dihydroergotoxine has been researched along with Disease-Models--Animal* in 11 studies
11 other study(ies) available for dihydroergotoxine and Disease-Models--Animal
Article | Year |
---|---|
Neuroprotective activity of alpha-dihydroergocryptine in animal models.
alpha-Dihydroergocryptine (alpha-DHEC) is a well known dopaminergic agent successfully employed in the treatment of Parkinson's disease. alpha-DHEC showed a neuroprotective activity against total cerebral ischemia induced by MgCl2 in mice and histocytic anoxia by NaCN in mice and rats. Moreover the drug promoted the recovery of locomotor activity in rats after cerebral ischemic damage and protected mice against convulsions induced by intracerebroventricular injections of NMDA and glutamate. alpha-DHEC showed a protective activity on neuronal degeneration induced by MPTP in monkeys, as evaluated through animal's behaviour and morphological-cytochemical changes in the substantia nigra, suggesting a preservative effect on neuronal morphology and brain architecture. In the MPTP-treated monkeys, the alpha-DHEC administration induced a restoration of the unstimulated MDA values to control levels. The neuroprotective activity of alpha-DHEC is related to its peculiar activity on antioxidative enzymes of GSH system and to reduction of lipid-peroxide-induced cellular degeneration. Topics: Animals; Brain Ischemia; Constriction; Dihydroergotoxine; Disease Models, Animal; Hypoxia, Brain; Injections, Intraventricular; Macaca fascicularis; Male; Mice; Mice, Inbred ICR; Motor Activity; Neuroprotective Agents; Parkinson Disease, Secondary; Rats; Seizures | 1995 |
Hypoxia-induced sleep disturbance in rats.
The effects of varying degrees of hypoxia on sleep-wake organization were studied in rats prepared for chronic electrophysiological recording. The influence of Piracetam (75, 50, and 500 mg/kg, i.p.) and Hydergine (0.5, 1, and 3 mg/kg, i.p.) on sleep-wake organization in 10.5% oxygen was also investigated. The sleep-wake organization of rats under the effect of 15.5% oxygen content was unchanged, compared to that of normoxic control. More extreme hypoxia (12.6 and 10.5% oxygen) produced dramatic changes in sleep organization without influencing gross behavior. Paradoxical sleep (PS) stages became less frequent and shortened and were totally absent in 10.5% oxygen. Frequent wakings caused disturbed and superficial sleep. Central biochemical mechanisms, peripheral chemoreceptor reflex pathways and, as a consequence, decrease of duration of deep sleep periods, may contribute to the development of hypoxic sleep disturbances. Piracetam alleviated and Hydergine moderately reversed the hypoxic sleep disturbance. Topics: Animals; Dihydroergotoxine; Disease Models, Animal; Hypoxia; Male; Piracetam; Rats; Sleep Stages; Sleep Wake Disorders | 1990 |
[Effect of interleukin-1 on animals with a fibrinolytic dysfunction].
Activating effect of the interleukin-1 on the fibrinolytic system was shown in hypofibrinolysis models. This polypeptide exerted an opposite effect on the fibrinolysis which had been activated with i.v. administration of dihydroergotoxine and thrombin. Topics: Animals; Blood Coagulation Disorders; Blood Coagulation Tests; Dihydroergotoxine; Disease Models, Animal; Drug Interactions; Fibrinolysis; Interleukin-1; Male; Rats; Thrombin; Time Factors | 1989 |
Anti-hypoxic potency of cerebroprotective drugs studied in a model of acute reversible respiratory failure.
The protective efficacy of pentoxiphylline, piracetam, and dihydroergotoxine against abrupt hypoxia was tested in a model of acute reversible respiratory failure, where repeated apnoeic attacks were induced by inhalation in repeated hypoxic exposures was reduced in control as well as in dihydroergotoxine-treated animals, it was increased after pentoxiphylline, and was not changed after piracetam. Repeated N2 inhalations reduced the duration of apnoea required for the development of mydriasis in all control cats. There were, however, no such reductions of the apnoeic interval in animals of the three groups treated with cerebroprotective drugs. The ratio between the total duration of hypoxia (hypoxic hyperventilation plus apnoea) and the time of recovery of breathing was significantly higher in the pentoxiphylline-treated animals already during the first hypoxic attack after drug application when compared both to the control and the dihydroergotoxine-treated animals. After piracetam the difference was apparent in the last hypoxic attack only. The model of acute reversible respiratory failure with apnoeic episodes induced repeatedly seems to be useful for testing some properties of cerebroprotective drugs during abrupt hypoxia. Topics: Animals; Brain Ischemia; Cats; Dihydroergotoxine; Disease Models, Animal; Electrocardiography; Hypoxia; Nitrogen; Pentoxifylline; Piracetam; Respiration, Artificial; Respiratory Insufficiency | 1989 |
Use of alpha-adrenoceptor antagonist dihydroergotoxin in experimental anticoagulant and fibrinolytic therapy.
The thrombolytic action of commercial plasmin-Fibrinolysin, heparin and complex Fibrinolysin-heparin in thecom bination with the alpha-adrenoceptor agent DET was studied in rats. The induction of venous thrombosis is accompanied by the manifestations of disseminated intravascular coagulation (DIC). The most efficient thrombolytic action in the hypercoagulemic stage of DIC had the complex Fibrinolysin-heparin in the combination with DET. The alpha-adrenoceptor antagonist blocked the compensatory reaction on plasmin excess, liberated vascular plasminogen activator and thus increased and prolonged thrombo- and fibrinolytic effects of this complex. Administration of this complex in the combination with DET resulted in a steady hypocoagulation and hyperfibrinolysis in blood stream. Topics: alpha-2-Antiplasmin; Animals; Anticoagulants; Dihydroergotoxine; Disease Models, Animal; Drug Therapy, Combination; Fibrinolysin; Fibrinolytic Agents; Heparin; Male; Rats; Thrombin Time; Thrombosis | 1988 |
Hepatic alpha 1-adrenergic receptor alteration in a rat model of chronic sepsis.
Catecholamine therapy is often ineffective in reversing the peripheral vasodilatation and hypotension of septic shock. This suggests that catecholamines might not be able to activate alpha 1-adrenergic receptors to cause vasoconstriction. Despite elevations in endogenous catecholamines, hypoglycemia is also a complication of human sepsis, suggesting that among many other causes, hepatic alpha 1-receptors might be altered. To better understand the pathophysiologic basis for this pharmacologic dilemma, we studied the effect of experimental sepsis on alpha 1-adrenergic receptors in hepatic tissue, a rich source of alpha 1-receptors, from septic and control Sprague-Dawley rats. alpha 1-adrenergic receptors were measured with [3H]-prazosin and data analyzed by a computerized nonlinear least-square regression algorithm. Twenty-four hours following cecal ligation with puncture, a decreased number of alpha 1-adrenergic receptors was noted in crude and purified plasma membrane fractions (23 and 40% reductions respectively) from septic animals. No changes in either agonist or antagonist affinity for receptors from septic animals were noted. These data indicate that the catecholamine refractoriness seen in septic shock may be a result of alterations in alpha 1-adrenergic receptor number or receptor-effector coupling. Topics: Animals; Bacterial Infections; Chronic Disease; Dihydroergotoxine; Disease Models, Animal; Glucose; Guanylyl Imidodiphosphate; In Vitro Techniques; Kinetics; Liver; Male; Prazosin; Rats; Rats, Inbred Strains; Receptors, Adrenergic, alpha; Shock, Septic; Tritium | 1986 |
Effects of dihydroergocriptine on mouse and rat resistance to acute anoxia: influence of repetition of treatment.
Topics: Animals; Asphyxia; Dihydroergotoxine; Disease Models, Animal; Dose-Response Relationship, Drug; Hypoxia; Hypoxia, Brain; Mice; Rats | 1981 |
Adenosinetriphosphate conservation by indoramin and other drugs.
Topics: Adenosine Triphosphate; Animals; Brain Edema; Brain Ischemia; Cerebral Cortex; Cyanides; Dihydroergotoxine; Disease Models, Animal; Hypoxia; Indoles; Indoramin; Rats | 1981 |
[Pathopharmacologic models of cerebral disorders].
Topics: Aging; Animals; Arteriosclerosis; Cerebrovascular Circulation; Dementia; Dihydroergotoxine; Disease Models, Animal; Dogs; Energy Metabolism; Glucose; Humans; Hypoxia, Brain; Memory; Neurons; Partial Pressure; Rabbits; Vincamine | 1979 |
Comparative effects of dihydroergotoxine (DHET) on CBF and metabolism changes produced by experimental cerebral edema, hypoxia and hypertension.
Dihydroergotoxine (DHET) perfused in the dog (100 microgram/kg) presenting a cerebral per-hypocapno-anemic syndrome reduces cerebral hyperemia, increases cerebral venous PO2, despite the rise in CMRO2 and favors glucose oxidation by the brain. DHET (20 mg/kg p.o.) is able to drop mean, diastolic and systolic arterial blood pressures in renal-hypertensive rats having a cerebral edema induced by triethyltin intoxication without affecting cerebral water and sodium levels which are increased in the controls. DHET (50 microgram/kg i.v.) can also improve EEG changes produced by a traumatic edema but does not exert (200 microgram/kg i.v.) any effect on EEG changes produced in the rabbit by lithium chloride intoxication. Topics: Anemia; Animals; Blood Gas Analysis; Blood Glucose; Brain; Brain Edema; Cerebrovascular Circulation; Dihydroergotoxine; Disease Models, Animal; Dogs; Electroencephalography; Electrolytes; Hypertension, Renal; Hyperventilation; Hypoxia, Brain; Lactates; Lithium; Oxygen Consumption; Rabbits; Triethyltin Compounds | 1978 |
[The phenomenon of experimental motor retardation as one of the manifestations of the Parkinsonian syndrome].
A low frequency stimulation of the head of the caudate nucleus in freely moving cats leads to an arrest of reactions with an increased muscular tone and tremor. This reaction may serve as an experimental model of one of the expressions of parkinsonism, inasmuch as its accomplishment depends upon the central dopaminergic mechanisms (confirmed on experiments with disulfiram and alpha-methyltyrosine). The similarity is also supplemented by the fact that the arrested reaction is weakened by antiparkinson drugs (d, 1-amphetamine, DOPA, artane) and is increased by neuroeptical preparation (aminazine, haloperidol, reserpine). Topics: Amphetamine; Animals; Catecholamines; Cats; Caudate Nucleus; Chlorpromazine; Dihydroergotoxine; Disease Models, Animal; Disulfiram; Electric Stimulation; Methyltyrosines; Motor Activity; Muscles; Parkinson Disease; Propranolol | 1975 |