate were examined using middle ear microscopy, pure tone audiometry, EMG of the tensor veli palatini muscle and MRI of the Eustachian tube. RESULTS: 8 of 15 patients had chronic middle ear disease. With 13 of 15 patients single motor unit action potentials could be recorded from the tensor veli palatini muscle. MRI of the Eustachian tube revealed two decisive observations in patients with chronic middle ear disease: in 4 patients the pterygoid hamulus could not be detected, in all otitis patients the continuity of tensor veli palatini muscle was interrupted or disturbed by medial or lateral fixation. CONCLUSION: Chronic middle ear disease with cleft palate patients is basically caused by impaired muscular compliance of the Eustachian tube. Thus integrity of hamulus as well as tensor veli palatini muscle must become of crucial interest in cleft palate surgery.     

Functional evaluation of paratubal muscles using electromyography in patients with chronic unilateral tubal dysfunction

Eustachian tube dysfunction is closely related to the development of otitis media and result from several factors including inflammation within the nasal cavity and nasopharynx, adenoid hypertrophy, cleft palate and nasopharyngeal carcinoma. To some extent, eustachian tube dysfunction may be related to weakness of the paratubal muscles, such as the tensor veli palatini and levator veli palatini muscles. The aim of the study is to find out myogenic factors in eustachian tube dysfunction using electromyography (EMG), and to evaluate the clinical feasibility of EMG. Ten patients with unilateral eustachian tube dysfunction were included in this study. The healthy side of each patient was used as a control. EMG tests on paratubal muscles were conducted under the view of a 30° endoscope or fiberoptic laryngoscope. EMG on the tensor veli palatini showed decreased amplitudes on the affected side in one patient during phonation. EMG on the levator veli palatini showed decreased amplitudes on the affected side in two patients during both deglutition and phonation, one patient during phonation only, and two patients during deglutition only. The only patient who had decreased amplitude on EMG of the tensor veli palatini also had decreased amplitude on EMG of the levator veli palatini. In conclusion, although it is generally accepted that the tensor veli palatini plays a major role in opening the eustachian tube, reduced activity of the levator veli palatini may be related to eustachian tube dysfunction. When assessing eustachian tube function, EMG is useful for evaluating myogenic factors.     

阻塞性睡眠呼吸暂停低通气综合征患者的血浆食欲素A水平测定及意义

目的：探讨阻塞性睡眠呼吸暂停低通气综合征（OSAHS）患者血浆食欲素A水平以及手术治疗对血浆食欲素A水平的影响。方法：对54例经PSG确诊的重度OSAHS患者（OSAHS组）行UPPP加舌骨悬吊术,另选择20例年龄、性别、BMI等均相匹配的健康者作为对照（对照组）。采用层析及放射免疫测定法,测定OSAHS患者术前、术后6个月血浆食欲素A水平,分析其与AHI、MAI及最低SaO2的关系及术前、术后血浆食欲素A水平的变化。结果：OSAHS组血浆食欲素A水平显著高于对照组（P〈0．01）,且与AHI、MAI呈正相关（r=0．658,0．464,均P〈0．05）,与最低SaO2呈负相关（r=-0．543,P〈0．01）,54例OSAHS患者术后6个月血浆食欲素A水平明显低于术前（P〈0.01）,且这种差异与BMI无关。结论：OSAHS患者血浆食欲素A水平升高,其原因可能与夜间反复多发作呼吸暂停及低氧血症有关,有效的手术治疗可使血浆食欲素A水平下降。     

The effect of tensor veli palatini stimulation on upper airway patency.

OBJECTIVE: To evaluate the effect of selective electrical stimulation of the tensor veli palatini muscle on upper airway patency. METHODS: Pressure-flow relationships were evaluated, in a feline isolated upper airway preparation, to determine the role of the soft palate musculature on airflow dynamics. The tensor veli palatini muscles were selectively stimulated while monitoring upper airway collapsibility (critical pressure), maximal inspiratory airflow, and the nasal resistance upstream to the flow-limiting site. RESULTS: Tensor veli palatini stimulation resulted (mean +/- SEM) in an increase in maximal inspiratory airflow from 74 +/- 13 mL/s to 93 +/- 18 mL/s (P= .04). The increase in maximal inspiratory airflow was associated with a decrease in critical pressure from -2.3 +/- 1.7 cm H2O to -4.7 +/- 2.7 cm H2O (P= .01) and an increase in nasal resistance from 32.4 +/- 24.3 cm H2O x L(-1) s(-1) to 50.8 +/- 29.7 cm H2O x L(-1) s(-1) (P= .02). CONCLUSIONS: Tensor veli palatini stimulation decreases upper airway collapsibility and is likely an integral component in maintaining airway patency. However, the effects of the isolated tensor veli palatini muscles are less significant than those seen previously with physiologic stimuli such as hypercapnia. These findings suggest that upper airway patency, although contributed to by the tensor veli palatini, requires the coordinated activation of palatopharyngeal muscles to adequately influence upper airway collapsibility.     

Muscular compliance of the auditory tube]

BACKGROUND: The simultaneous electromyographical assessment of innervation patterns of the mylohyoid and the tensor veli palatini muscle is introduced as a new technique for the examination of the auditory tube function. PATIENTS AND METHODS: Clinical studies were performed on 30 healthy volunteers and 50 patients suffering from chronic tubotympanic mucositis and cholesteatoma. Concentric needle electrodes were advanced into the tensor veli palatini muscle through the palate. The mylohyoid muscle was examined using surface electrodes. RESULTS: Innervation patterns of the tensor veli palatini muscle in volunteers were limited to the time interval of the mylohyoid innervation pattern only, i.e., the oral and pharyngeal phases of swallowing. In 14 of the chronic otitis patients these tensor muscle innervation patterns were found outside this interval. CONCLUSION: This observation provides a new pathophysiological explanation for the clinical concept of a relative closing failure of the auditory tube. These results emphasize the significance of coordination in muscular compliance of the tube.     

Bcl-2和Bax在自发性糖尿病小鼠耳蜗中的表达研究

目的观察自发性糖尿病小鼠耳蜗组织细胞凋亡及Bcl-2和Bax基因的表达。方法非肥胖性糖尿病（non-obese,diabetes,NOD）雌鼠分为糖尿病4周组（D4组）、糖尿病12周组（D12组）和正常对照组（C组）。应用吖啶橙-碘化丙啶（AO-PI）荧光染色和DNA缺口末端原位标记法（TUNEL）检测耳蜗凋亡细胞;免疫组织化学法和Western blot技术检测Bcl-2和Bax在糖尿病耳蜗组织中的表达。结果 NOD小鼠耳蜗可见大量凋亡细胞,D12组比D4组明显增多（P〈0.05）;两组底回毛细胞较顶回凋亡率明显增高（P〈0.05）。D4组耳蜗中Bax在细胞浆内呈阳性表达,Bcl-2在细胞核及细胞浆内均呈阳性表达;D12组Bax在细胞核及细胞浆内均呈阳性表达,而Bcl-2在细胞浆内呈阳性表达;与C组比较,D4组Bax与Bcl-2表达显著增高（P〈0.05）,D12组Bax表达显著增高（P〈0.05）,但Bcl-2表达下调（P〈0.05）;D4组Bax表达较D12组显著降低（P〈0.05）,但Bcl-2表达较D12组显著增高（P〈0.05）。结论自发性糖尿病小鼠耳蜗存在明显细胞凋亡,其损伤机制与Bax表达增高及Bcl-2表达降低有关。     

Clinical applications of pharyngeal electroneurography

Electroneurography of soft palate, Eustachian tube and pharynx was carried out in 60 normal adults and 187 patients. This test was performed on the 2-channel Schwarzer 2,000 electromyograph. The 2 cm long concentric needle electrodes were used for recording and were inserted into muscles of glossopalatinus, pharyngopalatinus, tensor veli palatini and levator veli palatini. Four cm long stimulating electrodes were used to stimulate the mandibular branch of trigeminal nerve and pharyngeal branch of vagus nerve. Stimuli of 100 voltage were delivered as rectangular pulses of 0.1-0.2 ms duration at a rate of 1-2 Hz. In normal subjects, the latency of the evoked wave induced from tensor veli palatini by stimulating the mandibular branch of trigeminal nerve was 1.8 +/- 0.6 ms. The latency of the evoked wave induced from levator veli palatini, glossopalatinus, pharyngopalatinus were 1.9 +/- 0.6, 2.0 +/- 0.4, 1.9 +/- 0.7 ms respectively. In 35 patients with paralysis of soft palate and pharynx, no evoked potential could be recorded in 18 cases, meaning complete nerve injury, latency delayed in 10 cases, indicating partial nerve injury, normal latency of evoked potential in 7 cases. One hundred and twenty-four cases of otitis media, 20 cases of myoclonus of soft palate and pharynx and 8 cases of cleft palate were also studied. Their electrogroms were normal. This technique may be used not only to measure nerve conductivity directly but also to make correct diagnosis of neuromuscular disorders of these structures without serious complications.     

凋亡相关蛋白Bcl-2和Bax在慢性鼻及鼻窦炎伴嗅觉障碍患者嗅黏膜中的表达

目的研究Bcl-2和Bax在慢性鼻及鼻窦炎（CRS）伴嗅觉障碍患者嗅黏膜中的表达,探讨其对嗅觉神经元（olfactory receptor neurons,ORNs）凋亡的调节作用。方法采用康涅狄格化学感受临床研究中心所采用的嗅觉检查法——CCCRC（Connecticut ChemosensoryClinical Research Center）对46例行功能性鼻内镜手术的患者进行嗅觉评分并分组：A组,CRS伴嗅觉障碍25例;B组,CRS不伴嗅觉障碍10例;C组,单纯鼻中隔偏曲行鼻中隔矫正术11例。免疫组织化学方法检测Bcl-2、Bax在3组患者嗅黏膜中的表达。结果在ORNs中,A组Bcl-2和Bax表达显著高于B组（q=3.24、4.29,P均〈0.05）和C组（q=8.56、12.99,P均〈0.01）,A组Bcl-2/Bax比值显著低于B组（q=3.76,P〈0.05）和C组（q=6.67,P〈0.01）;在基底细胞中,Bcl-2在3组表达无显著差异（q=0.68、0.69、1.06,P均〉0.05）,Bax在A组的表达显著高于B组和C组（q=9.54、11.98,P均〈0.01）,A组Bcl-2/Bax比值显著低于B组和C组（q=5.48、9.14,P均〈0.01）;在A、B、C 3组ORNs和基底细胞中,Bcl-2/Bax比值与嗅觉评分均呈正相关（rA分别为0.5631、0.8926,rB分别为0.5700、0.7991、rC分别为0.5694、0.8121,P均〈0.01）。结论细胞凋亡参与了CRS伴嗅觉障碍患者ORNs的减少,Bcl-2和Bax在此过程中起了重要的调控作用,Bcl-2/Bax比值决定细胞是否凋亡。