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Query: UMLS:C0040822 (tremor)
 18,428 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of arotinolol on the incomplete tetanic contractions of the cat soleus muscle was studied. Isoproterenol and epinephrine injected intravenously decreased the tension and degree of fusion of incomplete tetanic contractions of the soleus muscle in anesthetized cats. Intravenous arotinolol (> 3 micrograms/kg), propranolol (> 30 micrograms/kg) and pindolol (> 3 micrograms/kg) blocked the effects of isoproterenol and epinephrine, but atenolol (-300 micrograms/kg), prazosin (0.1-10 micrograms/kg) and phentolamine (10, 30 micrograms/kg) did not block them. These results indicate that the receptors involved can be classified as of the beta 2-type. It is proposed that arotinolol may inhibit beta 2-adrenoceptors in the extrafusal muscle fibers of slow muscle, and thereby reduces the amplitude of tremor by changing the incomplete tetanic contractions of the muscle to the complete ones.
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PMID:[Effect of arotinolol on the incomplete tetanic contractions of the cat soleus muscle--relation to its anti-tremorgenic action]. 769 Mar 40

Previous studies have suggested that racial differences may exist in beta-adrenoceptor-mediated responsiveness. However, no clear conclusions can be drawn based on these studies because of the confounding effect of the parasympathetic nervous system on responses to isoproterenol bolus doses. In this study, we blocked the effects of the parasympathetic nervous system with atropine, to determine whether racial differences exist in sensitivity to beta-adrenoreceptor stimulation and blockade. Sixteen healthy black and white men participated in the study. Atropine was administered before all studies to induce parasympathetic blockade. Isoproterenol sensitivity studies and treadmill exercise were then performed in the with and without beta-adrenoceptor blockade by propranolol. Responses measured included heart rate (HR), blood pressure (BP), and tremor. The average isoproterenol dose producing a 25-beat/min increase in HR was more than twofold higher in blacks than in whites (3.4 +/- 1.2 vs. 1.6 +/- 0.4 micrograms, respectively, p < 0.05). There were no racial differences in response to beta-adrenoreceptor blockade. Our results showed that during parasympathetic blockade blacks were less sensitive to the chronotropic effects of isoproterenol than whites. We conclude that these response differences are due to greater beta-adrenoceptor sensitivity in whites than in blacks.
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PMID:Racial differences in beta-adrenoceptor-mediated responsiveness. 772 60

A 21-year-old patient with right basal ganglial AVM was scheduled twice for cranioplasty under general anesthesia (nitrous oxide oxygen isoflurane anesthesia and modified neurolept anesthesia), after a surgery for removal of hematoma from the AVM three months previously. After this operation and before anesthesia for cranioplasties, he showed tremor-like seizure around the left arm and leg about once a day. During anesthesia for cranioplasties, he developed the similar and enhanced seizure frequently in response to intravenous injections of thiopental and midazolam, needle injections into the skin, intratracheal as well as oral suctions and other stimuli. The reason of decreased cerebral perfusion is probably due to the previous operation and administrations of thiopental and midazolam. Because of decreased perfusion around this cerebral lesion, concentrations of the anesthetics might have remained low around the lesion under general anesthesia. Therefore, the resulting hypoxia and prolonged light anesthesia in the basal ganglia, might have enhanced the seizure.
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PMID:[Preexisting seizure was enhanced under general anesthesia in a AVM patient]. 783 12

Tremor has been rarely described as a manifestation of stroke. A 21-year-old left-handed man developed severe action tremor of his distal left upper extremity and hand following a right parieto-occipital intracerebral hemorrhage. Strength of the left upper extremity improved gradually during a 3-month period but a severe action tremor developed. The patient was treated with the cardioselective beta-blocking agent, metoprolol, initially for elevated blood pressure and tachycardia at 25 mg twice daily for approximately 2 months. Metoprolol was then increased at weekly intervals by 25mg twice daily to a total of 100mg twice daily. Tremor intensity decreased clinically and graphically as monitored by a trace test by having the patient attempt to trace a horizontal and vertical axis and scoring the errors. The scores declined weekly from the first week (4,347), second week (3,786), third week (1,088), to the fourth week (484). No adverse cognitive or cardiopulmonary effects were noted. Action tremor should be considered as one of the movement disorders caused by hemorrhagic cerebral infarction. This case responded well to treatment with metoprolol.
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PMID:Metoprolol for action tremor following intracerebral hemorrhage. 808 22

We investigated whether the putative beta 3-adrenoceptors mediated metabolic responses to isoprenaline. Seven normal volunteers received infusions of isoprenaline, a (beta 1, beta 2 and beta 3-agonist), at 0.5-3.0 micrograms/min. They were pretreated with either placebo, 25 mg atenolol (a selective beta 1 antagonist), or 5, 20 and 80 mg nadolol (which blocks beta 1 and beta 2 but not beta 3-adrenoceptors). Isoprenaline markedly (30.6%) increased basal metabolic rate (BMR): this increase was significantly reduced by 25 mg atenolol but not by 5 mg nadolol. Significant beta 2-blockade (from tremor data) occurred with 5 mg nadolol but not with 25 mg atenolol. This suggests that beta 1 but not beta 2-adrenoceptors are involved in the mediating thermogenic effects of isoprenaline. However, the rise in BMR was not totally blocked even by 80 mg nadolol (9.5%), which produced complete beta 1/beta 2 blockade, as evidenced by the elimination of the chronotropic effect of isoprenaline. This implies that the thermogenic response has a non-beta 1/beta 2-mediated component. There were also significant increases in plasma free fatty acids, glycerol, glucose, insulin and lactate, but these were completely abolished by beta 1/beta 2 blockade. Overall, isoprenaline produced an increase in BMR which is only partly due to stimulation of beta 1-adrenoceptors, and which is not associated with beta 1/beta 2-mediated effects on carbohydrate and fat metabolism. This suggests the possibility of thermogenic beta 3-adrenoceptors in man, although their location and role remain unknown.
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PMID:Do beta 3-adrenoceptors mediate metabolic responses to isoprenaline. 825 74

The purpose of the present study was to investigate the presence of putative cardiac beta 3-adrenoceptors mediating chronotropic and inotropic responses in normal subjects. Isoprenaline (a known beta 1, beta 2 and beta 3-agonist) was infused to stimulate cardiac beta-adrenoceptors in the presence of antagonists at beta 1 (atenolol 25 mg) and beta 1/beta 2 (nadolol 5 mg, 20 mg and 80 mg) adrenoceptor subtypes. Dose-ranging with nadolol was performed to evaluate the lowest dose required to produce significant beta 2-blockade, since the higher doses might conceivably cause beta 3-blockade. Doppler echocardiography was used to evaluate stroke distance and minute distance, which are the linear analogues of stroke volume and cardiac output respectively. Nadolol 5 mg produced almost complete blunting of finger tremor (beta 2-blockade) whilst atenolol 25 mg had no significant effect. Chronotropic and Doppler minute distance responses to isoprenaline were consistent with stimulation of both beta 1 and beta 2-adrenoceptors with no evidence of a beta 3-mediated effect. However, isoprenaline produced an increase in systolic blood pressure and left ventricular stroke distance that was not attenuated by a dose of nadolol (20 mg) which produced complete blunting of beta 1 and beta 2-mediated responses. This infers the possibility of functional inotropic or lusitropic beta 3-adrenoceptors in the human heart. This study also brings into question possible differences in the validity of using stroke distance and systolic blood pressure as measures of inotropic response to beta-adrenoceptor stimulation and advocates the use of Doppler echocardiography as an additional tool for this purpose.
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PMID:Investigation of putative cardiac beta 3-adrenoceptors in man. 839 10

A 21-year-old woman presented to the emergency department complaining of head, neck, and abdominal pain after being assaulted. She denied a previous history or significant symptoms of hyperthyroidism. The physical examination was remarkable for lethargy, low-grade fever, tachycardia, facial abrasions, swelling of the anterior neck, and a tremor. A diagnosis of thyroid storm was made. An extensive work up excluded other causes of the patient's tachycardia, altered mental status, and neck swelling. A review of the clinical features and management of thyroid storm is presented. Relatively minor trauma can be a precipitating event for thyroid storm.
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PMID:Thyroid storm precipitated by trauma. 896 88

In the paper we have described a case of acute, unintentional intoxication with clenbuterol, a selective beta 2-agonist. A 21-year-old bodybuilder to improve his physical fitness and to increase his muscle bulk was using clenbuterol in a dose of two tablets (20 mg) daily for a week before poisoning. On a day of acute intoxication he drank orange juice containing 48 tablets (4.8 g) of clenbuterol, which had been placed there by his friends. The patient was admitted to our clinic with tachycardia at rate 160 bpm, headache, dizziness, tremor, sweats, muscle weakness, agitation. Serum potassium concentration was 2.6 mmol/L, blood glucose level 18.7 mmol/L. All the symptoms and biochemical abnormalities disappeared after intravenous treatment with propranolol (1.0 mg) and potassium chloride (60 mmol) within five hour period. This case indicates that more attention should be paid to clenbuterol widely used as a stimulant by athletes, especially by bodybuilders.
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PMID:Acute poisoning with clenbuterol--a case report. 947 4

Cocaine abuse is a well known cause of cerebrovascular complications. An inflammatory vasculopathy hypothesis has been proposed, but the medical literature has only reported a few pathological confirmations. We report a case with a biopsy demonstrating cerebral inflammatory vascular changes that are associated with cocaine abuse. A 21-year-old male, a twice weekly cocaine abuser, developed encephalopathy, apraxia and left hemiparesis with hemisensory loss during the first week after his last cocaine intake; postural tremor and dystonia appeared later. Laboratory data were unrevealing. Cerebral angiography showed a lack of vascularization in the left precentral and central arterial groups. A corticomeningeal cerebral biopsy demonstrated perivascular cell collection and transmural lymphomonocytic infiltration of the small cortical vessels. All symptoms improved with corticosteroid treatment, but 4 years later, the patient returned with a worsening of his encephalopathy and a severe memory impairment, emotional lability and apraxia. A cerebral magnetic resonance image (MRI) showed subcortical and periventricular lesions suggesting ischemic damage in small-size vessel areas as well as cortical atrophy. This new case supports the existence of an encephalopathy associated with vascular inflammatory changes in a cocaine abuser, although more clinical and experimental data are necessary to define its physiopathology.
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PMID:Encephalopathy and biopsy-proven cerebrovascular inflammatory changes in a cocaine abuser. 1021 Aug 20

The effect of nipradilol on the isoproterelol-induced depression of contractions of the soleus muscle of the anesthetized cats was studied. Isoproterenol (0.3 microg/kg) injected intravenously decreased the tension and degree of fusion of incomplete tetanic contractions of the soleus muscle of the anesthetized cats. The effect of isoproterenol was blocked by nipradilol (> or = 3 microg/kg), desnitro-nipradilol (> or = 10 microg/kg) and propranolol (> or = 10 microg/kg), but not by nitroglycerin (10-100 microg/kg). Nipradilol (30 microg/kg) and desnitronipradilol (300 microg/kg) almost completely antagonized the depressor effects of isoproterenol. These results coupled with evidence that nipradilol does not penetrate the blood-brain barrier indicate that nipradilol exerts an anti-tremor action by blocking peripheral beta2-adrenoceptors.
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PMID:The effect of nipradilol on the isoproterenol-induced depression of contractions in the cat soleus muscle. 1062 17


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