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)

Twenty-three children with advanced cancer refractory to conventional therapy received weekly iv doses of neocarzinostatin for 5 weeks. Doses were escalated from 500 to 6750 units/m2/week. Four types of toxic manifestations occurred: acute reactions consisting of shaking chills with or without fever and cyanosis (rigor), hypersensitivity, vomiting, and marrow depression. Evidence of oncolytic activity was limited to patients with acute leukemia in whom phase II trials at doses between 3000 and 4500 units/m2 appear warranted.
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PMID:Phase I study of neocarzinostatin in children with cancer. 15 67

Pigs in which venous catheters were positioned for long-term use were injected i.v. with high doses of nicotine in physiol. saline. The LD50 was 2.656 mg/kg body weight. Clinical symptoms were mainly: forced respiration, muscular tremor to tetanoid spasms, cyanosis of the skin, salivation and sometimes vomiting. The degree and duration of symptoms were dose-dependent. Ecg changes in anaesthesized pigs following intravenous nicotine injections of 0.126 mg/kg and 0.378 mg/kg at 15 minutes' interval were immediately commencing disturbances of the heart rate in form of bradycardia and asystolia. After 5 sec we observed extrasystoles, tachycardia, sino-auricular block and AV-block of first and second degree as well as a number of T- and P-changes. Changes of the ecg were observed generally for 10 to 15 min, however, the T-wave remained sometimes negative or biphasic-preterminal negative for some hours.
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PMID:Effect of high doses of nicotine in pigs. I. Changes of the electrocardiogram. 125 87

A 13-week oral repeated dose toxicity study of suplatast tosilate (IPD-1151T), a new anti-allergic agent, as well as a 5-week recovery study were carried out at dose levels of 0 (control), 50, 150, 450 and 1350 mg/kg/day using male and female beagle dogs. The results were as follows: 1. In general conditions, soft feces and diarrhea with specific smell were dose-dependently observed in males and females given 450 mg/kg/day or more. Both sexes given 1350 mg/kg/day, revealed reeling with dropped head, abnormal gait, dysstasia, lying at lateral or prone position, sedation, and tremor, and one male and one female in this group died after showing respiratory depression, collapse and cyanosis. 2. There were no significant or remarkable changes in body weight, food consumption, water consumption, ophthalmology, electrocardiogram, urinalysis, hematology, biochemistry, fecal occult blood test, and absolute and relative organ weights. 3. Pathological examination in dead animals revealed hemorrhagic change in the heart and slight vacuolar changes in hepatocytes. In survived animals, there were no pathological changes attributable to the IPD-1151T. 4. In electron microscopic examination, there were no abnormalities in the liver and kidney attributable to the IPD-1151T. 5. After 5-week recovery period, above-mentioned changes disappeared. 6. From the above results, the non-effective dose level and the toxic dose level were estimated to be 150 mg/kg/day and 1350 mg/kg/day, respectively, and no sex differences were found.
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PMID:[A thirteen-week oral repeated dose toxicity study of suplatast tosilate (IPD-1151T) in dogs]. 132 Dec 64

Acute toxicity of cefpirome sulfate (CPR) was examined in 6-week-old mice and rats and immature (5-day-old) rats. The LD50 values of CPR (mg/kg) were as follows: (1) mice: intravenous, 2420 (95% confidence limits, 2122-2758) for males and 2400 (2181-2640) for females; intraperitoneal, 3850 (3407-4351) for males and 4200 (3889-4536) for females; and oral, 16200 (14781-17755) for males and 18500 (17290-19795) for females. (2) 6-week-old rats: intravenous, 1900 (1784-2023) for males and 2080 (1953-2215) for females; intraperitoneal, 6550 (6179-6943) for males and 5800 (5311-6334) for females; subcutaneous, more than 10000 for both sexes; and oral, more than 8000 for both sexes. (3) 5-day-old rats: subcutaneous, between 1750 and 2500 for males and 2080 (1651-2621) for females. Major changes in general health conditions observed in 6-week-old mice and rats were decreased spontaneous activity, lying prone, tremor, respiratory changes (slow or deep respiration, gasping), clonic or clonic-tonic convulsions. In the 6-week-old rats dosed subcutaneously, vocalization, writhing and cutaneous changes at the injection site (dark reddening or blackening, swelling, exfoliation, depilation, induration) were also observed. In the 5-day-old rats dosed subcutaneously, the changes noted were slow respiration, writhing, cyanosis, and dark reddening and swelling of the skin at the injection site. After administration, transient depression of body weight gain or loss of body weight was observed in the mice and rats except the rats dosed orally. These changes disappeared at 7 days after administration at latest, and all surviving animals showed favorable body weight gain thereafter. Necropsies revealed hemorrhage under meninges in the brain in many of the mice and rats which died. Other findings included subcutaneous changes at the injection site in the 6-week-old and 5-day-old rats dosed subcutaneously (dark reddening, retention of dark red fluid, retention of red, white or dark red gelatinous material) and changes in the peritoneal cavity in the 6-week-old rats dosed intraperitoneally (red or dark red spots on the serous membrane, reddening of adipose tissues).
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PMID:[Acute toxicity study of cefpirome sulfate in mice and rats]. 207 98

Acute toxicity studies of miporamicin and its trace ingredients, degradations and metabolites were conducted in mice and rats. 1. Following oral administration of miporamicin (MPM), none died among mice or rats even at the highest dosage levels. Therefore, its LD50 values were estimated to be greater than 2,500 mg/kg for mice and greater than 2,000 mg/kg for rats. The LD50 value of MPM was the highest by oral route, followed, in order, by subcutaneous route and intravenous route. There was no difference in this respect between sexes of animals studied. 2. No signs of abnormalities were observed among mice or rats following oral administration of MPM. In animals dosed with MPM by subcutaneous route, such inflammatory reactions as swelling, subcutaneous hyperemia and hemorrhage, and loss of hair incrustation at the site of injection were noted. Animals among those given MPM by intravenous injection developed postdosing depression of motor activity, respiratory depression or arrest, tremor and convulsion. 3. Deaths from administration of MPM were estimated to be due to paralysis of respiratory function inasmuch as fatally affected animals exhibited respiratory depression and cyanosis and, subsequently, respiratory arrest was followed by cardiac arrest. 4. Trace ingredients, metabolites and degradation products of MPM proved to be essentially the same as MPM in acute toxicities.
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PMID:[Acute toxicity studies of miporamicin and its degradation products and metabolites in the mouse and rat]. 262 83

Cyclopiazonic acid (CPA) was found to have many pharmacological properties in common with the antipsychotic drugs chlorpromazine and reserpine. Thus, in mice CPA at ip doses of 5-14 mg/kg body weight produced hypokinesia, hypothermia, catalepsy, ptosis, sedation without loss of righting reflex, tremor, gait disturbance, dyspnoea, opisthotonus, atypical convulsion and prolonged barbiturate-induced sleep. The ip LD50 of CPA was found to be 13 +/- 0.05 mg/kg. The tremors induced by near-lethal doses of CPA were associated with voluntary or forced movements (action tremors); they worsened during the days following treatment, but they were weak compared with the exhausting and continuous tremors of the whole body caused by 20 mg tremorine/kg (used for comparison). When death occurred only 24-259 min after administration of CPA (11-14 mg/kg), it was preceded by dypsnoea, cyanosis, opisthotonus and clonic leg movements and tonic extension of hind legs (convulsions). When death was delayed (2-6 days after CPA administration), it was preceded by prostration, ptosis, hypothermia, tremor and cessation of food and water intake resulting in cachexia; convulsions were not seen in this group of mice. CPA did not affect the rate of convulsion or death caused by either maximal electroshock or metrazol administration but it did delay the onset of metrazol-induced seizures. In rabbits, 10 mg CPA/kg body weight initially produced tachycardia, tachypnoea and sedation with an activated electroencephalogram. Of three rabbits given 10 mg CPA/kg one died, and in this rabbit slow delta waves were seen just before and during a brief period with clonic leg movements. In this animal death was accompanied by tonic extension of the hind legs, respiratory arrest and cardiac fibrillation; and epileptiform EEG was not seen at any time. The unexpected EEG activation with sedation in rabbits treated with CPA was similar to the effect of reserpine on EEG.
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PMID:Toxicity and neuropharmacology of cyclopiazonic acid. 404 83

Thermal stress was induced experimentally in the hybrid pigs LW X L, weighing 45 to 52 kg. The trials were repeated in boxes heated to the temperature of 43 to 47 degrees C. The pigs were examined for the values of tremor, pH, partial pressure of carbon dioxide (pCO2), base excess (BE), buffer base (BB), standard and actual bicarbonate (SB and AB), total carbon dioxide (tCO2) and partial oxygen pressure in blood (pO2). Thermal stress caused marked tachycardia, polypnoea, higher body temperature, increased blood pH, reduction of partial carbon dioxide pressure. Respiratory alkalosis was accompanied by cardiovascular weakness, general excitation followed by apathy, cyanosis and dyspnoea.
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PMID:[The effect of heat stress on acid-base homeostasis in pigs]. 643 33

In guinea-pigs, the oral and subcutaneous LD50 values were very similar (cf. 0,173 mg/kg over 48 h with 0,116 mg/kg over 24 and 48 h). When dosed subcutaneously, a cumulative effect was observed. Intravenous administration of cotyledoside to anaesthetized guinea-pigs resulted in: dyspnoea, increased heart rates and blood pressures, and electrocardiagraphic changes typical of cardiac glycoside poisoning. A positive cardiac inotropic effect was succeeded by a positive chronotropic one. In sheep, acute and subacute intoxication resulted in ruminal, respiratory and cardiac changes. The signs included ruminal stasis, cyanosis, cardiac arrhythmia, ectopic foci and AV dissociation, followed by hypotension and progressive respiratory and cardiac failure. The skeletal muscles were affected in only 1 sheep vide infra. In chronically intoxicated sheep typical clinical signs of "krimpsiekte" developed, e.g. weakness, reluctance to stand, unsteadiness on feet, tremor and paresis of hindquarter muscles, paresis of the neck, arching of the back and standing with the feet close together. Respiratory function was affected in all 3 cases; ruminal stasis, with concomitant loss of appetite occurring in one, and a transient change in heart function in another. The syndrome induced by acute cotyledoside poisoning is similar to that of other cardiac glycosides, but the paretic signs of chronic intoxication resemble "krimpsiekte", a disease associated only with intoxication with the plants of the family Crassulaceae.
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PMID:Studies on South African cardiac glycosides. II. Observations on the clinical and haemodynamic effects of cotyledoside. 718 41

The oral toxicity of capsaicin was investigated in mice and rats. Oral LD50 values were 118.8 mg/kg for male and 97.4 mg/kg for female mice, and 161.2 mg/kg for male and 148.1 mg/kg for female rats. Major toxic symptoms in mice were salivation, erythema of skin, staggering gait, bradypnea and cyanosis. Some animals showed tremor, clonic convulsion, dyspnea and lateral or prone position and then died 4 to 26 min after dosing. Survivors recovered within 6 hr in mice and 24 hr in rats. Toxic symptoms of rats were almost the same as mice, but rats showing higher incidence of cyanosis, clonic or tonic convulsion, dyspnea and lateral position, and the recovery was later than mice. The cause of death by capsaicin may be due to hypotension and respiratory paralysis in both animals, although the pathophysiology of death is not clearly understood. At pathological examination, erosion and ulcer of gastric fundus were seen in dead animals, while no pathological change was seen in surviving ones.
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PMID:Acute oral toxicity of capsaicin in mice and rats. 888 88

This study examined the effects of Y-27632, a selective Rho-kinase inhibitor, on organophosphate-induced acute toxicity in rats. Rats were randomly divided into four groups as control (corn oil), dichlorvos (30 mg kg(-1) i.p.), 1 and 10 mg kg(-1) Y-27632 + dichlorvos groups. Cholinergic signs (fatigue, tremor, cyanosis, hyper-secretion, fasciculations) were observed in all the rats in the dichlorvos group and the mortality rate was 50%. No cholinergic findings and deaths were observed in the control and Y-27632 groups. Plasma cholinesterase activities were suppressed with dichlorvos and these reductions were attenuated with Y-27632 pretreatment. There was a marked increase in plasma malondialdehyde level in the dichlorvos group, but Y-27632 pretreatment abolished this elevation. Dichlorvos markedly depressed cardiac paraoxonase activity, but these changes were not markedly modified with Y-27632. Total antioxidant capacities, total oxidant status, oxidative stress index, total free sulfhydryl groups and catalase activities in plasma and cardiac tissues were not markedly different between the groups. No significant changes were observed with cardiac myeloperoxidase activities or plasma arylesterase and ceruloplasmin activities. In conclusion, our results suggest that Rho-kinase pathway is involved in organophosphate intoxication, and a decrease in cardiac paraoxonase activities may play a role in the pathogenesis of acute organophosphate poisoning in rats.
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PMID:Effects of a selective Rho-kinase inhibitor Y-27632 on oxidative stress parameters in acute dichlorvos poisoning in rats. 1863 19


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