Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

T-2 toxin was given to rats in three ways: Subcutaneous or intracerebral injection of a solution in dimethyl sulfoxide (DMSO) and by implantation of toxin, adsorbed on talc, into various regions of diencephalon and brain stem. The latter method proved to be most effective. Within a few hours after administration of 10-20 micrograms toxin, the animals became restless, ataxic and dyspneic. These early symptoms were followed by depression and immobility. Prior to death, tachypnea and/or convulsions developed. The rats succumbed to implantation of toxin within 1 - 7 days; no fatalities occurred at later dates. Histologically, the toxin pellets caused necrosis a few days after implantation; at a later stage, the necrotic areas were surrounded by inflammatory infiltrates around small blood vessels. These morphological changes were limited to the application site and were insufficient to explain the lethal effect of intracerebral administration. After intracerebral injections of toxin solutions, the animals died within 24 h. No marked histological changes could be seen after such rapid fatalities.
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PMID:Toxic and lethal effects of T-2 toxin upon intracerebral administration to rats. 407 29

The effects of ranitidine hydrochloride, a histamine H2-receptor antagonist, on development and general behavior of F1 generation of Crj: CD (SD) rats were examined. Ranitidine hydrochloride was intravenously administered once daily from day 7 to 17 of gestation at dose levels of 5, 15 and 40 mg/kg in base weight respectively. Two-thirds of females were killed on day 20 of gestation to examine the development of fetuses, the remaining females were allowed to litter naturally and the postnatal development of the offsprings was observed. Tachypnea, prone position and transient tremor were observed for approximately 15 from 30 seconds directly after an intravenous administration of ranitidine hydrochloride in the dose of 40 mg/kg, which were probably induced by a rapid fall in blood pressure. During the gestation period, there occurred a slight depression of the maternal body weight gain in the ranitidine-treated groups. At the stage of lactation, the body weights of dams showed slightly lower levels than control and their liver weights of dams were also inclined to decrease in 15 and 40 mg/kg groups. In the observation of the fetuses, there were no significant differences between the control and ranitidine-treated groups concerning fetal growth and development, external, skeletal and internal anomalies in fetuses. In delivery and postpartum observation, no influence of ranitidine administration was observed on the litter size, mortality rate of F1 pups. There was a tendency towards decrease in body weight in males of the ranitidine-treated groups. But no significant changes were observed in general behavior, postnatal development, various functions such as reflex response, learning and reproductive performances of F1 generation. Therefore, it was concluded that ranitidine hydrochloride had no effects on fetal and postnatal development, general behavior and various functions of F1 generation at the dose of 40 mg/kg/day or less.
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PMID:[Effects of intravenous administration of ranitidine hydrochloride to the pregnant rat in organogenesis period]. 609 57

Neuropharmacological mechanisms in central regulation of respiration in anesthetized rats were studied in a whole body plethysmographic model. Neurotransmitter agonists and antagonists were administered intracerebroventricularly or locally into the brain and the respiratory pattern was analysed. The four anesthetics: enflurance (E), halothane (H), pentobarbital sodium (P) and urethane (U) were found to have different effects on central respiratory regulation. Respiratory frequency was higher after H and U compared to after E and P. Animals anesthetized with H exhibited a lower inspiratory drive and a slightly depressed sensitivity to CO2. The responses to the neuropeptides substance P and TRH as well as the amino acid neurotransmitter GABA were partly modified after the different forms of anesthesia. Apomorphine (i.c.v) induced a biphasic, haloperidol reversible, respiratory response in H- and U- (but not in E- and P-) anesthetized rats. The initial bradypnoic response might be due to a decreased sensitivity to afferent vagal signals, while the following tachypnoic phase might be elicited by dopaminergic mechanisms at posterior diencephalic and upper midbrain levels (hypoxic, hypercapnic tachypnea). The tachypnoic response was inhibited by a graded exposure to CO2. The effects of different neurotransmitters were further analysed in H-anesthetized animals. GABA and the GABA agonist muscimol exerted a depressant effect on ventilation in contrast to the GABA-like drugs GHBA an baclofen. Exogenous GABA depressed all respiratory parameters studied exept for inspiratory time and was found to affect mainly respiratory timing mechanisms. An increase in endogenous GABA levels induced by the GABA transaminase inhibitor AOAA blunted the respiratory response to CO2 and induced a ventilatory depression similar to that seen after exogenous GABA. A significance correlation between brain stem GABA levels and respiratory duty cycle was found. The tripeptide TRH induced a marked tachypnea due to the extrahypothalamic actions of the peptide. A delay in the response was seen after local injection into the nucleus tractus solitarius and the tachypnea was abolished by CO2 exposure. The ventilatory effects might be elicited by mechanisms similar to those involved in the tachypnoic response to apomorphine. The tachypnea was potentiated by GABA (possibly due to that both agents act on inspiratory off-switch lowering mechanism) and by methylatropine or naloxone (possibly due to secondary pertubation by cholinergic or enkephalinergic mechanisms). A stimulation of ventilation (increase in tidal volume) was seen after substance P (SP) due to an increase in inspiratory drive and o
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PMID:Neuropharmacological aspects of central respiratory regulation. An experimental study in the rat. 620 94

Strychnine toxicosis is characterized by inducible tetanic seizures and metaldehyde poisoning by fine fasciculations progressing to generalized tremors and seizures. Intoxication with 1080 causes seizures, random running movements, vomiting, defecation, urination, acidosis and hyperglycemia. Intoxication with rodenticides causing coagulopathy is characterized by hemorrhage into body cavities but not necessarily external hemorrhage. Anticholinesterase insecticides cause salivation, urination and defecation, while chlorinated hydrocarbon insecticides cause CNS disturbances. Ethylene glycol intoxication results in ataxia, depression, coma, vomiting and tachypnea, followed by acute renal failure. Urea poisoning causes bloat and CNS signs in cattle. Monensin intoxication in horses lasts several days and causes stiffness, colic, uneasiness and recumbency. Salt poisoning results in depression, seizures and hypernatremia. Lead poisoning is associated with central and peripheral nervous system signs, as well as increased numbers of nucleated RBC and basophilic stippling of RBC. Arsenic poisoning results in GI pain, diarrhea, weakness and death. Copper toxicosis in sheep is manifested by hemolytic anemia, hemoglobinemia and hemoglobinuria. Plants that may intoxicate domestic animals include sorghum, greasewood, halogeton, water hemlock, Japanese yew, larkspur, lupine, milk-weed, philodendron, oleander, castor bean and precatory bean.
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PMID:Practical toxicologic diagnosis. 649 3

Adult intact conscious or anesthetized cats have been exposed to either hypoxia or low concentrations of CO in air. In addition, the ventilatory response to CO2 was studied in air, hypoxic hypoxia, and CO hypoxia. The results show that 1) in conscious cats, low concentrations of CO (0.15%) induce a slight decrease in ventilation and higher concentrations of CO (0.20%) induce first a small decrease in ventilation and then a characteristic tachypnea similar to the hypoxic tachypnea described in carotid-denervated cats; 2) in anesthetized cats, CO hypoxia induces only mild changes in ventilation; and 3) the ventilatory response to CO2 is increased in CO hypoxia in both conscious and anesthetized animals but differs from the increase observed during hypoxia. It is concluded that the initial decrease in ventilation may be caused by some brain stem depression of the respiratory centers with CO hypoxia, whereas the tachypnea originates probably at some suprapontine level. Conversely, the possible central acidosis may account for the potentiation of the ventilatory response to CO2 observed in either conscious or anesthetized animals.
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PMID:Ventilatory response of intact cats to carbon monoxide hypoxia. 662 36

In carotid body-denervated cats, moderate hypoxia, or even normoxia when compared to hyperoxia, provokes a significant depression of the respiratory output. This is observed in conscious or anesthetized or decerebrated animals. On the other hand, more severe hypoxia induces tachypnea (hypoxic tachypnea of Miller and Tenney, Respir. Physiol. 23: 31-39, 1975) in conscious cats, whereas the same hypoxia is followed by marked respiratory depression or apnea in the anesthetized or decerebrated animals. Hypoxic tachypnea can be partly or completely reversed by injection of dopa or xanthines such as caffeine or aminophylline. This suggests that alterations in brain monoamine metabolism by hypoxia may be responsible for the alterations in suprapontine respiratory control systems, resulting the tachypnea. Mild hypercapnia can also reverse hypoxic tachypnea. It is concluded that the ventilatory response to hypoxia of conscious animals results from stimulation of peripheral chemoreceptors, inhibition of brain stem neurons, and finally involvement of suprapontine structures that seems to be mediated by depletion of monoamines.
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PMID:Possible alterations in brain monoamine metabolism during hypoxia-induced tachypnea in cats. 677 76

The effects of graded brain hypoxia on respiratory cycle timing, the lung inflation reflex, and respiratory compensation for an inspiratory flow-resistive load were studied in unanesthetized goats. Two models, inhalation and CO and acute reduction of brain blood flow (BBF) were used to produce comparable levels of brain hypoxia. The lung inflation reflex was assessed as the ratio of inspiratory time of an occluded breath to that of the preceding spontaneous breath (TIoccl/TIspont). Compensation for flow-resistive loading was assessed as the effect of the load upon the airway occlusion pressure response to rebreathing CO2 (delta P 0.1/delta PCO2). Major findings were 1) severe brain hypoxia (HbCO of 60% or BBF of 42%) caused tachypnea due to a 50% or more reduction of expiratory time but only a 20% or less reduction of inspiratory time; 2) moderate carboxyhemoglobinemia (HbCO of 25-30%) enhanced TIoccl/TIspont from 1.5 +/- 0.1 at control to 2.1 +/- 0.1, while severe brain hypoxia (HbCO of 60% and BBF of 42%) reduced the ratio to 1.0 +/- 0.2; and 3) compensation for a flow-resistive load, manifested by increases of delta P 0.1/delta PCO2 of 75-300% in the control state, was abolished at HbCO of 45-50% and BBF of 60%. The data suggest that in unanesthetized animals brain hypoxia elicits tachypnea largely by an effect on the expiratory phase of the bulbopontine timing mechanism. The observed enhancement of the lung inflation reflex and abolition of flow-resistive load compensation are best explained by hypoxic depression of higher than brain stem neural function.
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PMID:Brain hypoxia and control of breathing: neuromechanical control. 678 50

A single breath of 100% CO2 produces depression of the monosynaptic reflexes, recorded from L7 or S1 ventral root, after stimulation of the Posterior Biceps and Semitendinosus nerve (PBST) in anaesthetised cats. As the depression could not be attributed to the J-reflex(1), the possible site of action of the CO2 induced depression of monosynaptic reflexes was worked out. PBST nerve threshold did not change after CO2 introduction and the depression persisted in paralysed cats under controlled ventilation, thus eliminating the possibility of movement effect of the spinal cord due to tachypnoea. Spinal cord sections at the level of L1 and C1 abolished the depression, whereas the depression persisted in the decerebrate preparation. Thus it is concluded that a single-breath of 100% CO2 depresses the monosynaptic reflexes at the supraspinal level. Blood gas tensions (PO2 and pCO2) measured before and after CO2 introduction showed a shortlasting increase in pCO2 and not much significant change in pO2 compared to the long lasting depression of monosynaptic reflexes.
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PMID:Effects and site of action of a single-breath of 100% CO2 on the monosynaptic reflexes in cats. 679 71

In 10 dogs the authors studied the effect of increasing doses of alfathesin on ventilation (VE, frequency, VT, blood gases), on the ventilatory pattern (TI, TE, TI/Ttot), on the neurological initiation of ventilation (VT/TI, occlusion pressure at 0.5 seconds), and on the Hering-Beurer reflex (duration of apnoea after occlusion of the airway at the end of inspiration). The results were compared with normal values taken from the literature. The correlation between the dose of alfathesin and the measured or calculated parameters was examined. Ventilation was stimulated by low doses of alfathesin, a stimulation, characterized by tachypnoea without change in tidal volume. Deepening of anaesthesia was accompanied by progressively increasing depression of respiration (diminution of VE, of frequency, of VT/TI and increase of PaCO2 and of the duration of apnoea). The mechanisms of the initial stimulation of ventilation and of respiratory depression are discussed. The authors conclude that the action of alfathesin on the central nervous system is biphasic, with stimulation during light anaesthesia followed by depression with associated depression of ventilation, despite increasing hypoxia and hypercapnia.
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PMID:[Respiratory effects of increasing doses of alfathesin in the dog]. 681 35

The present study retrospectively examined clinical and clinicopathological findings in horses with colic to determine which variables distinguished between medically treatable cases and cases which required surgical intervention. Heart rate, haematocrit, haemoglobin concentration, blood erythrocyte count, frequency of borborygmi and degree of mental depression showed the greatest differences (P less than 0.001) between medical and surgical groups. However, some variables which primarily evaluated cardiovascular function, ie, blood pressure, oral mucosal capillary refill time and blood lactate concentration, were not significantly different between medical and surgical groups. When several of the following findings are observed together surgery is suggested: moderate to marked colic signs; tacky to dry oral mucosa which is discoloured (especially when brick-red or blue); decreased to absent borborygmi, probably associated with absence of rectal faeces; nasograstric intubation producing refluent fluid; leucocytosis with a left-shift; and tachypnoea, tachycardia, elevated haematocrit, hyperglycaemia and uraemia.
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PMID:Assessment of the necessity for surgical intervention in cases of equine colic: a retrospective study. 688 11


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