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PubMed1975

Hemodynamic and ventilatory responses to fentanyl, fentanyl-droperidol, and nitrous oxide in patients with acquired valvular heart disease.

Fentanyl (10 mug/kh) or fentanyl (10 mug/kg) plus droperidol (100 mug/kg) administered intravenously during 20 minutes to adult patients with acquired valvular heart disease produced minimal circulatory changes. The trend during drug infusion was for mean arterial pressure and systemic vascular resistance to decrease, and for cardiac index and stroke volume index to increase without change in heart rate. Central venous pressure increased during drug infusion (P less than 0.05) but decreased to awake levels following controlled ventilation and skeletal-muscle paralysis, probably reflecting thoracoabdominal-muscle rigidity rather than a circulatory response. Hypoventilation during drug infusion necessitated assisted or controlled ventilation, with or without skeletal muscle paralysis, in 14 of 16 patients. Addition of 60 per cent nitrous oxide following fentanyl or fentanyl-droperidol infusion significantly decreased mean arterial pressure, heart rate, and cardiac index. All circulatory changes were similar in direction and extent to those previously found during morphine-nitrous oxide anesthesia. (Key words: Anesthetics, intravenous, fentanyl; Anesthetics, gases, nitrous oxide; Heart, effect of fentanyl, dorperidol, and nitrous oxide.).

Adult↗
PubMed1990

Pharmacodynamic effects of serotonin (5-HT) receptor ligands in pigs: stimulation of 5-HT2 receptors induces malignant hyperthermia.

In pigs, the serotonin-2 (5-HT2) receptor agonist 1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane (DOI), 0.8 mg/kg, induced "psychotic" behaviour (e.g., grimacing, backward locomotion, blank stare) and a muscular syndrome, which is known as malignant hyperthermia (MH) in pigs and humans. This syndrome is characterized by generalized skeletal muscle rigidity, leading to an increase in body temperature, marked acidosis, hyperkaliaemia, cyanosis and elevation of lactate, carbon dioxide and the muscle enzyme creatine kinase (CK) in plasma. In pigs which were selectively bred for susceptibility to MH induction by known triggering agents, such as halothane, the administration of DOI was fatal in 3 out of 5 animals. In genetically susceptible pigs, MH was also induced by 5-methoxy-N,N-dimethyltryptamine (5-MeO-DMT), 0.5-1.8 mg/kg, and D-lysergic acid diethylamide (LSD), 60-110 micrograms/kg. Furthermore, 5-MeO-DMT and LSD induced head shakes in the animals, which had not been observed after DOI and could not be blocked by 5-HT2-antagonists, ketanserin (0.5-5 mg/kg) and ritanserin (1-2.5 mg/kg). The psychotomimetic effects of 5-MeO-DMT could be blocked by ketanserin or ritanserin, which, depending on the dose, also reduced or totally prevented the hyperthermia and metabolic changes induced by 5-MeO-DMT in pigs. Administration of 5-MeO-DMT, 1.8 mg/kg, was fatal in 4 of 5 MH-susceptible pigs, whereas pigs injected with this dosage after pretreatment with ketanserin (0.5-5 mg/kg) or ritanserin (1-2.5 mg/kg) did not die. In pigs from MH-resistant littermates, administration of 5-MeO-DMT was not fatal. Comparison of metabolic changes in susceptible and non-susceptible pigs suggested that the marked increase in plasma potassium, which arises principally from damaged muscle cells, is primarily responsible for the fatal effect of DOI and 5-MeO-DMT in genetically susceptible individuals. In MH-susceptible pigs, which were anesthetized, relaxed and artificially ventilated, 5-MeO-DMT did not induce hyperthermia, thus substantiating that the marked hyperthermia observed in conscious pigs was a result of muscle activation and not due to effects on thermoregulation or blood pressure. The results indicate that hallucinogenic drugs with 5-HT2 agonistic effects trigger a life-threatening syndrome, MH, in genetically susceptible pigs. 5-HT2 antagonists, such as ketanserin or ritanserin, are capable of counteracting the fatality of this syndrome.

Amphetamines↗
PubMed1988

Respiratory muscle dysfunction in Parkinson's disease.

Patients with Parkinson's disease may have more difficulty performing repetitive motor acts than single motor acts because of bradykinesia and skeletal muscle rigidity. We thought that repetitive ventilatory tasks might be similarly limited and that this dysfunction would likely contribute to respiratory muscle fatigue. We studied 9 patients with Parkinson's disease who had no evidence of restrictive or obstructive lung disease and 5 normal age-matched control subjects who performed repetitive, forced inspiratory resistive-loaded tasks. The time a given mean airway opening pressure could be sustained, the incremental oxygen cost of breathing, and the work rate of breathing (W) were measured. Although maximal static inspiratory pressures were comparable in both groups, 8 of the 9 patients could not sustain as high a W in the resistive-loaded tasks as could the normal control subjects (41.0 +/- 23.0 versus 67.7 +/- 29.1 J/min; mean +/- SD, p less than 0.01) and the efficiency of breathing was reduced (2.0 +/- 0.8 versus 3.8 +/- 1.4%; p less than 0.01). These findings are similar to derangements of task performance by peripheral skeletal muscle groups in Parkinson's disease.

Aged↗
PubMed1992

Malignant hyperthermia: a review.

Malignant hyperthermia (MH) is a rare genetic myopathy that was first described as a fatal complication of general anesthesia in 1960. It is estimated to affect approximately 1 in 15,000 pediatric patients and 1 in 40,000 adult middle-aged patients. The mode of transmission is genetic: the severest form is autosomal dominant, and the less severe, autosomal recessive. Thus, both men and women can have MH, although there is a slightly higher incidence in the male pediatric population. Malignant hyperthermia is usually triggered by halogenated anesthetic agents with or without depolarizing muscle relaxants. The classic diagnostic triad consists of skeletal muscle rigidity, metabolic acidosis, and elevated body temperature. The definitive diagnosis is suspected susceptible individuals is revealed by exposing an intact muscle fiber to caffeine and halothane in varying concentrations. An abnormal contracture response is hypothesized to be the result of an increase in the release of calcium ion from the sarcoplasmic reticulum in response to neuronal stimulation leading to a hypermetabolic state. The mainstay of treatment is dantrolene, given either prophylactically in susceptible patients or immediately whenever a malignant hyperthermic episode is suspected.

Dantrolene↗
PubMed1995

[A 75-year-old man with parkinsonism and sudden death].

We report a 75-year-old man with parkinsonism who died suddenly. The patient was well until 64 years of the age when he had an onset of tremor in his left hand. He was treated with a medicine in another hospital, and his tremor subsided. Five years after the onset, he started to note difficulty in fine finger movements and gait disturbance. He tended to lean backward with frequent falls. He was treated with bromocriptine, trihexyphenydil, and L-dops without apparent improvement. He visited our out patient clinic on November 11, 1993 when he was 75 years of the age. Neurologic examination at that time revealed an alert and well oriented man in no acute distress. Higher cerebral functions were intact. In the cranial nerves, he showed restriction in the upward as well as down ward gaze (40% of normal). He showed masking of the face and spoke in small voice. He walked in a stooped posture with small steps; retropulsion was present. Muscle rigidity was moderately positive in the neck, however, no rigidity was noted in the limbs. No abnormal involuntary movements were seen. He showed moderate bradykinesia and difficulty in finger tapping. Muscle stretch reflexes were normally elicited and the plantar response was flexor bilaterally. Sensation was intact. The autonomic nervous system appeared intact. He was treated with 300 mg/day of Sinemet with marginal improvement in his balance. In February 4, 1994, he had a common cold. On the next day, his parkinsonism worsened and he became unable to walk by himself. He was found unconscious in the bathroom on the same day. He was brought to our hospital by an ambulance. Upon arrival, he was unresponsive and was not breathing. Blood pressure could not be measured. Pupils were dilated without reaction to light. Cardiac resuscitation was attempted, however, ventricular fibrillation appeared on an EEG monitor, and he was pronounced dead at eleven o'clock in the morning. The patient was discussed in a neurological CPC, and the chief discussant arrived at the conclusion that the patient had progressive supranuclear palsy because of vertical gaze palsy, axial rigidity, and poor response to levodopa. Regarding the cause of his sudden death, the chief discussant thought that he developed pulmonary embolism. Postmortem examination revealed non-bacterial thrombotic endocarditis in the heart, but this did not appeared to be related to his sudden death. Multiple disseminated small emboli were found occluding small arteries of the left lung; this was consistent with acute pulmonary embolism, and this was thought to be the cause of his sudden death. In the central nervous system, marked atrophy of the globus pallidus was noted; both internal as well as external segments showed marked atrophy; no myelinated fibers were seen in the globus pallidus. Neuronal cell loss was marked in the globus pallidus, the subthalamic nucleus, and the substantia nigra. No Lewy bodies or tangles were seen. The histologic diagnosis was consistent with pallido-nigro-luysian atrophy. Brownish pigments such as seen in Hallervorden-Spatz disease were seen in the globus pallidus. In addition, formy spheroids were seen in the substantia nigra. However, iron deposits were not so strong as to suggest Hallervorden-Spatz disease. Pallido-nigro-luysian atrophy is a rare neurodegenerative disorder. It is interesting to note that this condition may mimic progressive supranuclear palsy or pure akinesia clinically.

Aged↗
PubMed1993

The ischiocavernosus and bulbospongiosus muscles in mammalian penile rigidity.

The role of the perineal muscles in erection physiology is currently controversial. Specifically, confusion persists as to the function, if any, the ischiocavernosus (IC) and bulbospongiosus (BS) muscles possess in nonejaculatory erections. An extensive review of the evidence for and against such an erectile role across five orders of mammalian species indicates that the IC muscles create rigidity by producing suprasystolic intracavernous pressures. The BS muscles, on the other hand, are primarily involved in expelling semen during ejaculation. Beckett and coworkers were the first to demonstrate a clear relationship between IC muscle contractions, suprasystolic intracavernous pressures and rigidity. This Beckett model is used to differentiate an erect phase from a rigid erect phase in the erection cycle. The involvement of these muscles in sleep-related erection physiology is also reviewed. Clinical implications and directions for future research are discussed.

Animals↗
PubMed1998

An early onset muscular dystrophy with diaphragmatic involvement, early respiratory failure and secondary alpha2 laminin deficiency unlinked to the LAMA2 locus on 6q22.

We present four subjects from one family and one subject (with an affected sibling who had died) from a second, unrelated family, with early onset, Duchenne-like, muscular dystrophy who presented with proximal girdle weakness, calf and generalized muscle hypertrophy, selective wasting of the sternomastoid muscles, rigidity of the spine and contractures of the tendo Achilles. Intellect was normal. Serum creatine kinase was grossly elevated and the muscle biopsies showed a dystrophic picture. All five subjects have developed early respiratory failure due to severe diaphragmatic involvement; two have already died aged 4 and 7 years of age and the remaining three are dependent on night time ventilation. There has been very little deterioration over time in the skeletal muscle function, and the survivors remain ambulant, the oldest being 11 years. Immunocytochemical studies of the muscle biopsy showed a normal pattern for dystrophin and the dystrophin-associated glycoproteins, but a reduction of the laminin alpha2 chain of merosin. Magnetic resonance imaging of the brain was normal. The disease did not link to the LAMA2 locus for laminin alpha2 on chromosome 6q, so that these families seem to represent a new form of autosomal recessive muscular dystrophy with a secondary merosin deficiency. The primary protein deficiency has not yet been identified.

Age Factors↗
PubMed2006

Effects of caffeine, halothane, and 4-chloro-m-cresol on skeletal muscle lactate and pyruvate in malignant hyperthermia-susceptible and normal swine as assessed by microdialysis.

BACKGROUND: Skeletal muscle fibers from malignant hyperthermia (MH)-susceptible humans and swine are markedly more sensitive to ryanodine receptor (RyR1) agonists than those from normal individuals. Reproducible shifts in the dose-response of skeletal muscle to caffeine and halothane are the basis of the current in vitro diagnostic caffeine-halothane contracture test. In an attempt to develop a less invasive MH diagnostic test, the authors determined the effects of RyR1 agonists (caffeine, 4-chloro-m-cresol [4CmC], and halothane) on the adductor muscle with respect to the lactate-pyruvate (L/P) system that was percutaneously dialyzed using a microdialysis technique in homozygous MH-susceptible compared with normal swine. METHODS: Animals were anesthetized (ketamine-propofol) and artificially ventilated. Sets of six CMA/20 microdialysis catheters were implanted; each catheter was perfused with different RyR1 agonist concentrations. After a 30-min equilibration after implantation, one of the catheters was perfused (2 microl/min) with vehicle (0.9% saline or lipid emulsion), and the other five were perfused with caffeine (1-64 mM), 4CmC (0.1-8 mM), or halothane (prepared in lipid emulsion; 10-500 mM). Outflow dialysate fractions collected at 10-min intervals and L/P parameters were measured enzymatically. RESULTS: Only in the MH-susceptible group did all RyR1 agonists increase dialysate L/P in a dose-dependent manner. The dose-effect relations were most prominent with 4CmC. With the halothane lipid emulsion, data scatter was high compared with that of the caffeine group and especially the 4CmC group. There were no signs of global muscle rigidity, systemic hypermetabolism, or a clinical MH episode during microdialysis RyR1 perfusion. CONCLUSIONS: The authors data demonstrate that the in vivo muscle microdialysis of the porcine L/P system reveals distinct differences between MH-susceptible and MH-normal muscle, especially in response to highly specific RyR1 agonists such as 4CmC. The microdialysis L/P technique seems to have an MH diagnostic potential in the clinical setting.

Anesthesia, General↗
PubMed2003

A case of malignant syndrome associated with a parkinsonism patient.

Malignant syndrome is usually triggered by an excessive use of neuroleptics and dehydration. In the patients with Parkinson's disease, it is sometimes provoked by discontinuation of anti-Parkinsonism agents. Nevertheless, there are few reports describing malignant syndrome in Parkinson's disease patients and no typical therapeutic strategy had been established in such cases. We recently experienced a case of malignant syndrome associated with a familial Parkinsonism patient, which was brought about by surgical invasion and a break in the administration of anti-Parkinsonism agents. Respiratory muscle paralysis, megacolon, and nocturnal delirium observed in this patient might have partially resulted from the use of dantrolene administered during the course of the treatment. Since an increase in the sensitivity to certain drugs is presumed in Parkinson's disease patients, we should be sufficiently cautious about drug administration. We should administer dantrolene, recognizing the fact that the use of dantrolene is one of the symptomatic treatments for muscle rigidity.

Antiparkinson Agents↗
PubMed2003

[Botulinum toxin A in the treatment of stiff man syndrome].

Stiff-Person Syndrome (SPS) is a very rare disorder characterised by progressive fluctuating muscle rigidity and episodic spasm. So far, only two reports have demonstrated a significant clinical improvement in the patients with SPS when muscle were injected with Botulinum Toxin A (BTA). We investigated the effectiveness of intramuscular injections of BTA in a patient with clinical, biochemical and electrophysiological evidence of SPS. A 41-year-old woman with coexisting epilepsy and insulin-dependent diabetes mellitus was hospitalised in our Department because of stiffness and paroxysmal spasm of trunk and proximal limbs muscles. Because of not sufficient results of the pharmacological treatment the injections of BTA into involved muscles were done. Clinical observations included measure of pain, frequency of spasm, well-being and selection's activities were performed at baseline and in 1, 2, 7, 11, 16, 20, weeks. Significant improvement started one week after injections and lasting about 4 months was observed. Using BTA injections into involved muscles for the treatment of SPS can be followed by marked functional improvement and reducing the need for systemic drugs.

Adult↗
PubMed1984

[A comparison of the effects of baclofen and some other muscle relaxants on alpha-rigidity in rats].

Muscle relaxant effects of baclofen were compared with those of dantrolene, diazepam, chlordiazepoxide and tolperisone. When administered intraduodenally (i.d.), baclofen and dantrolene but not diazepam suppressed the sustained rigidity of forelimbs in anemically decerebrated rats, and ED50 values of the former two drugs were 2.9 and 22 mg/kg, respectively. Baclofen, dantrolene and diazepam reduced the phasic rigidity of the decerebrated animals induced by mechanical stimulation of hindlimbs, with their respective ED50 values of 6.2, 140 and 1.4 mg/kg, i.d. Both the rigidities were almost insensitive to chlordiazepoxide and tolperisone. With the exception of tolperisone, these drugs also produced a muscle relaxation in intact animals as measured by traction (rats), rotarod (mice), and grip-strength (mice) tests. ED50 or eD25 values were calculated to be in the following ranges: 5.6 approximately 12 mg/kg, p.o. for baclofen, 15 approximately 35 mg/kg, p.o. for dantrolene, 2.1 approximately 6.5 mg/kg, p.o. for diazepam and 33 approximately 64 mg/kg, p.o. for chlordiazepoxide. These results suggest that baclofen, unlike other drugs, may be effective in reducing both tonic and phasic rigidities at lower doses than those causing muscle relaxation in intact animals.

Animals↗
PubMed1999

A halothane test to detect turkeys prone to developing pale, soft, and exudative meat.

The turkey industry suffers from pale, soft, and exudative meat (PSE) that is unsuitable for further processing because of excessive color variation, poor meat binding, and depressed water holding ability. This condition is caused by accelerated postmortem muscle metabolism and is thought to be related to a similarly inherited condition in swine. A quick, nondestructive method of screening animals is needed to avoid further propagation of PSE in breeding flocks. In this study, a halothane test used with swine was evaluated as a possible detection method for PSE-susceptible turkeys. In Experiment 1, a commercial strain of 4-wk-old male turkeys (n = 116) was exposed to 3% halothane gas for 3 min (6 L/min) and examined for leg muscle rigidity. Experiment 2 followed similar testing measures, using two strains of growth-selected turkeys (n = 504). Measurements of pH, R-value (ratio of inosine:adenosine), color, and expressible moisture content were made from each bird's breast fillet to determine whether the muscles of the responding birds would develop PSE characteristics. Five percent of tested birds in the first experiment and 2% in the second experiment exhibited rigid legs, indicating some of the discriminating power of this test. However, the data indicated that the characteristics of muscles from these birds did not differ from those of the nonresponding birds (P < 0.05). Possibly, the birds may need to be screened or slaughtered at a different age or using different methods.

Adenosine↗
PubMed1981

[Possible malignant hyperthermia as reaction to an overdose of myotonolytic, antidepressive and sedative drugs (author's transl)].

A 51-year-old male patient with no history of musculo-skeletal or myopathic abnormalities, but suffering from manic-depressive psychosis, attempted suicide with an overdose of dolpersin hydrochloride (Mydocalm), dipenzepine hydrochloride (Noveril), meprobamate (Mepronox) and nitrazepam (Mogadon). He developed high fever, muscle rigidity, tachycardia, arrhythmias, hypotension and mottled cyanosis, symptoms well-known in persons with malignant hyperthermia, an autosomally inherited disease of skeletal muscle. There is also discussed the manifestation and the symptoms of an acute rhabdomyolysis. The diagnosis was confirmed by chemical pathological laboratory findings, including respiratory and metabolic acidosis, myoglobinaemia accompanied by myoglobin diuresis, and elevated creatine phosphokinase (CPK values up to 2790 U/l). Electron microscopic examination of muscle tissue revealed signs of myolysis and mitochondrial reactions with pleoconic hyperplasia. No inhalation anaesthetics or skeletal muscle relaxants, such as succinyl choline, were used in this case. Therefore, malignant hyperthermia might have been induced by a combination of drugs which were not known to induce this abnormal muscular reaction. However, the muscle relaxant effect of dolpersin hydrochloride may have acted as a possible inducer of the attack.

Bipolar Disorder↗
PubMed2002

Fatal malignant hyperthermia--delayed onset and atypical course.

A case of malignant hyperthermia (mh) in a 27-year-old man is described. In a first anaesthesia using isoflurane and succinylcholine, the end-tidal CO(2) rose from 39 to 49 mmHg 2.75 h post-intubation and the body temperature rose to 39.8 degrees C 14 h post-intubation but was normal again the next day. In a second anaesthesia using the same medication, the maximal end-tidal CO(2) was 44 mmHg and the body temperature rose to 39 degrees C after 9 h. After 4 days, the fever rose to 40 degrees C, and to 42 degrees C when death occurred 10 days after the second anaesthesia. Masseter spasms or muscle rigidity were never present. According to the death certificate, death was due to multi-organ failure from sepsis. At autopsy, the skeletal muscles were pale and oedematous. Histology demonstrated focal necroses in the skeletal muscles, shock kidneys with myoglobin excretion and myoglobin clots in small blood vessels of the lungs. Hence, the postmortem diagnosis "malignant hyperthermia" was established but accusations of medical maltreatment were rejected because of the atypical and protracted clinical course and because uncharacteristic signs of malignant hyperthermia were attributable to the clinically suspected sepsis.

Adult↗
PubMed1977

Congestive cardiomyopathy in uraemic patients on long term haemodialysis.

Five uraemic patients who developed progressive cardiac failure with clinical evidence of congestive cardiomyopathy at the start or during haemodialysis treatment were studied. The diagnosis of cardiomyopathy, for which there was no apparent cause, was confirmed by angiocardiographic and haemodynamic studies. These showed a significant increase in left ventricular end-diastolic volume over normal values obtained in 12 patients without uraemia. The mean velocity of myocardial fibre shortening was significantly decreased, as was the index of normalised rigidity. Three of the five patients presented the complete picture of the disease. The other two also had considerable ventricular dilatation and a decreased index of normalised rigidity but normal ejection fraction and only moderately decreased myocardial contractility indices. This suggests that there may be primary involvement of normalised heart muscle rigidity followed by secondary changes in myocardial contractility in uraemic patients with congestive cardiomyopathy.

Adult↗
PubMed2001

Neuroleptic malignant syndrome associated with long-term clozapine treatment: report of a case and results of a clozapine rechallenge.

Clozapine has recently been found to be associated with neuroleptic malignant syndrome (NMS) after long-term treatment. Here, I report on a 34-year-old Taiwanese woman who had been diagnosed with schizophrenic disorder 17 years previously. She had received clozapine 250 mg/day monotherapy for 7 years. She had sudden onset of NMS signs with high fever, profuse diaphoresis, severe muscular rigidity, elevated creatine phosphokinase level and consciousness disturbance. Brain computed tomography, blood culture and cerebral spinal fluid studies were negative. She had no muscle rigidity and fever after treatment with normal saline 1500 ml/day and diazepam 30 mg/day for 8 days. On day 15, a rechallenge with clozapine was done with caution because the patient was experiencing auditory hallucinations and delusions of persecution. The dose was slowly increased to 250 mg/day over 18 days. She had no active psychotic symptoms or NMS again in the following year. I reported this case to remind readers of the possibility of induced NMS with long-term use of clozapine and successful clozapine rechallenge.

Adult↗
PubMed1978

Pharmacological profile of N-(2,6-DIMETHYLPHENYL)-N-(1-methyl-2pyrrolidinylidene)urea, xilobam, a new centrally acting skeletal muscle relaxant.

The pharmacological profile of a new centrally acting skeletal muscle relaxant, xilobam, is described and compared to that of existing skeletal muscle relaxants. The potencyof xilobam, administered intravenously, is approximately ten times that of methocarbamol in the linguomandibular assay in the cat. When evaluated in the strychnin assay in the mouse, the potency of xilobam is approximately seven times that of chlorzoxazone and eleven tomes that of methocarbamol and five times that of metaxalone. In contrast to methocarbamol, xilobam exhibits little or no sedative activity and appears devoid of antianxiety properties. When administered to non-anesthetized dogs, xilobam and other centrally acting muscle relaxants, such as chlorzoxazone and methocarbamol, increased arterial pressure and heart rate. Mydraiasis, vocalization and muscle rigidity were concomitantly observed. These effects appear to be centrally induced. It is concluded that xilobam appears to be a potent centrally acting muscle relaxant which should not be sedating or anxiolytic in man.

Animals↗