Fusimotor reflexes to antagonistic muscles simultaneously assessed by multi-afferent recordings from muscle spindle afferents

Several single agonist/antagonist primary muscle spindle afferents were simultaneously recorded in chloralose anaesthetized cats. It was shown that their dynamic and static sensitivity to sinusoidal muscle stretches could be increased or decreased via the fusimotor system by extension and flexion of the contralateral hind limb as well as by stretch of ipsilateral muscles and stimulation of ipsilateral skin nerves. The results seem to support the hypothesis that the primary muscle spindle afferents convey complex multisensory messages to the central nervous system (CNS).     

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     

安吉复口服液的耐缺氧,耐低温和抗疲劳作用

采用缺氧、寒冷和负重游泳等方法,观察了安吉复口服液(0.025、0.1和0.4mg·kg~(-1),ig,qd×14d)对小鼠的耐缺氧、耐低温及抗疲劳作用.结果表明,安吉复口服液0.1、0.4mg·kg~(-1)可延长KCN中毒小鼠的存活时间及延长小鼠在寒冷环境中存活时间,而0.4mg·kg~(-1)可延长常压缺氧条件下小鼠存活时间及延长小鼠负重游泳时间.     

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。     

Mechanisms of fatigue in normal intercostal muscle and muscle from patients with myasthenia gravis

Fatigue mechanisms in normal intercostal muscle and muscle from patients with myasthenia gravis (MG) were evaluated by monitoring the compound muscle action potential (CMAP) and tetanic tension responses to repetitive nerve or muscle stimulation in vitro. When fatigue was induced by nerve stimulation at 30 Hz for 0.5 s every 2.5 s, about half of the original tension decreased after 30 min in normal muscle and 5 min in MG muscle. Analysis of the changes in area of CMAPs and tension indicated that impairment of neuromuscular transmission, muscle membrane excitation, and excitation-contraction (E-C) coupling and contractility accounted for 40%, 29%, and 31% of fatigue in normal muscle, and 83%, 0%, and 17% of fatigue in MG muscle. When fatigue was induced by muscle stimulation at 30 Hz, tension declined by a quarter after 30 min in normal muscle, but by a half after 17 min in MG muscle. Impairment of muscle membrane excitation and E-C coupling and contractility accounted for 58% and 42% of fatigue in normal muscle, and 22% and 78% of fatigue in MG muscle. Thus, fatigue of normal muscle is caused by impairment of at least four processes, and enhanced fatigue of MG muscle is caused by greater impairment of neuromuscular transmission, E-C coupling, and contractility. © 1993 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.