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At least 199 records · Page 11Linked to original sources
PubMed1974

Effect of p-chlorophenylalanine on brain monoamines and behaviour during ethanol withdrawal in mice.

The administration of p-chlorophenylalanine to mice prevents the rise in brain 5-hydroxytryptamine concentration associated with ethanol withdrawal but does not affect the increase in brain catecholamines which occurs at the same time. The locomotor excitement, piloerection, tremor and handling convulsions which occur during ethanol withdrawal were not affected. These results suggest that the increase in brain 5-hydroxytryptamine which occurs in ethanol withdrawal is a consequence of increased 5-hydroxytryptamine synthesis and that it is probably not involved in the above behavioural changes of ethanol withdrawal.

Amines↗
PubMed1978

Effects of propylbenzilylcholine mustard on injection into the liquor space of cats.

In unanaesthetized cats the effects were examined of propylbenzilylcholine mustard (PrBCM) on injection into the cannulated cerebral ventricles and cisterna magna. Extreme motor excitation, vocalization, shivering leading to fever, tachypnoea, panting, piloerection and salivation were produced on ventricular, vigorous scratching bouts on cisternal, injections. The sites of these actions are discussed. None of the effects was produced by atropine similarly injected. All effects were suppressed by anaesthetizing doses of pentobarbitone sodium injected intraperitoneally.

Animals↗
PubMed1980

Selective inhibition of thermogenesis by tributyl S,S,S,-phosphorotrithioate (DEF).

1 Rats and mice given tributyl S,S,S,-phosphorotrithioate (DEF) showed large dose-related falls in body temperature which lasted several hours to several days at environmental temperatures below thermoneutrality (30 to 31 degrees C). 2 DEF produced only mild sedation and a remarkable degree of motor control was retained even when body temperatures fell below 30 degrees C. At the dose producing maximal hypothermia only 2% of rats died within the first 24 h, although prolonged hypothermia was usually lethal. 3 Hypothermia was associated with a complete block of cold-induced thermogenesis, with relatively little effect on basal metabolism at thermoneutrality. 4 Heat conservation mechanisms (peripheral vasoconstriction and piloerection) appeared to be unaffected by DEF and retained their usual temperature thresholds. 5 Adrenal catecholamine secretion in response to handling or acute cold exposure was normal in DEF-treated rats but the fall in body temperature could be markedly reduced by large intraperitoneal injections of noradrenaline, although not atropine. The increase in oxygen consumption produced by injected catecholamines was also unaffected by DEF treatment. 6 It is concluded that the block of cold-induced thermogenesis probably results from a lack of catecholamine release at the tissue level. That this is likely to be mediated at a peripheral site is suggested by the lack of effect of intracerebroventricular DEF.

Animals↗
PubMed1987

Acute toxicity studies of aluminium compounds: antidotal efficacy of several chelating agents.

Four aluminum compounds--nitrate, chloride, sulphate and bromide--were administered orally and intraperitoneally to rats and mice. The LD50-values (14 days) were determined. The majority of deaths occurring during the first four days. The clinical and physical signs appearing after intoxication include among other lethargy, decreased locomotor activity, piloerection, weight loss and perorbital bleeding. After 14 days no alterations in liver and renal functions were detected in the animals which received intraperitoneally the LD50-values of aluminum nitrate as a single dose. Aluminum concentrations were highest in liver and spleen. No histopathological lesions could be observed. To compare the efficacies of nine chelating agents on the toxicity of aluminum in mice, the therapeutic index and the therapeutic effectiveness of each chelating agent have been calculated. Malic, succinic, oxalic and malonic acids showed the best results with malic and succinic acids being the most effective. Deferoxamine mesylate (DFOA), sodium salicylate, L-cysteine and citric acid were not so effective as antidotes for acute aluminum toxicity. Aurin tricarboxylic acid (ATCA) should not be used due to its high toxicity.

Alum Compounds↗
PubMed1988

Renal sympathetic nerve activity during morphine abstinence in sino-aortic baroreceptor-denervated rats.

This study was undertaken to investigate the influence of the arterial baroreceptors on the response of renal sympathetic nerve activity (rSNA) during naloxone-precipitated morphine abstinence in rats. In chronically baroreceptor-denervated, morphine-dependent rats, rSNA, mean arterial pressure (MAP) and heart rate (HR) were studied before and after repeated i.v. bolus doses of naloxone (0.005-5 mg kg-1), during chloralose anaesthesia or in the conscious state. In the anaesthetized animals, naloxone doses of 0.05-5 mg kg-1 caused a pronounced inhibition of rSNA, reaching a level 61% below pre-naloxone activity. This was accompanied by increases in MAP and HR. In the conscious rats, the lower doses of naloxone elicited an initial state of increased somatomotor activity. This was paralleled by slight increases in rSNA and MAP. After 4-5 min, the behavioural excitation faded and was replaced by lethargy. The rats exhibited still signs of withdrawal in the form of piloerection, chromodacryorrhoea and defaecations. Concomitantly, rSNA returned towards the pre-naloxone level, while MAP showed a sustained increase. The higher naloxone doses exacerbated the hypertension without any further changes in rSNA or in behaviour. We conclude that the influence of the baroreceptors is of minor significance for the inhibition of rSNA during naloxone-precipitated abstinence in anaesthetized rats. In conscious, intact rats, however, the baroreceptors seem to contribute to rSNA inhibition since no significance decrease of rSNA occurred in baroreceptor-denervated rats in the present study. This is in contrast to our previous finding of a marked inhibition of rSNA in rats with intact baroreceptors.

Animals↗
PubMed1981

Withdrawal syndrome after continuous infusion of clonidine in the normotensive rat.

The effects on heart rate and arterial pressure of continuous subcutaneous infusion of clonidine (500 microgram kg-1 day-1) via an ALZET miniosmopump and sudden termination of this treatment were studied in conscious normotensive rats. No consistent decreases of heart rate and blood pressure were observed during the clonidine infusion. Within a few hours following removal of the minipumps, a pronounced and long-lasting tachycardia developed. Mean arterial pressure did not exceed control level consistently, but transient blood pressure 'upswings' were observed. The withdrawal phenomena were accompanied by a small, significant rise in plasma noradrenaline content. During the clonidine-infusion period piloerection and sedation were prominent. The present study indicates, that the occurrence of the withdrawal phenomena following cessation of clonidine treatment is not dependent upon a decrease of blood pressure and heart rate preceding clonidine withdrawal. Furthermore, the model presented may be suitable for the study of withdrawal phenomena of other anti-hypertensive drugs.

Animals↗
PubMed1971

The role of sodium and calcium ions in the hypothalamus in the control of body temperature of the unanaesthetized cat.

1. Isolated regions of the anterior, posterior and other areas of the hypothalamus of the unanaesthetized cat were perfused by means of push-pull cannulae lowered through permanently implanted guide tubes. Each site was perfused for a 30 min interval at a rate of 50 mul./min. Concentrations of sodium, calcium, potassium and magnesium ions in the perfusate were altered selectively.2. Sodium ions in a concentration which varied from 13.6 to 68.0 mM in excess of the level in extracellular fluid caused a steep rise in the temperature of the cat when the solution was perfused at sites located within the posterior hypothalamic area. Shivering, vasoconstriction, and piloerection accompanied the increase in temperature. When the chloride was replaced in the perfusate by the toluene-p-sulphonate salt of sodium, the hyperthermia was equally intense. Solutions containing excess sodium ions perfused within the anterior and other hypothalamic areas produced either a slight fall or rise in temperature as well as other physiological changes.3. Calcium ions in a concentration which varied from 2.6 to 10.4 mM in excess of the physiological level perfused at the same sites within the posterior region of the hypothalamus produced a sharp fall in body temperature, which was accompanied by vasodilatation and a decrease in the activity of the cat. When solutions containing excess calcium were perfused in the anterior and other hypothalamic areas, no consistent change in temperature occurred.4. Potassium or magnesium ions in concentrations which varied from two to ten times the level in extracellular fluid had virtually no effect on the temperature of the cat when they were perfused in the anterior, posterior or other areas of the hypothalamus.5. We conclude that the constancy in the ratio between sodium and calcium ions in the posterior hypothalamus may be the inherent mechanism by which the set-point for body temperature is determined.

Animals↗
PubMed1971

Changes in body temperature of the unanaesthetized monkey produced by sodium and calcium ions perfused through the cerebral ventricles.

1. In the unanaesthetized Rhesus monkey, solutions containing sodium, calcium, potassium or magnesium in excess of the normal concentration of extracellular fluid were perfused from a lateral to the fourth ventricle through chronically implanted cannulae.2. Sodium (11.0-88.0 mM in excess of the physiological concentration) perfused through the ventricles, caused an immediate rise in body temperature which was accompanied by vasoconstriction, piloerection and shivering. The latency of the hyperthermia was related directly to the rate of perfusion and the concentration of sodium, whereas the magnitude of the response depended upon the concentration only. When the perfusion was terminated, shivering ceased and the temperature of the monkey returned to the base line level.3. When calcium ions were perfused in concentrations 2.5-47.9 mM in excess of that of extracellular fluid, a fall in the temperature of the animal occurred. The magnitude of the decreases depended upon the concentration of calcium in the perfusion fluid. Vasodilatation, sedation and a reduction in withdrawal reflexes accompanied the calcium-induced hypothermia. After the perfusion ended, the temperature continued to fall until the monkey began to shiver and vasoconstriction was observed in many skin areas.4. The perfusion through the cerebral ventricles with modified Krebs solution alone or with the Krebs solution which contained potassium or magnesium ions in concentrations five to ten times normal had virtually no effect on the temperature of the monkey.5. Since the temperature of the monkey was unchanged as long as the physiological ratio of sodium to calcium in the perfusion fluid remained constant, we conclude that the balance between these two essential cations within the brain stem could determine the neural mechanism whereby the set-point for body temperature of the primate is established.

Animals↗
PubMed1971

Effects on body temperature of prostaglandins of the A, E and F series on injection into the third ventricle of unanaesthetized cats and rabbits.

1. Prostaglandins were injected into the third ventricle of unanaesthetized cats and rabbits whilst rectal temperature was recorded.2. In cats prostaglandin E(1) and E(2) (PGE(1) and PGE(2)) produced hyperthermia which mostly began within a minute of injection and lasted 1 or more hours. With PGE(1) the hyperthermia was shown to be dose dependent between 10 ng and 10 mug (2.8 x 10(-11) and 2.8 x 10(-8)M). The hyperthermia was associated with vigorous shivering, skin vasoconstriction and piloerection. In several experiments a secondary rise in temperature occurred a few hours after the injection but such an effect was sometimes observed with control injections of 0.9% NaCl solution as well.3. None of the other prostaglandins (A(1), F(1alpha), F(2alpha)) examined in cats had an immediate or strong effect on temperature comparable to the hyperthermia produced by PGE(1) and PGE(2).4. In rabbits PGE(1) (2 mug) also caused hyperthermia which began shortly after the injection and lasted for hours. PGF(2alpha) and PGA(1), did not affect temperature.5. In cats it was seen that an intraperitoneal injection of 4-acetamidophenol (paracetamol 50 mg/kg) did not affect the initial strong hyperthermia produced by PGE(1) and PGE(2) but abolished the secondary rise.6. The possibility is discussed that PGE(1) plays a role as a central transmitter or modulator in temperature regulation.

Acetaminophen↗
PubMed1980

The course of post-ganglionic sympathetic fibres distributed with the trigeminal nerve in the cat.

1. The course of post-ganglionic sympathetic fibres to the jaws, face and eye was investigated in cats by observing the effects of nerve sections on responses evoked by stimulation of the cervical sympathetic trunk. 2. Sympathetic fibres were present in the infraorbital and inferior alveolar nerves. From the superior cervical ganglion, all of these fibres travelled in the internal carotid nerve and all but a few passed through the foramen lacerum and joined the trigeminal nerve at its ganglion. 3. Compound action potentials were recorded from sympathetic fibres in six out of twenty-seven teeth. These fibres followed the route described above. 4. Sympathetic fibres to the pupil and levator palpebrae superioris passed from the internal carotid nerve to the eye via the foramen lacerum and the superior orbital fissure. Some fibres causing piloerection in front of the ear travelled by the same route and some travelled with the maxillary division of the trigeminal nerve. 5. Sympathetic fibres to the nictitating membrane followed a similar route to those supplying the pupil except that they entered the cranial vault through the pterygoid foramen. 6. The secretomotor fibres to the submandibular salivary gland and some vasoconstrictor fibres to the lip did not travel with the internal carotid nerve or major branches of the trigeminal nerve.

Action Potentials↗
PubMed1981

Salivary syndrome in horses: identification of slaframine in red clover hay.

An outbreak of salivary syndrome in horses in North Carolina was investigated. Rhizoctonia leguminicola was the predominant fungus isolated from toxic red clover hay. The fungus was less prevalent in the hay after 10 months of storage, and the hay had also decreased in biological activity after 10 months. Toxic hay caused extreme salivation, piloerection, respiratory distress, and increased frequency of defecation when fed to guinea pigs, and purified extracts of toxic hay and pure slaframine elicited these same responses when injected intraperitoneally into guinea pigs. The freshly acquired hay, based on the biological (slobber-producing) activity in hay and in purified extracts, contained the equivalent to 50 to 100 ppm (50 to 100 microgram/g) of slaframine, but this level had decreased after 10 months by about 10-fold to about 7 ppm. Slaframine and seven synthetic derivates of slaframine were used in presumptive gas-liquid chromatographic identification of this mycotoxin. Slaframine (1-acetoxy-6-amino-octahydroindolizine) was identified in purified extracts of toxic hay by gas-liquid chromatography-mass spectrometry after preparative thin-layer chromatography. This was the first direct identification of slaframine in toxic red clove hay.

Alkaloids↗
PubMed2000

IL-18 and IL-12 induce intestinal inflammation and fatty liver in mice in an IFN-gamma dependent manner.

BACKGROUND: In murine models of inflammatory bowel disease, colonic inflammation is considered to be caused by an aberrant Th1-type immune response. AIM: To investigate if systemic administration of interleukin (IL)-12 and IL-18 to wild-type BALB/c mice induces liver injury and intestinal inflammation, and if pathological changes are observed, what cytokines are involved. METHODS: Mice (BALB/c-wild-type (wt), MRL-lpr/lpr, BALB/c-interferon gamma knock out (IFN-gamma KO), C57BL/6-inducible nitric oxide synthase (iNOS) KO, and BALB/c tumour necrosis factor alpha (TNF-alpha) KO) were injected intraperitoneally each day with IL-12 (20 ng/g/mouse) and/or IL-18 (200 ng/g/mouse). RESULTS: Administration of IL-12 and IL-18 to BALB/c-wt mice induced prominent intestinal mucosal inflammation and fatty liver, leading to piloerection, bloody diarrhoea, and weight loss. IL-12 and IL-18 induced striking elevations in serum levels of IFN-gamma that caused NO production, although increased NO had no exacerbating effect on mice. Moreover, iNOS KO mice, or MRL lpr/lpr mice lacking functional Fas were equally susceptible to IL-12 and IL-18. Administration of IL-12 and IL-18 did not induce TNF-alpha production in wild-type mice, and the same treatment to TNF-alpha KO mice induced intestinal mucosal inflammation. Furthermore, they had diffuse and dense infiltration of small fat droplets in their hepatocytes associated with an increase in serum levels of liver enzymes. In contrast, the same treatment in IFN-gamma KO BALB/c mice and iNOS KO mice did not induce these changes. CONCLUSIONS: Our study strongly indicates that IL-18 together with IL-12 induces intestinal mucosal inflammation in an IFN-gamma dependent but TNF-alpha, NO, and Fas ligand independent manner, and fatty liver is dependent on IFN-gamma and NO.

Animals↗
PubMed1976

Observations on sensory and sympathetic function during intrathecal analgesia.

A dilute solution of procaine in glucose solution was injected by slow drip into the lumbar theca of patients to cause a differential block. Vasodilatation of the skin vessels of the lower limbs always occurred before any change in sensibility. The first changes in sensibility were inability to fell painful stimuli and warm stimuli; these two forms of sensibility were usually coextensive and occurred at the same time. When this was not so, either form of sensibility could be more extensively disturbed than the other. When warmth sensibility was removed, cold sensibility was either normal or diminished or cold stimuli caused non-thermal sensations such as non-thermal wetness or pressure. It is concluded that the nerve fibres signalling warmth are the smaller delta fibres or non-myelinated fibres or both. As two groups of investigators who recorded from the non-myelinated fibres in man found no non-myelinated fibres responding to cold, it is condluded that fibres signalling cold cover the same delta range as those signalling warmth, together with a proportion of larger delta fibres. When fibres subserving pain, warmth, and cold were blocked, tactile sensibility could be normal. It is concluded that, if there are tactile fibres in man in the smaller delta and non-myelinated ranges, their contribution to tactile sensibility is insignificant. It is also concluded that the pre-galglionic B fibres are the most susceptible of all fibres of the nerve roots to local anaesthetic agents. On two occasions, piloerection occurred when the pre-ganglionic sympathetic fibres were blocked. In two patients spontaneous itching occurred when all peripheral nerve fibres were blocked except large tactile fibres.

Anesthesia, Epidural↗
PubMed1989

Progressive encephalomyelitis with rigidity: a case report with magnetic resonance imaging findings.

A 52 year old woman presented with pain in the back and upper limbs and progressive weakness and sensory impairment of the upper and lower limbs. She developed frequent episodes of severe generalised muscle spasms associated with piloerection and hyperventilation. Nerve conduction studies and electromyography were normal. MRI demonstrated a lesion of the cervical spinal cord and lower brainstem. A biopsy of the cord revealed perivascular cuffing with mononuclear cells and inflammatory changes in the parenchyma, with increased numbers of microglia, reactive astrocytes and plasma cells. Following treatment with corticosteroids she showed substantial improvement.

Brain Stem↗
PubMed1985

Standardized intraabdominal abscess formation with generalized sepsis: pathophysiology in the rat.

Gelatine capsules containing Escherichia coli and Bacteroides fragilis in a standardized mixture with rat colonic content and barium sulfate were implanted intraabdominally into rats. Capsules of 0.75 g gave approximately 50% mortality whereas 0.35 and 1.10 g caused no or 100% mortality, respectively. In subsequent experiments, using the 0.75 g capsule, all animals became ill with signs of tachypnea, piloerection, low physical activity and hypersecretion of saliva 6-8 h after the implantation. The animals reduced their water and food intake substantially and the body weight decreased. A significant reduction in blood pressure, glucose and leukocyte and platelet counts was found 12 h after challenge. Blood cultures obtained at 12, 24, 48 and 60 h all grew E. coli but none B. fragilis. Succumbed animals revealed diffuse peritonitis with growth of E. coli and B. fragilis at autopsy, whereas surviving animals showed abscess formation at investigation on day 8 after challenge. It was concluded that the model closely resembled intraabdominal abscess formation with sepsis in man.

Abdomen↗
PubMed1987

A new screening method for anti-ulcer agents: psychological stress produced by intraspecies emotional communication.

Psychological stress produced by intraspecies emotional communication in a communication box was studied to see whether it could be applied to a new screening method for anti-ulcer agents. There were two groups of mice, the 'sender' mice that received electrical foot shocks and showed emotional responses such as piloerection, abnormal squealing and jumping, and the 'responder' mice that were affected by the sender's emotional responses without foot shock. The gastric lesions (erosions) produced by conditioned emotional stimuli were observed in both groups. The effects of the anti-ulcer drugs cetraxate, cimetidine and gefarnate were examined. In 'senders', the gastric lesions were significantly suppressed by the administration of cetraxate at a dose of 200 mg/kg (p.o.) or cimetidine at doses of 30 and 100 mg/kg (p.o.). The gastric lesions in 'responders' were significantly suppressed by two administrations of cetraxate at doses of 100 and 200 mg/kg (p.o.), cimetidine at doses of 10-100 mg/kg (p.o.) or gefarnate at a dose of 200 mg/kg (p.o.). The gastric lesions of 'responders' were more sensitive to anti-ulcer drugs. The present results indicate that the gastric erosions of 'responders' are useful for the evaluation of anti-ulcer agents.

Animal Communication↗
PubMedDate not supplied

Effect of pharmacological doses of 3-0-methyl-D-glucose and 2-deoxy-D-glucose on rat brain glucose and lactate.

The present investigation examined the effects of two glucose analogues, 3-0-methyl-D-glucose (30MG) and 2-deoxy-D-glucose (2DOG) on basal levels of rat brain glucose and lactate. The results showed that pretreatment (iv) with 30MG up to 2 g/kg caused a transient drop in brain glucose levels to 42% of control value within 2.5 min and a drop in lactate levels to 75% of control value by 5 min. 2DOG administration (2 g/kg) affected glucose in a biphasic response with an initial drop to 46% of control value seen by 2.5 min, followed by a progressive increase to 290% of the control value by 40 min. This elevated level of glucose was sustained for approximately 40 min. Lactate levels responded to 2DOG administration by a decrease to 37% of control value within 10 min post-injection and returned to near basal levels by 160 min. A dose response was also examined for both compounds. Behaviorally 30MG had no apparent effects. However, the response to 2DOG was a reduction in voluntary movements, piloerection, irregular clonic jerks, splayed limbs and fits of wild running. These experiments were designed to evaluate the potential of 30MG or 2DOG for attenuating the well documented rise in brain lactate levels following an ischemic insult. Our results suggest that under certain experimental conditions either 30MG or 2DOG could prevent brain lactate rise and might have beneficial effects in minimizing the neuropathological consequences of ischemic damage that could be related to increases in brain lactate.

3-O-Methylglucose↗
PubMedDate not supplied

Characterization of carbon disulfide neurotoxicity in C57BL6 mice: behavioral, morphologic, and molecular effects.

Female C57BL6 mice were exposed to 0 or 800 ppm carbon disulfide (CS2), 6 h/d, 5 d/wk for 20 weeks. The neurologic function of all mice was assessed once at the end of exposures using a functional observational battery. General health effects included a decrease in body weight gain, piloerection, hunched body posture, and ptosis. Treatment-related effects included altered gait (uncoordinated placement of hind limbs and ataxia) and impaired function on an inverted screen test. In addition, rearing and locomotor movement were decreased in treated mice. Focal to multifocal axonal swelling was seen predominantly in the muscular branch of the posterior tibial nerve, and occasionally giant axonal swelling was detected in the lumbar segment of the spinal cord. Electron microscopic examination revealed swollen axons with massive accumulation of neurofilament proteins within the axoplasm. Covalent cross-linking of erythrocyte spectrin (surrogate protein to neurofilament protein) was demonstrated in mice exposed to CS2 but not in mice receiving filtered air. These data provide supportive evidence that covalent cross-linking of neurofilament proteins is a significant feature of the axonal swellings in mice produced by inhalation exposure to CS2.

Administration, Inhalation↗