Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0040822 (tremor)
 18,428 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

7 alpha-Hydroxysteroid dehydrogenase (EC 1.1.1.159) production by Escherichia coli strain 080 was highest when the organism was grown in brain heart infusion broth at pH 6.5 for 72-96 h with shaking at 37 degrees C. The oxygen consumption rate had a strong effect on the production of this constitutive enzyme. Glucose and lactose at 0.2-0.4%, detergents, and ethylenediaminetetra-acetic acid were found to increase the enzyme production.
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PMID:Optimization of 7 alpha-hydroxysteroid dehydrogenase production by Escherichia coli 080. 225 13

Electromyographic (EMG) recordings of the 6th to 7th intercostal space (thoracic EMG) and abdominal muscles, ventilatory pattern, and the work of breathing were studied in 4 human subjects exposed for 12 days to 46 ATA of helium-oxygen (density = 8.7 g.liter-1) then of nitrogen-helium-oxygen gas mixture (ternary mixture) (density = 11.1 g.liter-1). We found that the respiratory muscle work necessary for eupneic ventilation was multiplied by 4 at 46 ATA. During quiet breathing as well as during forced inspiratory maneuvers, the power spectrum of thoracic EMG shifted to the left in three individuals during the sojourn at maximal pressure, whichever gas mixture was inhaled. This was corroborated by the decreased ratio of EMG power in a high to that in a low band of frequencies. These alterations disappeared at the end of the decompression period, suggesting the existence of inspiratory muscle fatigue at high pressure. Hyperbaric tremor was recorded on the thoracic EMG and was maximal with He-O2 inhalation. It disappeared at the end of the period at 46 ATA (He-N2-O2).
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PMID:Electromyographic study of respiratory muscles during human diving at 46 ATA. 232 17

Eighteen professional divers (age range 24-33 yr, mean 28.3) participated in one simulated dive to 360 meters of seawater (msw) in a helium-oxygen (heliox) atmosphere with equal compression and decompression profiles. All divers were given an extensive neurologic examination before diving. Clinical neurologic symptoms observed during the dives were equilibrium disorder, sleep disturbances, fatigue, nausea, loose stools, stomach pain, tremor, mental disturbances, reduced appetite, and headache. Symptoms were scored individually by each diver. The symptoms were analyzed statistically by factor analysis, which grouped them into four factors. These symptoms are presumably related to functional disturbances in the brain stem and the cerebellum. Factor 3 symptoms (tremor, mental disturbances, reduced appetite) correlated significantly to a history of predive decompression sickness (P = 0.006) and to cerebral concussion (P = 0.023). Three divers were periodically unable to work at bottom due to equilibrium disorder, diarrhea, or nausea. One diver with mild polyneuropathy and slight cerebral atrophy as seen by computerized tomography and another diver with abnormal electroencephalography were periodically unable to work due to equilibrium disorder and nausea, respectively. We advocate that divers with signs of central or peripheral nervous system dysfunction should not be selected for deep diving.
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PMID:Analysis of neurologic symptoms in deep diving: implications for selection of divers. 232 22

Higher doses of inhaled albuterol have been shown to cause slightly more bronchodilatation than standard doses from a metered-dose inhaler in patients with severe chronic airflow limitation. Higher doses, however, carry an increased risk of side effects, and the optimum dose balancing benefit and adverse effects have yet to be established. We have therefore looked at objective and subjective evidence of beneficial and adverse effects after 4 doses of albuterol in 30 patients with chronic bronchitis, severe airflow limitation, and less than 200 ml increase in FEV1 after 200 micrograms inhaled albuterol. Subjects were given placebo, 400 micrograms, 1 mg, 2 mg, and 4 mg albuterol by dry powder inhaler in random order on separate days in a double-blind study, and FEV1, relaxed VC, PEFR, 12-min walk distance, finger tremor, oxygen saturation, heart rate, and arrhythmias were measured at intervals over 6 h. With increasing doses of albuterol, there was a significant dose-related increase in FEV1, VC, and PEFR, the maximal mean changes being 196 ml, 480 ml, and 50 L/min, respectively. The duration of effect was longer with the higher doses. There was a dose-related increase in heart rate, tremor amplitude, and supraventricular ectopic beats and a dose-related fall in oxygen saturation. There was no drug-related effect on the frequency of ventricular ectopic beats either at rest or during the walk tests. The largest increases in walk distance occurred after the 1 and 2 mg doses and the least after the 4 mg dose.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:High-dose inhaled albuterol in severe chronic airflow limitation. 246 83

Recovery from inhalation anesthesia is often marked by the occurrence of postoperative tremor that resembles shivering, which is known to be associated with an increase in oxygen uptake (VO2), CO2 output (VCO2), and minute ventilation (VE). This study determined the time course of the ventilatory changes observed during the first hour of recovery from isoflurane anesthesia. Ten patients (ASA PS 1) scheduled for minor orthopedic surgery (knee arthroscopy) were included in this study. Anesthesia was induced with thiopental (5 mg/kg) and maintained with 70% N2O and isoflurane (1-2%) in oxygen, allowing spontaneous ventilation. In the recovery room, after N2O had been discontinued, patients were connected to a Beckman Metabolic measurement cart, which allowed a continuous monitoring of VE, VO2, VCO2, and PETCO2. Postoperative tremor was observed in all patients within 7.1 +/- 1.2 min (mean +/- SEM) after isoflurane discontinuation and was associated with a marked increase in the following: VO2, from 173 +/- 26 ml/min at the end of anesthesia to 457 +/- 88 ml/min; VCO2, from 149 +/- 18 ml/min at the end of anesthesia to 573 +/- 98 ml/min; and VE, from 6.8 +/- 0.7 l/min at the end of anesthesia to 16.6 +/- 2.8 l/min (values obtained 20 min after isoflurane discontinuation). In three patients during intense shivering, VO2, VCO2, and VE reached peak values higher than 800 ml/min, 1,300 ml/min and 30 l/min, respectively. This study shows that postoperative tremor following isoflurane anesthesia may be associated with prolonged and large increases in oxygen uptake, CO2 output, and minute ventilation.
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PMID:Changes in ventilation, oxygen uptake, and carbon dioxide output during recovery from isoflurane anesthesia. 249 61

Temporal changes of plasma erythropoietin (Epo) in mice exposed to hypobaric hypoxia were studied by a fetal mouse liver cell culture method. Since a colony formation inhibitory activity was found in the mouse plasma, thirteen pretreatment procedures for bioassay were compared and the procedure of shaking with chloroform followed by dialysis was concluded to be the best. When normal mice (P50 = 40.4 +/- 2.2 Torr) were exposed to hypoxia of 350 Torr, the plasma Epo level was elevated, with peak at the 2nd to 3rd day, and afterwards declined gradually. On the contrary, cyanated mice (P50 = 30.1 +/- 1.5 Torr) showed much less of the Epo response when exposed to 350 Torr. Under 200 Torr hypoxia, both mice exhibited a similar and remarkable extent of the response. These results suggest that the renal Epo-producing tissue or its oxygen-sensing system is less hypoxic in cyanated mice than in normal mice under 350 Torr, and that the physiologically optimal oxygen affinity of blood is variable depending on hypoxic degrees. The fact that the inhibitory activity showed an inverse temporal change to that of Epo, suggested a possible important role of this activity in the regulation of erythropoiesis under hypoxia.
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PMID:Temporal changes of plasma erythropoietin level in hypobaric hypoxic mice and the influence of an altered blood oxygen affinity. 263 99

Cultured cells often exhibit alterations in energy metabolism (increased glycolytic activity and decreased oxidative metabolism) during adaptation to the culture environment. The role of hypoxia as a mediator of these effects was examined by comparison of metabolism in primary rabbit renal proximal tubule (RPT) cultures maintained in stationary culture dishes (DISH), shaking Erlenmeyer flasks (SHAKE), and DISH cultures transferred back to SHAKE conditions (RESHAKE). Both oxidative metabolism and transport capacity were fully preserved in SHAKE cultures over a 24-h period. In contrast, within 6 h, DISH cultures exhibited a continuous decline in transport-dependent and -independent oxygen consumption, respiratory capacity, and ATP and K+ contents. The loss of oxidative metabolism in DISH cultures was accompanied by stimulation of lactate production, detectable within 1 h after plating. Comparison of metabolic properties of DISH cultures to those of RPT exposed to graded levels of hypoxia suggested that medium oxygen tensions may be as low as 1-3% in DISH cultures. RESHAKE cultures exhibited metabolic properties comparable to those of SHAKE cultures, indicating reversibility of DISH culture metabolism on reoxygenation. We concluded that DISH cultures rapidly become hypoxic as a consequence of static culture conditions. Shaking suspension cultures may provide a more metabolically appropriate model for long-term in vitro studies.
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PMID:Glycolytic and oxidative metabolism in primary renal proximal tubule cultures. 276 94

The clinical use of interleukin-2 (IL-2) is limited by severe cardiopulmonary dysfunction. This study examines the mechanism of respiratory failure related to IL-2, using sheep with chronic lung lymph fistulae. Awake animals were infused with an intravenous (I.V.) bolus of IL-2 10(5) U/kg (n = 5) or its excipient (EXC) control (n = 3), every 8 hours for 4 to 5 days. Cardiopulmonary function was monitored daily for at least one 8-hour period. Within 2 hours after each IL-2 administration, mean pulmonary arterial pressure (MPAP) rose. On Day 1, the mean rise was from 13 to 26 mmHg (p less than 0.05), and on Day 5, to 29 mmHg (p less than 0.05). MPAP returned to baseline levels after 2-3 hours. Pulmonary arterial wedge pressure was unchanged from 4 mmHg. There were transient falls in arterial oxygen tension, from 88 to 77 mmHg on Day 1 and to 73 mmHg (p less than 0.05) on Day 5. Lung lymph flow (QL) rose from 2.4 to 6.8 ml/30 minutes (p less than 0.05) on Day 1, and from 4.7 to 10.2 ml/30 minutes (p less than 0.05) on Day 5, whereas the lymph/plasma protein ratio increased on Day 1 from 0.69 to 0.83 (p less than 0.05) and from 0.63 to 0.71 (p less than 0.05) on Day 5. This documents an increase in pulmonary microvascular permeability. Thromboxane (Tx)B2 levels increased transiently after each IL-2 injection in plasma from 195 to 340 pg/ml (p less than 0.05) and in lung lymph from 222 to 772 pg/ml (p less than 0.05) on Day 1, and to similar levels on Day 5. There was a progressive rise in cardiac output from 5.7 to 8.6 1/minute (p less than 0.05) during the 5 days of infusion. Systemic blood pressure did not change. Temperature rose from 39.1 to 41.2 C (p less than 0.05), and shaking chills were common. There was a progressive fall in leukocyte count, from 8.4 to 3.2 X 10(3)/mm3 (p less than 0.05) by Day 5, reflecting a 77% fall in lymphocytes. Lung lymph lymphocyte counts rose, and lymphocyte clearance increased.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The rapid induction by interleukin-2 of pulmonary microvascular permeability. 278 63

Interleukin (IL)-2 administration leads to respiratory dysfunction due to increased vascular permeability. This study examines the role of thromboxane (Tx)A2 in IL-2 induced lung injury in sheep with chronic lung lymph fistulae. This preparation enables evaluation of permeability prior to the development of gross edema. IL-2, 10(5) units/kg (n = 6), or its excipient control (n = 5) was given as an i.v. bolus over 2 min. After 2 h of IL-2 administration, plasma TxB2 increased from 168 to 388 pg/ml (P less than 0.05) and lung lymph TxB2 from 235 to 694 pg/ml (P less than 0.05). Mean pulmonary artery pressure (MPAP) rose from 13 to 29 mm of Hg (P less than 0.05) at 30 min and remained elevated for 4 h while the pulmonary artery wedge pressure was unchanged at 4 mm of Hg. Arterial oxygen tension (PaO2) fell from 88 to 77 mm of Hg (P less than 0.05). Lung lymph flow (QL) rose from 2.2 to 3.8 ml/30 min (P less than 0.05) at 1 h and to 6.4 ml/30 min at 3 h. This rise coincided with an increase in the lymph/plasma (L/P) protein ratio from 0.67 to 0.77 (P less than 0.05). In contrast, the non-IL-2-infused sheep (n = 3) recruitment of the lung vasculature by left atrial balloon inflation led to a rise in QL from 2.4 to 8.2 ml/30 min, whereas the L/P ratio declined from 0.62 to 0.25, suggesting that the protein-rich lymph flow after IL-2 administration reflected increased microvascular permeability. In further proof of an increase in permeability, IL-2 administration into sheep (n = 2) with an inflated left atrial balloon led, after a pressure-independent L/P protein ratio had been achieved, to an increase in L/P protein ratio and decrease in protein reflection coefficient. At 2 h after IL-2, the blood leukocyte count fell from 8156 to 4375/mm3 (P less than 0.05) primarily due to a 73% drop in lymphocytes. The platelet count declined from 292 to 184 x 10(3)/mm3 (P less than 0.05). Body temperature rose from 38.9-40.3 degrees C (P less than 0.05), and shaking chills were common. Pretreatment with the Tx synthetase inhibitor OKY 046 (n = 7) lowered baseline plasma and lymph TxB2 levels to 22 and 52 pg/ml (P less than 0.05) and prevented the IL-2-induced increase in plasma and lung lymph TxB2 (P less than 0.05).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Role of thromboxane in interleukin 2-induced lung injury in sheep. 278 52

Beta 2-Agonists are safe and effective bronchodilator drugs. Their major adverse effects of skeletal muscle tremor, tachycardia and various metabolic effects are mediated by beta-adrenoceptor stimulation and are reversible. Skeletal muscle tremor is the most frequent dose-limiting side effect. It may be reduced by commencing treatment with a low dose and if it persists another beta 2-agonist may be tried. Other side effects such as cardiac arrhythmias and reduction in PaO2 are a serious potential problem in some susceptible asthmatics. However, they are infrequent or of a mild degree and are generally outweighed by the good control of asthma produced by beta 2-agonists. Side effects from beta 2-agonist therapy can be minimised by use of the inhaled route which selectively delivers the drug to the airways. Furthermore, selective tolerance develops to their side effects. The dose of a beta 2-agonist should be assessed on the basis of therapeutic effect and the level of tolerance to its side effects. Recommended doses of beta 2-agonists used for long term therapy do not cause clinically significant desensitisation of airway beta-adrenoceptors, although this may become a relevant problem in patients who are regularly receiving very high doses. Intravenous beta 2-agonists have a place in the treatment of severe asthma not responding to nebuliser therapy. In this life-threatening situation with severe airflow obstruction, monitoring of heart rate, PaO2, plasma potassium and the electrocardiogram should be mandatory and supplemental oxygen given so that serious adverse effects are presented.
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PMID:Adverse reactions to beta 2-agonist bronchodilators. 287 44


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