Extensive pectoral muscle necrosis after defibrillation: nonthermal skeletal muscle damage caused by electroporation

A 37-year-old Italian male developed a myocardial infarct with subsequent ventricular fibrillation. He was defibrillated seven times with up to 360 Joules. Thirteen days later the patient died of recurrent myocardial infarct due to thrombotic occlusion of the left circumflex coronary artery. At autopsy, necrosis of the right pectoralis muscle was observed. Electroporation is the pathogenetic mechanism of skeletal muscle damage due to multiple defibrillations with high energy levels. Received: 8 January 1998 Accepted: 15 April 1998     

Lactate/H+ transport kinetics in rat skeletal muscle related to fibre type and changes in transport capacity

 Lactate/H⁺ transport kinetics were determined by means of the pH-sensitive probe BCECF in sarcolemmal giant vesicles, obtained from rat skeletal muscle, and related to variations in lactate/H⁺ transport capacity. Vesicle preparations were made from red and white muscles, mixed muscles, denervated muscles, muscles of old rats and rats that had been subjected to high-intensity training, endurance training, repeated exposure to hypoxia, and hypothyroid or hyperthyroid treatments. The lactate/H⁺ transport capacity of red muscles was greater than that of white muscles, and this difference was associated with a higher maximal transport rate (V _max) in red muscles, whereas the K _m was similar in the two muscle types. High-intensity training and hyperthyroidism increased the lactate/H⁺ transport capacity by enhancing V _max without affecting K _m. Similarly, a reduced transport capacity with old age and hypothyroidism was due to a decrease in V _max. The denervation-induced decline in lactate/H⁺ transport capacity resulted from both an increased K _m and a reduced V _max. The present data show that muscle type differences and most changes in the lactate/H⁺ transport capacity are mediated by modifications in V _max, which is expected to represent the number of membrane transporter molecules. K _m is unaffected by most treatments and appears to be independent of fibre type. Received: 10 February 1998 / Received after revision: 21 April 1998 / Accepted: 24 April 1998     

断肢断腕断掌再植后手内在肌挛缩51例分析

探讨断肢断腕断掌再植术后手内在肌挛缩的发病机理,结合临床经验提出分类、预防和治疗方法。方法:对51例断肢(腕、掌)再植,分别采用术中切开骨间肌肌筋膜、掌腱膜及腕横韧带;术后严重肿胀时早期切开骨筋膜室;缺血时间超过10小时者,除上述措施外尚须切断或部分切除拇收肌和骨间肌肌腹。结果:采用上述预防措施后,手内在肌挛缩的发生率明显降低。结论:本症重在预防,如能及时、果断地采取措施,效果良好。一旦发生中、重度手内在肌挛缩应尽早手术。     

Evidence of an abnormal intramuscular component of fatigue in multiple sclerosis

The goals of this study were to investigate muscle fatigue in patients with multiple sclerosis (MS), and to determine the relationships between muscle fatigue, clinical status, and perceived fatigue. The fatigability of the anterior tibial muscle was quantitated in patients and controls during 9 min of intermittent stimulation (used to eliminate central sources of muscle fatigue). During exercise, the decline in tetanic force, phosphocreatine, and intracellular pH was greater in patients than in controls. The compound muscle action potential amplitude did not decrease during exercise, indicating that there was no failure of neuromuscular transmission during fatigue. Thus, the excessive fatigue in MS developed from sources beyond the muscle membrane. Following exercise, the recovery of tetanic force was delayed in patients (a pattern that suggests abnormal excitation–contraction coupling), whereas the recovery of metabolites was complete in both groups. Muscular fatigue was correlated with clinical disability but not with perceived fatigue. These results suggests that fatigue in MS has both central (perception, upper motor neuron dysfunction) and peripheral (impaired metabolism and excitation–contraction coupling) components.© 1995 John Wiley &Sons, Inc.     

Respiratory muscle rigidity in a preterm infant after use of fentanyl during Caesarean section

Fentanyl is in many neonatal intensive care units the sedative of choice. One side-effect is, however, the possibility of muscle and/or chest wall rigidity. A pregnant woman with a critical pulmonary valve stenosis had a balloon dilatation at 26 weeks of gestation. She was put on propranolol, but went into a severe cardiac failure. In week 31, she developed pregnancy induced hypertension. Periodically absent diastolic flow in the umbilical cord was demonstrated. A Caesarean section was performed using fentanyl as analgesia. A boy weighing 1440 g, had a 1 min Apgar score of 3 without respiratory movements. Mask ventilation was tried, but chest wall expansion was not achieved despite using high pressures. He was intubated and positive pressure ventilation attempted, with the same result. Despite the use of high pressures up to 60–70 cm H₂O, no chest movement could be achieved. An intravenous line was established in order to give naloxone and pancuronium. Just before the drugs were given, chest wall movements were achieved and the heart rate normalized. Conclusion This is the first report on chest wall rigidity in a neonate after administration of fentanyl to the mother during Caesarean section. Received: 15 August 1997 and in revised form 30 January 1998 / Accepted 3 February 1998     

Hypertrophy without increased isometric strength after weight training

Summary Eight men (20–23 years) weight trained 3 days week^–1 for 19 weeks. Training sessions consisted of six sets of a leg press exercise (simultaneous hip and knee extension and ankle plantar flexion) on a weight machine, the last three sets with the heaviest weight that could be used for 7–20 repetitions. In comparison to a control group (n = 6) only the trained group increased (P<0.01) weight lifting performance (heaviest weight lifted for one repetition, 29%), and left and right knee extensor cross-sectional area (CAT scanning and computerized planimetry, 11%, P<0.05). In contrast, training caused no increase in maximal voluntary isometric knee extension strength, electrically evoked knee extensor peak twitch torque, and knee extensor motor unit activation (interpolated twitch method). These data indicate that a moderate but significant amount of hypertrophy induced by weight training does not necessarily increase performance in an isometric strength task different from the training task but involving the same muscle group. The failure of evoked twitch torque to increase despite hypertrophy may further indicate that moderate hypertrophy in the early stage of strength training may not necessarily cause an increase in intrinsic muscle force generating capacity.     

Neuroleptic malignant syndrome in the intensive therapy unit

A case of the neuroleptic malignant syndrome occurred in a 40-year-old male after administration of chlorpromazine while on an Intensive Therapy Unit. Treatment with dantrolene sodium was successful, and a muscle biopsy was examined in the recovery phase of the illness. The importance of this condition and the difficulties in establishing a diagnosis at an early stage in patients on an Intensive Therapy Unit are discussed, along with implications for treatment.     

Development of an animal model for neuroleptic malignant syndrome: heat-exposed rabbits with haloperidol and atropine administration exhibit increased muscle activity, hyperthermia, and high serum creatine phosphokinase level

The neuroleptic malignant syndrome (NMS) is a life-threatening complication of neuroleptic treatment. To elucidate the pathogenesis of NMS, an animal model has been developed. Experimental rabbits treated with haloperidol (1 mg/kg) by intramuscular injection, were studied for the diagnostic symptoms of increased muscle rigidity, elevated body temperature, and high serum creatine phosphokinase (CPK) level. Administration of haloperidol (1 mg/kg) and atropine (0.4 mg/kg), and exposure to high ambient temperature (35°C) induced a significant increase in electromyographic activity with muscle rigidity similar to that observed in patients with NMS. Such rabbits also showed elevated body temperature and serum CPK value. In addition to the similarity of the signs and symptoms, all parameters measured (muscle rigidity, body temperature, and serum CPK level) were normalized by dantrolene treatment. The effectiveness of dantrolene in the experimental animal partially confirms the validity of this animal model for NMS. This experimental animal model for NMS may be useful to elucidate the pathogenesis of NMS.     

Muscle growth and myosin isoform transitions during development of a small teleost fish, Poecilia reticulata (Peters) (Atheriniformes, Poeciliidae): a histochemical, immunohistochemical, ultrastructural and morphometric study

The myosin composition of lateral muscle in Poecilia reticulata from birth to adult was studied by ATPase histochemistry and immunostaining with myosin isoform-specific antibodies. At birth the muscle consists of two layers containing developmental isoforms of myosin. In deep layer fibres the developmental myosin is replaced by the adult fast-white isoform soon after birth. In the epaxial and hypaxial monolayer fibres the myosin composition present at birth (J1) is replaced within 3 days by another (J2). In some fibres, this J2 composition is retained in the adult, but in others it is slowly replaced by the adult slow-red muscle isoform. Close to the lateral line, all monolayer fibres are already in transition between the J2 myosin and the adult slow-red form at birth, and rapidly complete the transition to slow-red form. These fibres, together with others generated de novo in an underlying hyperplastic zone, form the red muscle layer of the adult. The pink muscle develops during the first month after birth, and by 31 days it consists of an outer, middle and inner layer. A few middle layer fibres are already present at birth, while the outer layer fibres first appear 3 days after birth. The thin inner layer is probably a transitional form between the middle pink and adult white types, and appears at about 31 days. A morphometric analysis showed that growth of the white muscle occurs principally by hypertrophy. Even at the magnification level of the electron microscope, no satellite cells or myoblasts which could give rise to new fibres were found in the white muscle, except in the far epaxial and hypaxial regions and only in the first 10 days. A zone of hyperplastic growth was also found lying just under the superficial monolayer close to the lateral line, and this presumably contributes fibres to the red and pink muscle layers.     

慢性应激对大鼠血管平滑肌细胞的效应及与焦虑行为的关系

目的探讨慢性精神应激对血管平滑肌细胞的影响及与焦虑行为的关系。方法将38只SD大鼠按照随机数字表随机分为精神应激组(30只)和对照组(8只)。对应激组采用限制应激和饮水冲突应激,持续2个月;分别于应激前、应激后1,2个月用空场实验和高架十字迷宫实验观察大鼠焦虑水平,计算出中央格爬行次数、外周格爬行次数、开放臂进入次数及停留时间、闭合臂进入次数及停留时间。以免疫组化方法测定主动脉血管局部增殖细胞核抗原(PCNA)表达,并用苏木素-伊红染色法观察主动脉结构变化。结果(1)与对照组比较,应激1个月后,应激组大鼠在开放臂的次数和时间、闭合臂的次数少(P<0·05),闭合臂的时间多(均P<0·01);应激2个月后,应激组大鼠在外周格爬行的个数和闭合臂时间多(P<0·01),开放臂时间少(P<0·01)。(2)应激组大鼠主动脉失去原有的正常结构,中层血管平滑肌细胞排列紊乱,数目增多。(3)应激组大鼠血管壁PCNA表达的阳性细胞数为(16485±10694)个/MM2,对照组大鼠为(4012±2256)个/MM2,T=4·359,P<0·01。(4)中度焦虑组大鼠PCNA表达与大鼠焦虑呈正相关(PEARSON相关系数为0·718,P=0·004)。结论大鼠中度焦虑时,其血管平滑肌细胞增殖率与焦虑情绪呈正相关。