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PubMed1996

Prevention of endotoxin-induced mortality by antitissue factor immunization.

BACKGROUND: Microvascular thrombosis with intravascular fibrin deposition is a characteristic pathologic alteration during endotoxic shock. This effect is predominantly mediated by expression of the cellular procoagulant tissue factor by endothelial cells and cells of monocyte or macrophage lineage, resulting in acceleration of the coagulation cascade and fibrin deposition. OBJECTIVE: To determine whether modulation of this response by treatment with an antitissue factor antibody might have beneficial effects. DESIGN: A polyclonal antibody to murine tissue factor was prepared by injecting rabbits with a synthesized peptide sequence of murine tissue factor. To determine the activity of the antibody, elicited murine peritoneal macrophages were treated for 4 hours with 10-micrograms/mL lipopolysaccharide (LPS), and procoagulant activity was determined via a clotting assay (milliunits of activity per 10(6) macrophages). RESULTS: The tissue factor antibody abrogated LPS-induced macrophage procoagulant activity, confirming activity of the antibody (macrophages, 236 +/- 28 mU/10(6) macrophages; macrophages/LPS, 3801 +/- 190* mU/10(6) macrophages; macrophages/LPS/alpha-tissue factor, 753 +/- 92* mU/10(6) macrophages; n = 3; the asterisk indicates P < .05 by an analysis of variance). Additionally, antibody-protein affinity was confirmed by Western blot analysis. Having determined the activity of the antibody in vitro, we tested its efficacy in vivo in a lethal endotoxemia model. Mice were immunized with 200 microL of antiserum intraperitoneally 2 hours before injection with 250 micrograms of LPS intraperitoneally and 24 hours later. Control animals received 200 microL of saline solution. All animals initially exhibited lethargy and piloerection, characteristic of the predicted response to LPS. However, immunized animals had a significantly (P < .05) reduced mortality compared with control animals. Fibrinogen levels were significantly (P < .05) higher in the immunized mice, suggesting decreased consumption of coagulation factors, a finding consistent with an antitissue factor effect. Further, plasma tumor necrosis factor levels 90 minutes after LPS injection were similar in both groups, suggesting normal induction of the cytokine cascade. CONCLUSIONS: Modulation of microvascular fibrin deposition by abrogating tissue factor-mediated coagulation significantly (P < .05) improved survival in this model without attenuating the initiation of the cytokine cascade. These findings suggest a pathogenic role for coagulation in the induction of acute organ injury during sepsis.

Amino Acid Sequence↗
PubMed1996

Noradrenergic mechanisms in stress and anxiety: I. Preclinical studies.

There is considerable preclinical evidence for a relationship between noradrenergic brain systems and behaviors associated with stress and anxiety. The majority of noradrenergic neurons are located in the locus coeruleus (pons), with projections throughout the cerebral cortex and multiple subcortical areas, including hippocampus, amygdala, thalamus, and hypothalamus. This neuroanatomical formation of the noradrenergic system makes it well suited to rapidly and globally modulate brain function in response to changes in the environment, as occurs during the presentation of stressors. Stress exposure is associated with an increase in firing of the locus coeruleus and with associated increased release and turnover of norepinephrine in brain regions which receive noradrenergic innervation. Increased firing of the locus coeruleus is also associated with behavioral manifestations of fear, such as arched back and piloerection in the cat. Exposure to chronic stress results in long-term alterations in locus coeruleus firing and norepinephrine release in target brain regions of the locus coeruleus. Norepinephrine is also involved in neural mechanisms such as sensitization and fear conditioning, which are associated with stress. These findings are relevant to an understanding of psychiatric disorders, such as panic disorder and post-traumatic stress disorder (PTSD), the symptoms of which have been hypothesized to be related to alterations in noradrenergic function.

Adrenergic Fibers↗
PubMed2001

Age differences in arousal and vigilance in California ground squirrels (Spermophilus beecheyi).

Newly emerged pup, juvenile, and adult California ground squirrels (Spermophilus beecheyi douglasii) were videorecorded at a seminatural field site in northern California. Video data revealed age differences in the budgeting of ground squirrel behavior, habitat use, and physiological arousal as indicated by morphometric analyses of tail piloerection. Adults and juveniles devoted their time to foraging in the open at feeding stations while displaying low to moderate levels of arousal, respectively. Pups remained vigilant on the fringe of covered habitats while displaying comparatively higher levels of arousal. Higher pup arousal may facilitate memory formation during early stages of development.

Aging↗
PubMed1990

Cytokine-related syndrome following injection of anti-CD3 monoclonal antibody: further evidence for transient in vivo T cell activation.

In vivo injection of the hamster anti-murine CD3 monoclonal antibody 145 2C11 into BALB/c mice induces a massive systemic release of several cytokines. Very high circulating levels of tumor necrosis factor are detected both by enzyme-linked immunosorbent assay and L-929 bioassay 90 min following a single injection of 10 micrograms/mouse 145 2C11. Peak circulating levels of exclusively T cell-derived products such as interferon-gamma, interleukin 2 and interleukin 3 are also detected 90 min to 8 h post-injection. Importantly, this cytokine release is transient since none of these cytokines are still present 12 to 24 h post-injection. In parallel to cytokine release, 145 2C11-treated mice (10 micrograms/mouse) exhibit somnolence, hypomotility (quantified by actimetry), hypothermia, diarrhea and piloerection. At this dosage, the physical reaction is not lethal and reverses in all mice by 48 h post-injection. Severe but again reversible anatomopathological changes are also observed: massive cellular depletion, necrosis and edema of lymphoid organs, leakage syndrome and inflammatory cell infiltrates of the lung, cell vacuolization, necrosis and vascular congestion of the liver. All these data are similar to the clinical and immunological manifestations of the OKT3-induced reaction in patients and, thus, provide an invaluable experimental tool to study its mechanisms and explore its prevention.

Animals↗
PubMed2005

Development of pregnancy in rats treated with Hypericum perforatum.

St John's wort (Hypericum perforatum) is a medicinal plant used in the treatment of depression and other psychiatric disorders. In the present paper, the toxicity of H. perforatum administered to female rats during the period of organogenesis (day 9-15 of pregnancy) was evaluated. Thirty inseminated Wistar rats were randomly distributed into control and treated groups, which received, by gavage, 0.5 mL of saline and 36 mg/kg body weight of Jarsin dried extract diluted into 0.5 mL of saline, respectively. Maternal toxicity was evaluated through: water and food intake, body weight gain, piloerection, locomotor activity, diarrhea and death occurrence. Animals were killed on day 21 of pregnancy, when fetuses and placentas were removed and weighed. The indices of implantation and resorption were calculated. Clinical signs of maternal toxicity were not observed and none of the variables analysed showed statistically significant differences. In the dose administered in the experimental model used, H. perforatum does not seem to be toxic to the mother nor to interfere with the progress of gestation during organogenesis.

Administration, Oral↗
PubMed1999

Molecular design of conjugated tumor necrosis factor-alpha: synthesis and characteristics of polyvinyl pyrrolidone modified tumor necrosis factor-alpha.

We conjugated tumor necrosis factor-alpha (TNF-alpha) with the synthetic polymeric modifier polyvinyl pyrrolidone (PVP) to facilitate its clinical use for anti-tumor therapy. TNF-alpha was chemically conjugated with the terminal carboxyl-bearing PVP at one end of its main chain, which was radically polymerized via the formation of an amide bond between the lysine amino groups of TNF-alpha and carboxyl group of PVP. In vitro specific bioactivity of PVP-conjugated TNF-alpha (PVP-TNF-alpha) relative to that of native TNF-alpha gradually decreased with increases in the degree of PVP attachment. In contrast, PVP-TNF-alpha in which 40% of TNF-alpha lysine residues were coupled with PVP (MPVP-TNF-alpha) exhibited the highest anti-tumor activity among the conjugated derivatives examined. MPVP-TNF-alpha had more than 200-fold higher anti-tumor efficacy than native TNF-alpha, and the anti-tumor activity of MPVP- TNF-alpha was more than 5-fold stronger than that MPEG- TNF-alpha which had the highest anti-tumor activity among PEG-conjugated TNF-alphas examined. Additionally, a high dose of native TNF-alpha induced toxic side-effects such as body weight reduction, piloerection and tissue inflammation, while no side effects were observed following i.v. administration of MPVP-TNF-alpha. The plasma half-life of MPVP-TNF-alpha (360 min) was about 80 and 3-fold longer than those of native TNF-alpha (4.6 min) and MPEG-TNF-alpha (122 min), respectively. These results suggested that PVP is a useful polymeric modifier for increasing the anti-tumor activity of PVP.

Animals↗
PubMed1995

The evaluation of the developmental toxicity of hydrochlorothiazide in mice and rats.

Timed-pregnant CD-1 outbred albino Swiss mice and CD Sprague-Dawley rats were administered hydrochlorothiazide (HCTZ, USP) in corn oil by gavage during major organogenesis, Gestational Days (GD) 6 through 15. The doses administered were 0, 300, 1000, or 3000 mg/kg/day for mice and 0, 100, 300, or 1,000 mg/kg/day for rats. Maternal clinical status was monitored daily during treatment. At termination (GD 17, mice; GD 20, rats), confirmed pregnant females (20-27 per group, mice; 36-39 per group, rats) were evaluated for clinical status and gestational outcome; each live fetus was examined for external, visceral, and skeletal malformations. In mice, no maternal mortality was observed. However, clinical signs including dehydration, piloerection, lethargy, and single-day weight loss appeared to be dose-related. HCTZ had no effect on maternal weight gain or water consumption, gravid uterine weight, relative maternal liver weight, or relative maternal kidney weight. There was no definitive evidence of embryotoxicity or fetal toxicity for mice on GD 17. Thus, the no observed adverse effect level (NOAEL) for both maternal and developmental toxicity was 3000 mg/kg/day. In rats, HCTZ had no effect on maternal survival, clinical signs, or water consumption. Clinical signs were not dose-related. Maternal weight gain during treatment was depressed at 1000 mg/kg/day. Gravid uterine weight and relative maternal liver weight were unaffected. Relative maternal kidney weight was slightly (7-8%) increased at all dose levels, but there was no evidence of a dose response. Thus, the maternal NOAEL for rats was 300 mg/kg/day, based on decreased maternal weight gain during treatment at 1000 mg/kg/day.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

Long-lasting hypothermic effects of vincristine in rats.

The effects of vincristine given intravenously on deep and superficial body temperature were assessed in rats kept at ambient temperature within the thermoneutral range. Vincristine (0.5 and 1 mg/kg i.v.) produced a gradual but marked hypothermic response which was dose-dependent, reached its maximum after approximately 3 h and lasting approximately 48 h. Vincristine induced a decrease in deep body temperature which was accompanied by piloerection and a decrease in skin temperature. Pretreatment with phentolamine, an alpha-adrenoceptor blocking agent (0.5 mg/kg i.v. 15 min before) prevented the hypothermic effects induced by subsequent administration of vincristine (0.5 mg/kg i.v.). These experiments showed that vincristine produced a marked hypothermic response in rats. However, the precise site of action remains to be established.

Animals↗
PubMed1984

Behavioural and electrocortical spectrum power changes after intraventricular injection of patulin in rats.

The effects of patulin when given into the third cerebral ventricle of rats, on behaviour and electrocortical spectrum power have been investigated. Patulin (10 micrograms i.v.t.) produced behavioural sedation, hypoalgesia, tail rigidity, piloerection and postural changes. This symptomatology lasted approx. 3 h and was accompanied by slower frequency and larger amplitude potentials in the electrocorticogram (ECoG) and by an increase in total voltage power. A larger dose (50 micrograms) produced a more dramatic picture characterized by catatonic posture with kyphosis, loss of the righting reflex, tail rigidity and on a few occasions short-duration episodes of tonic-clonic convulsions. Such a symptomatology was accompanied by a flattening of ECoG activity with a significant fall in total voltage power, as well as in preselected bands (0-3, 3-6, 6-9, 9-12, and 12-16 Hz). A lower dose (1 microgram) of patulin, on the other hand, produced behavioural sedation without significant changes in ECoG spectrum power.

Animals↗
PubMed1992

Attenuation of the morphine withdrawal syndrome by inhibition of catabolism of endogenous enkephalins in the periaqueductal gray matter.

We have investigated the effects of the local administration into the periaqueductal gray matter of thiorphan, a selective inhibitor of endopeptidase 24.11 "enkephalinase", kelatorphan, (R)-3-(N-hydroxy-carboxamido-2-benzylpropanoyl)- L-alanine, and RB 38 A, (R)-3-(N-hydroxy-carboxamido-2-benzylpropanoyl)-L-phenylalanine, two almost complete inhibitors of enkephalin metabolism, on the naloxone-precipitated morphine withdrawal syndrome in rats. Local administration of these inhibitors decreased the severity of the withdrawal syndrome. Jumping, chewing, diarrhea, piloerection, salivation and hypothermia were decreased by all drugs. Lacrimation and weight loss were reduced by kelatorphan and RB 38 A whereas teeth chattering, tremor, eye twitch and rhinorrhea were decreased only by RB 38 A. The rise in plasma corticosterone levels was only slightly reduced by the three inhibitors. Wet dog shakes and ptosis remained unchanged. These results indicate that during the morphine withdrawal syndrome in rats there is a tonic or/and naloxone evoked release of opioid peptides, presumably enkephalins, into the periaqueductal gray matter and that inhibition of their degradation strongly decreases the severity of the withdrawal syndrome.

Analgesics↗
PubMed1983

Comparative assessment of dopamine agonist aporphines as anticonvulsants in two models of reflex epilepsy.

The anticonvulsant action of various aporphine derivatives that act on dopamine receptors has been investigated in two genetically determined animal models--DBA/2 mice with sound-induced seizures and baboons Papio papio with photically-induced seizures. Protection against the clonic and tonic phases of the seizures response in DBA/2 mice was seen for 15-60 min after (-)2,10,11-trihydroxy-N-n-propylnoraporphine (1.25 mg/kg) and (-)10,11-methyl-enedioxy-N-n-propylnoraporphine (0.625-1.25 mg/kg) and for 30-60 min after (-)2,10,11-trihydroxyaporphine (31.25 mg/kg). Short-lasting protection (up to 30 min) was seen following (-)2,10,11-trihydroxy-N-ethyl-noraporphine (1.25-6.25 mg/kg). Changes in audiogenic seizure susceptibility were accompanied by piloerection, ptosis and loss of spontaneous locomotor and exploratory behaviour. No protection was seen after (-)norapomorphine (0.05-18.75 mg/kg). All the compounds (including norapomorphine) significantly lowered rectal temperature, although the time course of this effect was often longer than that of protection against audiogenic seizures. In baboons, marked reductions in photomyoclonic responses were seen following (-)10,11-methylenedioxy-N-n-propylnoraporphine (0.25 mg/kg, lasting up to 2h); (-)2,10,11-trihydroxy-N-n-propylnoraporphine (0.5-2.5 mg/kg, lasting up to 7 h); (-)2,10,11-trihydroxyaporphine (5 mg/kg, duration of action 1-4 h) and (-)2,10,11-trihydroxy-N-ethylnoraporphine (6.25 mg/kg, lasting 2 h). Little change in responsiveness followed administration of (-)norapomorphine 1.25 or 6.25 mg/kg. Changes in photosensitivity were accompanied by yawning and pupil dilatation. (-)10,11-Methylenedioxy-N-n-propylnoraporphine (0.5-6.25 mg/kg) was also administered orally in baboons.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1980

Continuous-access phencyclidine self-administration by rhesus monkeys leading to physical dependence.

IV phencyclidine (PCP) self-administration was studied in five rhesus monkeys. The animals were given 23 h per day access with each respose producing an injection. For the first seven sessions saline was made contingent on responding. For the next 30 sessions responses produced 0.01 mg/kg PCP and for the next 20 sessions responses produced 0.05 mg/kg PCP. Withdrawal signs and symptoms were evaluated every 4 h during the subsequent saline-access period. All animals responded for 0.01 mg/kg injections at rates higher than their initial saline rates. Response rates decreased but total PCP intake increased during access to the higher dose. The levels of PCP self-administered resulted in severe intoxication. Evidence for physical dependence development was obtained. The symptoms emerged within 4--8 h after access was terminated, peaked at 12--16 h, and subsided by 24--48 h. The syndrome could be reversed by IV PCP administration. The most common symptoms were vocalizations, hyperresponsivity, bruxism, oculomotor hyperactivity, and diarrhea. During withdrawal the animals refused preferred food. In some of the animals piloerection, tremors, ear and facial twitches, and priapism occurred. Rhythmic abdominal contractions and emesis were seen in one subject and convulsive activity was seen in one subject.

Animals↗
PubMed1979

Percutaneous epidural neurostimulation in modulation of paraplegic spasticity. Six case reports.

Six cases of paraplegic, post-traumatic spasticity, alleviated by percutaneous epidural neurostimulation with temporary or permanent implanted neuroelectrodes from the L1 to L4 intervertebral levels are presented. Modulation of this spasticity and secondary beneficial physiological effects were achieved, including regulation of bowel regimens, production of sweating and piloerection below the level of the lesion, and morning erections. The main advantages of percutaneous epidural neurostimulation in modulating spasticity are the avoidance of destructive neurosurgical procedures, the regulation of secondary physiological and autonomic responses, the avoidance of antispasticity medications, and the reversibility of the neurostimulation procedure.

Adolescent↗
PubMed1995

Subjective and objective symptoms in relation to plasma methadone concentration in methadone patients.

Two rating scales, which were originally developed for measurements of objective and subjective signs of opiate withdrawal, were used to evaluate potential estimates (correlates) of methadone effects in relation to plasma methadone concentrations. Patients participating in our regular methadone maintenance treatment project were studied during 24 h after the intake of the daily methadone dose. Methadone concentrations in plasma were compared to the subjective (estimated by the patients) and objective (estimated by the investigator) signs of the drug effects before, and 2.5, 5, 9 and 24 h after intake of methadone. Some new items possibly related to rising methadone concentrations were added to the subjective scale. Results indicated that, for subjective ratings, the majority of the items investigated corresponded well with the plasma methadone concentrations. The most significant associations were found for the following items: low psychomotor speed, alertness, running nose, yawning and anxiety. For objective ratings, only the items rhinorrhea, piloerection and signs of anxiety were significantly associated with the methadone concentrations. These rating scales may, together with plasma methadone determinations, be of considerable value when making dose adjustments for methadone maintenance patients. Further work is, however, needed to establish concentration-effect relationships.

Adult↗
PubMed1995

Increase of extracellular dopamine in the medial prefrontal cortex during spontaneous and naloxone-precipitated opiate abstinence.

Abstinence from chronic morphine has been shown to reduce extracellular dopamine in the nucleus accumbens as measured by brain microdialysis (Acquas et al. 1991). In the present study, we investigated if similar changes take place in the prefrontal cortex. Withdrawal from a schedule of increasing doses of morphine administered intraperitoneally twice a day for 9 days up to a daily dose of 60 mg/kg resulted in doubling of basal extracellular concentrations of dopamine in the prefrontal cortex and in a mild withdrawal syndrome (ptosis, piloerection, hunched-back posture). Administration of a low dose of naloxone (0.5 mg/kg SC) to rats withdrawn from chronic morphine resulted in a full withdrawal syndrome with wet dog shakes and diarrhoea and an increase of extracellular dopamine that peaked at 40 min and returned to the pre-naloxone values by 80 min. The results show that dopamine neurotransmission in the medial prefrontal cortex responds to opiate withdrawal in a manner opposite to dopamine transmission in the nucleus accumbens and indicate that the dopamine system is affected by abstinence in a topographically specific manner, consistent with a different functional role of mesocortical as compared to mesolimbic dopamine systems.

Animals↗
PubMed1988

Hyperglycemic suppression of morphine withdrawal signs in the rat.

Male Sprague-Dawley rats maintained under controlled lighting and temperature conditions were used in this experiment. Morphine dependency was induced by giving increasing doses of morphine by intraperitoneal injection (IP group) or by the ingestion of morphine through drinking water (PO group). Animals were injected with 10, 20, 30 and 50 mg/kg morphine sulfate at days 1, 2, 3 and 4, respectively. Another group of animals received increasing concentrations of morphine through drinking water from 0.1, 0.2, 0.3 to 0.4 mg/ml at 48 h intervals. Morphine dependent animals were given naloxone by the intraperitoneal route to precipitate withdrawal. Glucose (3 g/kg or 10 g/kg) was given 10 min prior to the administration of naloxone to the respective groups. Another two groups of animals were made diabetic by the administration of streptozotocin. In one group, animals received increasing concentrations of 10, 20, 30 and 50 mg/kg morphine sulfate by the IP route at days 1, 2, 3 and 4, while the other group was not treated with morphine but was assessed for withdrawal signs to serve as the control. Withdrawal signs were assessed by observing the presence of diarrhea, tremor, piloerection, hunchbacked posture, teeth chattering, salivation, erection, restless activity, territorial exploring, irritability to handling, vocalization and jumping. Results obtained indicate that glucose administration at 10 g/kg abolished most of the withdrawal signs, and we were unable to induce the same degree of morphine dependency in diabetic animals as compared to the non-diabetic groups. It was concluded from this study that hyperglycemia could suppress morphine withdrawal signs.

Animals↗
PubMedDate not supplied

The effect of furazolidone and furaltadone on drug metabolism in rats.

This work examines the effect of oral treatment of rats with the nitrofuran drugs furazolidone (FZ) and furaltadone (F) at doses of 100, 200 and 400 mg/kg for 4 days, or F in the drinking water at concentrations of 0.1, 0.2 and 0.4% w/v for 14 days, on drug metabolism in vivo. FZ at doses of 200 and 400 mg/kg, and F at a dose of 400 mg/kg or at a concentration of 0.4% w/v in water depressed growth and prolonged pentobarbitone-induced sleeping time. Treatment also significantly increased the blood concentration of metronidazole when measured 30 and 40 min after metronidazole administration. Administration of tremorine (25 mg/kg, i.p.) to control vehicle-treated rats produced within 2-3 min tremors, piloerection, profuse salivation, defecation urination and chromodacryorrhesis (red tears). The onset of appearance of these signs was delayed to 7-12 min in rats pretreated with FZ or F (100 mg/kg, 4 days) or cimetidine (50 mg/kg, i.p.) given 45 min earlier. Taken together, these results suggest that FZ and F inhibit drug metabolism in rats. Treatment with these nitrofuran drugs may alter the disposition of certain drugs which may be given concomitantly with them.

Animals↗
PubMed2000

Precipitated and spontaneous withdrawal in rats tolerant to anandamide.

RATIONALE: There is evidence that cannabinoids cause tolerance and physical dependence in humans and animals. OBJECTIVES: The aim of this work was to study whether the endogenous ligand for the cannabinoid receptor, arachidonylethanolamide (anandamide), induced behavioral tolerance and physical dependence in rats. METHODS: Rats were injected with anandamide (20 mg/kg i.p.) daily for 2 weeks. To assess tolerance, on days 1, 8 and 15 of treatment rats were observed and behavior was tested. Two common methods were employed to assess physical dependence: interruption of anandamide dosing and vehicle substitution or administration of the cannabinoid CB1 receptor antagonist SR141716A (3 mg/kg i.p.). RESULTS: Full or partial tolerance developed to the classical behavioral effects elicited by the cannabinoids: hypothermia, catalepsy, hypomotility, decrease in stereotypic activity (rearing and grooming) and hindlimb splaying. No tolerance to anandamide was observed for reduced defecation. An abstinence syndrome appeared after abrupt cessation of cannabinoid intake and after withdrawal precipitated by SR141716A; the withdrawal signs were scratching, licking and biting, eating of feces, ptosis, arched back, wet dog shakes, head shakes, myoclonic spasms, writhing, forepaw fluttering, teeth chattering and piloerection. CONCLUSIONS: These findings indicate that the endogenous cannabinoid ligand, administered exogenously, induces both tolerance and physical dependence in rats.

Animals↗