大鼠氧化乐果中毒致呼吸衰竭的实验治疗

目的 探讨不同剂量氯磷定和阿托品联合呼吸机治疗氧化乐果中毒所致呼吸肌麻痹的疗效。方法 所有实验大鼠均给予2LD50的氧化乐果染毒,并以10mg/kg的阿托品有效对抗量碱能症状,当大鼠出现呼吸频率减慢,呼吸困难征象时即行气管插管并辅助机械通气（A组除外）,B组阿托品继续原剂量治疗,C、D、E组氯磷定依次按15、20、40mg/kg于呼吸机治疗即刻及治疗后1、2、3h肌肉注射,阿托品减至首剂量的1／3－2／3,以维持阿托品化为度。经联合治疗后1、2、3h试行脱机,若大鼠在上述时间中任何一次脱机＜60min,则视为联合治疗成功,一镒脱机后大鼠存活超过60min或第3次脱机后迅速死亡,均需取游离膈神经膈肌标本经MS－302生理药理分析仪作膈肌功能测定。结果 B组膈肌功能恢复不佳,无一只大鼠脱机成功;C组膈肌功能恢复良好,3h脱机成功率高达100％;D、E两组虽膈肌功能测定也较好,但脱机成功率极低,结论 只有适量氯磷定联合阿托品并辅助呼吸机治疗氧化乐果中毒所致的呼吸肌麻痹,才能加速中毒大鼠膈肌功能恢复,大大降低中毒大鼠病死率。     

内毒素血症大鼠膈肌功能障碍和肌浆网钙泵基因表达的变化

目的探讨内毒素血症大鼠膈肌功能和膈肌肌浆网钙泵基因(SERCA)表达的变化。方法直接采用腹腔注射内毒素12 mg/kg建立大鼠内毒素血症模型,32只成年雄性SD大鼠随机分成四组:生理盐水对照组和内毒素24 h组,48 h组,96 h组,即分别在注射内毒素24、48、96 h后处死大鼠,应用体外灌流大鼠膈肌条的方法,分别测量其单收缩张力(Pt)、最大强直张力(Po)、峰值收缩时间(CT)、半舒张时间(1/2RT)、张力-频率曲线,电镜观察大鼠膈肌超微结构,采用RT-PCR检测大鼠膈肌SERCA mRNA表达。结果大鼠膈肌的各项力学指标:单收缩张力和最大强直张力,内毒素血症组较对照组明显降低(P<0.01);单收缩的峰值收缩时间和半舒张时间,内毒素血症组较对照组明显延长(P<0.01);在给予大鼠膈肌条10、20、40、60、100 Hz刺激时,内毒素血症组的大鼠膈肌各频率下的收缩张力明显低于对照组(P﹤0.01);超微结构显示内毒素对大鼠膈肌组织损伤明显,肌纤维断裂,肌浆网扩张,线粒体水肿,数目减少,脊断裂,空泡化或囊泡化;RT-PCR检测实验结果提示内毒素血症大鼠膈肌SERCA表达较对照组明显降低(P<0.01)。结论内毒素可损伤大鼠膈肌超微结构,导致膈肌收缩和舒张功能障碍,并引起膈肌SERCA基因表达明显降低。     

氨茶碱提高切断膈神经大鼠的通气

氨茶碱(AP)可兴奋呼吸.除了对呼吸中枢的作用外,同时亦影响呼吸肌的收缩性.以往曾报道AP 对膈肌的作用,本文观察其对切断膈神经大鼠吸气肌的作用.方法实验用Wistar 种雄性大鼠57只,体重260～320g.全麻后行气管切开术,接微型呼吸流速仪测定呼吸频率、潮气量、气管内压及最大吸气压.于颈部切断双侧膈神经.动物随机分为6组,其中5组静注AP,剂量每公斤分别为5、10、20、40和80mg,第6组静注等量生理盐水作为对照。于膈神     

孕激素对卵巢切除大鼠子宫肌层发育的影响

目的　探讨孕激素对卵巢切除大鼠子宫肌层发育的影响。方法　将4 0只幼年大鼠随机分为A、B、C、D组,每组各10只。A组为假手术组,只行开关腹手术;B、C、D组均切除双侧卵巢,其中C组及D组分别加用大剂量及小剂量孕激素。连续给药6周后,测量各组大鼠子宫重量,用HE染色法加计算机图像分析技术观察子宫内膜、肌层及垂体、肾上腺的组织形态学变化。结果　B组子宫重量明显减轻至(14 5 .0 0±31.0 8) mg,C组子宫重量由(14 5 .0 0±31.0 8) mg增至(5 4 0 .30±86 .30 ) mg;肌细胞直径由(4.83±0 .2 5 ) μm增至(16 .5 2±0 .4 6 ) μm,与B、D组比较P均<0 .0 5。各组大鼠垂体及肾上腺无明显组织学改变。结论　大剂量孕激素可促进卵巢切除大鼠子宫肌层的发育。     

内毒素对大鼠膈肌收缩功能及线粒体超微结构的影响

目的 观察内毒素(革兰阴性菌细胞壁的脂多糖成分)对大鼠膈肌收缩功能及线粒体超微结构的影响,为探索呼吸衰竭发生机制提供新思路.方法 将28只SD大鼠按随机数字表法分为:(1)对照组(10只)气管内灌注生理盐水;(2)实验组气管内灌注内毒素,浓度为200 ?g/ml,剂量为0.5 ml/kg,制备急性肺损伤(acute lung injury,ALI)动物模型,再分为观察4 h(内毒素4 h组,9只)及24 h(内毒素24 h组,9只)2组.然后,取膈肌肌条,用体外电生理方法测定膈肌的最大收缩力、颤搐收缩峰值及疲劳指数.另外取膈肌标本固定后做电镜检测.采用SPSS 15.0统计软件分析数据,组间比较用单因素方差分析及q检验.计量资料以x-±s表示.结果 (1)内毒素4 h组膈肌的收缩力及颤搐收缩峰值[(3.4 ±1.9)及(0.9±0.4)N/cm2,经肌肉横截面积校正]均明显低于对照组[(6.7±4.3)及(2.2±1.7)N/cm2,F值分别为3.59、3.78,P＜0.05];内毒素24 h组膈肌的收缩力及颤搐收缩峰值[(4.1±1.2)和(1.2±0.7)N/cm2]较内毒素4 h组明显恢复.(2)膈肌的疲劳指数在内毒素4 h及24 h组(分别为0.07±0.06和0.12±0.07)均较对照组(0.26±0.14)明显下降(F=9.27,P＜0.01).(3)内毒素4 h组及24 h组电镜下显示膈肌间线粒体肿胀、嵴减少,外膜模糊、变形,部分溶解破坏等超微结构的改变.结论 内毒素可导致ALI大鼠膈肌的收缩力下降并易于疲劳,这可能是导致呼吸功能衰竭的原因之一.     

氧化乐果中毒大鼠膈肌的病理及血肌酸激酶变化

目的:探讨氧化乐果中毒大鼠膈肌损伤致呼吸肌麻痹(RMP)的机制.方法:60只Wistar大鼠随机分为3组:盐水对照组、中毒组、阿托品治疗组,测定各组中毒后24 h血液胆碱酯酶(ChE)和肌酸激酶(CK)水平,观察中毒后不同时间膈肌组织病理及超微结构的改变.结果:中毒组和阿托品治疗组血CK明显升高,部分大鼠膈肌发生坏死.结论:氧化乐果中毒大鼠膈肌损伤严重,膈肌纤维坏死是急性有机磷农药中毒(AOPP)致RMP的可能原因之一.     

不同剂量的氯解磷定联合阿托品对急性敌敌畏中毒大鼠的治疗效果

目的:探讨不同剂量的氯解磷定联合阿托品对急性敌敌畏中毒大鼠模型的治疗效果。方法 :将204只健康雄性大鼠按照随机数字表法分为对照组(n=12)、染毒组(n=48)、治疗组(n=144)。对照组给予1 mL生理盐水一次性灌胃。染毒组和治疗组按照30 mg/kg敌敌畏一次性灌胃。治疗组在灌胃后立即腹腔注射阿托品15 mg/kg,同时加以30、45、60 mg/kg的氯解磷定腹腔注射。观察动物中毒表现和存活情况,分别于染毒后2、24、48和72 h处死大鼠,取血标本和肺组织。测定血清中乙酰胆碱酯酶(AChE)、丙二醛(MDA)、超氧化物歧化酶(SOD)的含量;苏木素-伊红(HE)染色观察肺组织病理变化。结果:与染毒组相比,治疗组大鼠翘尾、流涎、肌束震颤、翻正反射消失发生率明显降低,同时存活率增加,且差异具有统计学意义(均P<0.05);与染毒组相比,治疗组大鼠动脉血中AChE、SOD含量增加,MDA含量明显减少,高剂量的氯解磷定效果更明显(均P<0.05)。HE结果显示,氯解磷定治疗组大鼠肺组织损害减轻,炎细胞减少,且高剂量的氯解磷定效果更显著。结论:氯解磷定联合阿托品对急性敌敌畏中毒大鼠具有治疗作用,且高剂量的氯解磷定效果更加明显。     

莪术对大鼠结肠平滑肌收缩的促进作用及机制

目的:观察莪术对离体大鼠结肠平滑肌收缩运动的影响,并初步探讨其作用机制.方法:制备大鼠结肠平滑肌肌条,以9 g/LNaCl溶液(NS)为对照组,观察不同浓度莪术对结肠平滑肌的收缩效应;以莪术为对照组.分别观察酚妥拉明、维拉帕米和阿托品3种阻断剂孵育肌条后,莪术对肌条的收缩效应.结果:莪术高浓度组对离体大鼠结肠平滑肌的促进作用明显,与NS对照组比较,莪术1g/L、10 g/L组引起的肌条最大收缩振幅和曲线下面积均有统计学意义(63.92±2.06,76.27±2.28vs100%;44.09±11.10,55.66±10.29vs100%,P<0.05或<0.01);与单独莪术组比较,阻断剂维拉帕米和阿托品对莪术引起的肌条收缩有抑制作用,其最大收缩振幅和曲线下面积均有统计学意义(87.35%±50.49%,73.80%±9.37%vs 100%,33.97%±15.18%,27.55%±11.56% vs 100%,P<0.05或<0.01).结论:莪术对大鼠结肠平滑肌的收缩活动有兴奋作用,且与剂量呈正相关,其引起的收缩效应可被阿托品和维拉帕米阻断,而未能被酚妥拉明阻断.     

四磨汤对大鼠胃窦平滑肌影响及其机制的研究

临床证实四磨汤可改善胃肠动力障碍疾病的症状。但机制不明。目的：研究四磨汤对大鼠离体胃窦平滑肌收缩活动的影响及其机制。方法：处死Sprague-Dawlev大鼠后收集胃窦纵行和环行平滑肌条,检测不同剂量四磨汤（1μl、5μl、25μl、50μl、100μl、150μl和200μl）对胃窦平滑肌收缩的影响,同时观察M受体阻断剂阿托品（100mol／L）、M受体激动剂乙酰胆碱（10-6mol／L）对四磨汤诱导的胃窦平滑肌收缩的影响。结果：低一中剂量（1～100μl）四磨汤剂量依赖性地诱导大鼠胃窦纵行肌和环行肌收缩增强,但两者之间的作用无明显差异。阿托品可完全阻断四磨汤对胃窦环行肌、纵行肌的促收缩作用,且对环行肌的阻断效应更明显。以乙酰胆碱预处理后,四磨汤对胃窦纵行肌和环行肌的促收缩作用进一步增强．且对环行肌的作用更明显。结论：四磨汤对大鼠胃窦纵行肌和环行肌具有明显的促收缩作用．该作用主要通过M受体介导。     

茶碱对呼吸肌作用的研究进展

茶碱改善呼吸肌功能的作用引起人们极大的关注。除少数资料外,无论在离体试验、动物实验、正常人还是患者中,均证明茶碱能增加健康的或疲劳的膈肌对低频刺激的收缩力。有3份资料提示茶碱还能淡最大强直收缩力增加,这种变化可能取决于最大肌动蛋白-肌球蛋白横桥相互作用中收缩物质的内在潜能,而并非茶碱对于肌肉本身的作用。此外,在体内可达到的血清茶碱浓度并不能使膈肌或其它骨骼的肌力增加。以往所谓茶碱改善呼吸肌的收缩性,系指低频刺激时搐搦性收缩力(Twitch tension)或非融合性强直性收缩力(Unfused tetanic force)增加。最近发现茶碱能促进仰卧位麻醉狗呼气肌的恢复。从而降低肺功能残气量,使膈肌增长,改变膈肌的前负荷。同时胸腹部呼气肌的张力性收缩等增加其吸气肌的后负荷。茶碱是否促进 COPD 患者呼气肌的恢复尚待进一步观察。最近证实茶碱并不能改变大鼠和狗膈肌的最大融合性强直收缩力,而有使狗膈肌的最大强直收缩力减低的趋势。与以前的报道相一致,茶碱可增加搐搦性收缩与强直性收缩的比率和搐搦性收缩的张力。上述作用有种属差异,当茶碱浓度为500mg/L 时大鼠膈肌的搐搦性收缩与强直性收缩比约增加50%;而当     

Hypothyroidism presenting with respiratory muscle weakness

A 58-yr-old woman presented with recurrent chest infections, breathlessness, and orthopnea. She complained of nonspecific tiredness and aching limbs. A chest radiograph showed an elevated right hemidiaphragm. Thyroid function tests showed her to be severely hypothyroid (T4 = 23 nmol/L; TSH greater than 50 mU/L). Measurement of maximal respiratory mouth pressures (expiratory: 50 cm H2O, normal, 94 +/- 33; inspiratory: 15 cm H2O, normal, 71 +/- 27) suggested global respiratory muscle weakness. Severe bilateral diaphragm weakness was demonstrated by a greatly reduced maximal transdiaphragmatic pressure (Pdi) (Pdi Pimax = 0, normal, 65 +/- 31 cm H2O; sniff Pdi = 25 cm H2O, normal, 121 +/- 25). No Pdi was detectable on stimulation of the right phrenic nerve, whereas, on the left, it was 11 cm H2O (normal 7 to 15 cm H2O). Phrenic nerve conduction time was prolonged to both sides (right, 12 ms, left, 10 ms; normal, less than 9.5 ms). The relaxation rate of Pdi after a maximal sniff and after bilateral phrenic nerve stimulation was abnormally slow (7.4%/10 ms, 6.3%/10 ms, respectively). Three months after starting treatment with thyroxine she had become euthyroid, and phrenic nerve conduction times and Pdi relaxation rates had returned to normal. Maximal respiratory pressures, vital capacity, and maximal voluntary ventilation improved progressively on treatment, although maximal respiratory pressures still had not reached the normal range after six months. We conclude that hypothyroidism may present with breathlessness due to respiratory muscle weakness and/or phrenic nerve neuropathy and is reversible with treatment.     

Effect of corticosteroids on diaphragm function and biochemistry in the rabbit

The effects of corticosteroid administration for 2 weeks on diaphragm histology, biochemistry, and function were assessed in the rabbit at rest and during inspiratory loading to respiratory failure, and compared to the extensor digitorum longus and untreated control animals. There were marked pathologic changes in the diaphragm after corticosteroid administration and significant alterations in diaphragm glycogen level (118.7 +/- 2.8 versus 56.2 +/- 1.0 mmol/kg wet weight, p less than 0.01) and lactate level (5.3 +/- 0.3 versus 3.5 +/- 0.4 mmol/kg wet weight, p less than 0.01) with only minimal changes in the skeletal muscle. Although respiratory muscle endurance in the control group increased from 142 +/- 17 min at baseline to 155 +/- 20 at Week 1 and 183 +/- 13 at Week 2 (p less than 0.05), it fell progressively from 135 +/- 19 min at baseline to 99 +/- 5 at Week 1 and 88 +/- 9 at Week 2 (p less than 0.01) in the corticosteroid-treated animals. On the other hand, there was no significant change in resting Pdimax after corticosteroid administration. In addition, there was no significant change in Pdimax, Pdi/Edi ratio, or glycogen level at the point of respiratory failure, but diaphragm lactate levels were increased (8.5 +/- 0.8 versus 5.3 +/- 0.3, p less than 0.05). When variable degrees of diaphragm dysfunction were induced by phrenic nerve pacing and/or thoracoabdominal binding, the degree of biochemical change associated with diaphragm dysfunction was significantly greater in corticosteroid-treated animals. We conclude that corticosteroid administration in the rabbit alters diaphragm histopathology and biochemistry as well as respiratory muscle endurance, but not strength.(ABSTRACT TRUNCATED AT 250 WORDS)     

Endurance training does not affect diaphragm mitochondrial respiration

We sought to determine if chronic endurance training would increase mitochondrial respiration or protein content in rat diaphragm muscle. To this end, 20 male Wistar rats were randomly assigned to control (C) or an 8-week endurance training (T) group, n = 10 per group. At the end of T, VO2 max was 13% greater in T (83.3 vs 73.8 ml X kg-1 X min-1) and peak max power output was 32% greater (2.63 vs 1.98 kg X m X min-1). Mitochondrial specific activities of pyruvate-malate and cytochrome oxidase (expressed per mg mitochondrial protein) in both plantaris and diaphragm were similar in C and T rats, as were ADP/O and respiratory control ratios. When expressed per gram wet weight, whole muscle homogenate oxygen uptake (pyruvate + malate) and cytochrome oxidase activity increased 36 and 23%, respectively (P less than 0.05) in plantaris from T rats but did not change in diaphragm. Control oxidative capacity and mitochondrial protein content in the diaphragm were ca. 2-fold those in control plantaris. Plantaris mitochondrial protein content increased ca. 50% with T while the diaphragm was unaffected. We conclude that: plantaris muscle oxidative capacity adapts to training by increasing mitochondrial protein content, since there was no evidence for functional improvement of existing mitochondria, and in the face of a substantial training effect in whole animal and plantaris, the T stimulus was not sufficient to induce mitochondrial protein changes in the diaphragm. This finding is the result of either a 'pre-adaptation' secondary to the diaphragm's high chronic activity, or a sub-threshold increase in diaphragm recruitment during the exercise conditions studied.     

Diaphragm pacing and continuous positive airway pressure

The effect of changes in continuous positive airway pressure (CPAP) on the tidal volume generation by the diaphragm during electrical stimulation of the phrenic nerves in a quadriplegic patient is presented. Measurements of tidal volume, end-tidal PCO2, arterial PCO2, oxygen consumption, physiologic dead space to tidal volume ratio, diaphragm length, and thoracic and abdominal dimensions were made at values of CPAP from 0 to 20 cm H2O during periods of diaphragm pacing. Total respiratory compliance (TRC) was measured during controlled ventilation with incremental positive end-expiratory pressure (PEEP) from 0 to 20 cm H2O. A significant negative correlation was found between increasing CPAP and generated tidal volumes. This correlation was seen to occur even when TRC was constant at degrees of CPAP from 0 to 7.5 cm H2O. When phrenic nerve stimulation was commenced, oxygen consumption rose significantly from values obtained during controlled ventilation, but there was no significant correlation between changes in CPAP and the rise in oxygen consumption. Using inductance methods, thoracic and abdominal diameters were seen to rise as CPAP was increased. As suggested by the decrease in the length of the vertical and horizontal portions of the diaphragm in the chest roentgenogram, the conformation of the diaphragm also changed. It is suggested that the operating length and conformation of the diaphragm are principal factors affecting tidal volume generation during electrical stimulation of the phrenic nerves.     

Effect of dexamethasone on diaphragmatic and soleus muscle morphology and fatigability

In spite of the extensive use of corticosteroids, its myopathic effect on respiratory muscle is unknown with relation to the dose and duration of therapy. The present study examined the effects of dexamethasone on the morphology and function of respiratory (diaphragm) as compared to skeletal (soleus) muscle. Control rats were compared to those that received low, high and prolonged doses of dexamethasone. Body mass was reduced proportionally to the dose and duration of therapy. Atrophy of the diaphragm was greater than that of the soleus when normalized to body mass. Absolute tension and tension as a function of cross sectional area was significantly (P less than 0.05) less in the diaphragm and soleus at the high and prolonged dosages. Dexamethasone had no effect on fatigability except in the soleus after prolonged treatment. Furthermore, after prolonged therapy, it had converse effects on the Pt and 1/2RT in the diaphragm as compared to the soleus muscle. Dexamethasone improved the recovery times in the diaphragm alone. Our data suggest that dexamethasone weakens the diaphragm and soleus by reducing its mass and apparently also through some effect on the intrinsic contractile apparatus.     

Respiratory failure due to diaphragmatic dysfunction in Charcot-Marie-Tooth disease: a case report]

A 56-year-woman with type 2 respiratory failure due to diaphragmatic dysfunction in Charcot-Marie-Tooth disease (CMT) is reported. The patient, who had a 50-year history of CMT, was referred to our hospital because of nocturnal dyspnea. Arterial blood gas analysis on admission showed marked hypoxia with hypercapnia, and physical examination revealed thoracoabdominal paradoxus in the supine position. Chest radiography revealed elevation of both sides of the diaphragm. The vital capacity and arterial blood gas pressure in the sitting position were markedly higher than those in the supine position. Electrical phrenic nerve stimulation failed to produce any convincing muscle action potential in the diaphragm. These findings suggested that her respiratory failure was induced by both diaphragmatic dysfunction caused by bilateral phrenic nerve palsy due to CMT. Treatment of this patient was started at home with a pressure support ventilator, resulting in satisfactory clinical improvement. In general, respiratory muscle impairment is a rare phenomenon in a patient with CMT. However when a patient with CMT complains of dyspnea or if unexpected heart failure develops, it is important to keep in mind that CMT may be associated with phrenic nerve palsy.     

Respiratory response during arm elevation in isolated diaphragm weakness.

Upper extremity exercise is associated with a significant metabolic and ventilatory cost that is particularly evident in patients with severe chronic airflow obstruction. In these patients abnormal ventilatory muscle recruitment has been hypothesized to relate to impaired diaphragm function resulting from hyperinflation. Similar data have never been reported in patients with isolated diaphragm weakness but without airflow obstruction or hyperinflation, a group that would ideally define the role of diaphragm function during arm elevation (AE). We prospectively studied 15 patients with isolated diaphragm weakness of varying severity (Pdi(sniff), 31.74 +/- 3.75 cm H(2)O) as contrasted with eight normal subjects (Pdi(sniff), 111. 77 +/- 13.35 cm H(2)O) of similar age. Patients with diaphragm weakness demonstrated significant lung volume restriction with normal DL(CO)/VA. There was no difference in resting oxygen consumption (V O(2)), carbon dioxide production (V CO(2)), minute ventilation (V E), and tidal volume (VT) between the two groups; however, a borderline difference in resting breathing frequency (f(b)) (p = 0.056) was evident. Both groups demonstrated a rise in V O(2), V CO(2), and V E during 2 min of AE anteriorly. Normal subjects demonstrated a statistically significant rise in VT but a statistically insignificant rise in f(b) during AE. In contrast, patients with diaphragm weakness demonstrated a statistically significant rise in f(b) during AE but a statistically insignificant rise in VT. In patients the observed rise in VT directly correlated with baseline Pdi(sniff) (r = 0.59, p = 0.02) and Pdi(max) (r = 0.81, p = 0.002). Both groups demonstrated a rise in Pdi during AE. The rise in Pdi during AE directly correlated to Pdi(sniff) in the patients (r = 0.69, p = 0.004). Observed end-expiratory Ppl rose during arm elevation in both the patient group and in the normal control group, but no evidence of a differential response to AE was found. In those patients with greater diaphragm weakness (Pdi(sniff) < 30 cm H(2)O), abnormal respiratory muscle function (lesser rise in Pdi) and a lesser increase in VT during AE were more evident. These data highlight the importance of diaphragm function in determining the metabolic and respiratory muscle response to arm elevation.     

Laparotomy-induced gastric protection against ethanol injury is mediated by capsaicin-sensitive sensory neurons

Laparotomy significantly attenuates ethanol-induced gastric mucosal lesions in the rat. The effects of sensory denervation by capsaicin, indomethacin, atropine, guanethidine, and hexamethonium on laparotomy-induced protection were studied in the rat. Gastric mucosal injury was induced by the intragastric instillation of 1 mL of 75% ethanol. The laparotomy-induced protection against ethanol injury was abolished by sensory denervation by capsaicin (total dose, 125 mg/kg, SC) and also by pretreatment with indomethacin (5 mg/kg, SC). In contrast, pretreatment with atropine (0.5 mg/kg, IP), guanethidine (total dose, 20 mg/kg, SC), or hexamethonium (20 mg/kg, IP) had no significant effect on laparotomy-induced protection. These data indicate that capsaicin-sensitive sensory afferent neurons, but not cholinergic or adrenergic autonomic neurons, mediate laparotomy-induced protection against ethanol injury. The hypothesis is put forward that the protective response to laparotomy arises from a somatovisceral and/or viscerovisceral axon reflex of capsaicin-sensitive afferent neurons. Prostaglandins might play a mediator role in the activation by laparotomy of somatic and/or visceral branches of the afferent neurons.     

Diaphragmatic dysfunction and dyspnoea in amyotrophic lateral sclerosis.

Amyotrophic lateral sclerosis (ALS) is a progressive disorder of unknown origin. Respiratory involvement is the principal cause of death, and dyspnoea is a major source of discomfort. In this study, diaphragm function is described and its relationship with dyspnoea examined in 48 ALS patients (32 male, age 26-80 yrs). The detailed neurological and respiratory evaluation (clinical examination, pulmonary function tests, static pressures, mouth twitch pressures (Pm,t), electromyographic responses to phrenic nerve stimulation and cortical magnetic stimulation were analysed after stratification according to dyspnoea. Dyspnoeic (group I) and nondyspnoeic (group II) patients were similar, bulbar signs being more frequent in group I. Vital capacity was lower in group I (mean+/-SD 67.9+/-22.7 versus 87.9+/-15.6% of the predicted value, p=0.0028), as were maximal static inspiratory pressure (41+/-24 versus 60+/-27% pred, p=0.0242) maximal static inspiratory pressure (18+/-11 versus 32+/-14% pred, p=0.0042), and Pm,t (3.71+/-2.5 versus 7.26+/-3.45 cmH2O, p=0.0011). Abdominal (Abd) paradox and respiratory pulse were frequent in group I (15 of 25 and 14 of 25) but absent or rare in group II (0 of 23 and four of 23) (p<0.05). The electromyographic responses to phrenic and cortical stimulation were generally abnormal in group I but subnormal in group II. Multivariate analysis selected only signs of diaphragm dysfunction (namely, Abd paradox and abnormal electromyographic responses) as significant predictors of dyspnoea. It is concluded that dyspnoea in amyotrophic lateral sclerosis patients should prompt diaphragm function tests.