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PubMed1998

Metamizol potentiates morphine effects on visceral pain and evoked c-Fos immunoreactivity in spinal cord.

In a model of visceral pain consisting of intraperitoneal injection of acetic acid (writhing test), simultaneous administration of subanalgesic doses of metamizol (150 mg/kg) and morphine (0.2 mg/kg) resulted in a potent analgesia (19 +/- 1 vs. 2.3 +/- 0.8 writhes; P < 0.05). While the analgesic effect of morphine (2 mg/kg) was antagonized by naloxone (1 mg/kg), the opioid antagonist did not reverse the analgesia induced by the combination of metamizol and morphine. Potentiation by metamizol was also observed as a bilateral decrease in stimulus-evoked c-Fos induction in superficial laminas (I-II) of the dorsal spinal cord after drug combination compared to single administration (66.5 +/- 2.2 vs. 80.7 +/- 4.2; P < 0.05). Conversely, the number of nuclei immunostained with an antibody that recognizes all proteins of the Fos family was not modified by the same dose combination compared to single treatment (21.1 +/- 1.3 vs. 20.2 +/- 1.2). Furthermore, in a model of somatic pain consisting of peripheral thermal stimulation of the paws, simultaneous administration of metamizol (100-250 mg/kg) and morphine (0.5 mg/kg) failed to modify flexor reflex latency.

Acetic Acid↗
PubMed1998

Neurochemical effects of the enantiomers of mirtazapine in normal rats.

The present study was designed to examine the neurochemical effects of (+/-)-mirtazapine (10 mg kg(-1) i.p.) and its enantiomers in rats. Male Sprague-Dawley rats received either (+)-mirtazapine, (-)-mirtazapine, (+/-)-mirtazapine or vehicle, by intraperitoneal injection for two weeks. Maximum change in temperature from baseline, following a single dose of the 5-HT1A receptor agonist 8-Hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT) (0.15 mg kg(-1) s.c.), was used to assess the function of the 5-HT1A receptors. Chronic drug treatment potentiated this response, with (+/-)-mirtazapine > (-)-mirtazapine > (+)-mirtazapine. Receptor changes were also observed with a slight decrease in beta1-adrenoceptor density, although this failed to reach significance. A significant decrease in beta1-adrenoceptor affinity was observed following (-)-mirtazapine treatment. All drugs tested significantly reduced the density of the 5-HT2 receptors. Results of the present study suggest that in so far as alterations in these receptor populations are important for the therapeutic action of antidepressants, neither of the enantiomers appear to be more active than the racemic mixture.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed2002

Role of endocrine status and cell type in adhesion of human endometrial cells to the peritoneum in nude mice.

OBJECTIVE: To investigate the role of different cellular types (epithelial and stromal endometrial cells and peritoneal cells) in the ectopic implantation of endometrium and to evaluate the importance of endocrine environment on the adhesion of endometrial cells to the peritoneum. DESIGN: Experimental prospective study. SETTING: University hospital, department of cell biology. ANIMAL(S): One hundred one nude mice. INTERVENTION(S): Monolayer culture of human epithelial and stromal endometrial cells obtained from patients undergoing hysterectomy or laparoscopy for benign disease. Intraperitoneal injection of cells into nude mice. MAIN OUTCOME MEASURE(S): Two weeks after cell injection, adhesion of endometrial cells was evaluated by histological and immunohistochemical examination. RESULT(S): Mixed cultures of stromal and epithelial cells, but not purified epithelial or stromal cells alone, adhered to the mouse peritoneum and led to endometriotic-like nodules. Pretreatment of cells with estrogen alone or with estrogen and progestin resulted in a higher percentage of animals developing endometriotic-like nodules, whereas treatment with progestin alone did not affect endometriotic implantation. CONCLUSION(S): Our data indicate that the success of endometrial cell implantation is dependent on the cooperativeness between stromal and epithelial endometrial cells, as well as on the endocrine environment of endometrial cells, but not that of recipient animals. The results emphasize the role of both endometrial cell types for ectopic implantation.

Adult↗
PubMed1990

Fluorescent detection of rabbit endometrial implants resulting from monodispersed viable cell suspensions.

A model for early stage endometriosis was prepared in rabbits by intraperitoneal injection of monodispersed viable endometrial cells. With this model, we have found that DHE fluorescence increases the sensitivity of detection of endometrial tissue. The potential experimental and clinical significance of ectopic endometrial detection by porphyrin fluorescence is enhanced by the recent report of endometrial transplant destruction by PDT. Although caution must be exercised for extrapolation from animal experiments to human conditions, these results encourage further evaluation of photosensitization for the study and potential treatment of disorders involving endometrial tissue.

Animals↗
PubMed1997

In vitro hatched oncospheres of Asian Taenia from Korea and Taiwan develop into cysticerci in the peritoneal cavity of female scid (severe combined immunodeficiency) mice.

In vitro hatched (but not activated) oncospheres of Asian Taenia obtained in Korea and Taiwan, prepared by the sodium hypochlorite method, rinsed with sterile PBS several times and adjusted to 5 x 10(4)/0.5 ml PBS, were injected intraperitoneally or subcutaneously into male or female scid mice of 3 different strains. When these scid mice were sacrificed 4 months later, the females harboured fully developed cysticerci either in the peritoneal cavity or under the back skin, whereas males did not. All cysticerci from the peritoneal cavity were easily recovered by rinsing the abdomen with PBS. Although most cysticerci recovered from pig liver usually become calcified within 1-2 months, in female scid mice they all increased in size and were viable. Intraperitoneal (i.p.) injection of in vitro hatched oncospheres is recommended for easier recovery of Asian Taenia metacestodes in laboratory animals.

Animals↗
PubMedDate not supplied

Tacrolimus-rapamycin combination therapy for experimental autoimmune uveoretinitis.

Tacrolimus and rapamycin both belong to a new family of immunosuppressants, immunophilin ligands, but the mechanisms by which they inhibit T cell activation are different. Therefore, we tested the immunosuppressive effects of combination therapy with low doses of tacrolimus and rapamycin on experimental autoimmune uveoretinitis (EAU) in rats. Male Lewis rats, immunized with S-antigen (S-Ag) were given intraperitoneal injection of the combined drugs for 14 days after the immunization with S-Ag. Effects were evaluated by clinical observations, histological examination and immune response. The combination therapy with tacrolimus (0.1 mg/kg per day) and rapamycin (0.03 mg/kg per day) achieved 100% suppression of clinical EAU and 66.7% suppression of histological EAU; tacrolimus combined with a higher dose of rapamycin (0.1 mg/kg per day) caused 100% suppression clinically and histologically. Therapy with either drug alone achieved only partial suppression: tacrolimus alone (0.1 or 0.2 mg/kg per day) or rapamycin alone (0.03-0.2 mg/kg per day). Doubling the dose of either drug produced only 16.7% suppression with rapamycin or 50% suppression with tacrolimus. The serum antibody levels to S-Ag and proliferative response of lymphocytes to S-Ag were also significantly suppressed by the combination therapy with low doses of tacrolimus and rapamycin.

Animals↗
PubMed2003

Polymorphonuclear neutrophils promote rFGF-2-induced angiogenesis in vivo.

BACKGROUND: The role of neutrophils in angiogenesis remains largely unknown. Recent evidence has shown that polymorphonuclear neutrophils (PMNs) produce several proangiogenic cytokines, including VEGF, TNF-alpha, IL-1, IL-6, and IL-8. In addition, PMN-derived proteinases promote endothelial cell migration. We hypothesized that PMNs may facilitate angiogenesis and that reducing circulating PMNs might alter the host angiogenic response. MATERIALS AND METHODS: We utilized a corneal pocket assay to compare rFGF-2-induced vessel formation in the corneas of mice with normal levels of circulating neutrophils to those in a neutropenic state. Circulating PMNs were reduced using serial intraperitoneal injections of monoclonal antibody to Gr-1. Slow release rFGF2 pellets were implanted into the corneas of neutropenic mice and controls. Corneal neovascularization, measured as vessel length and area of vessel in-growth, was quantified using slit-lamp microscopy on day 7. RESULTS: The average number of circulating PMNs was significantly reduced in the experimental group compared to the control group on days 1-7 (P < 0.05). No statistical differences in circulating monocytes or lymphocytes were observed from days 0 to 6. Mice in the experimental group had a vascular area of 2.58 +/- 0.2 mm(2) compared to 3.55 +/- 0.3 mm(2) in the control group (P < 0.05). CONCLUSIONS: Corneal neovascularization in response to rFGF-2 is diminished by PMN depletion. PMNs play an important role in facilitating rFGF-2-induced angiogenesis.

Animals↗
PubMed2001

The H3 receptor is involved in cholecystokinin inhibition of food intake in rats.

We investigated the peripheral effects of an H3-receptor agonist and an H3-receptor antagonist (R)alpha-methylhistamine (Ralpha-MeHA) and thioperamide, respectively, on basal feeding and the CCK8-induced inhibition of food intake in rat. Intraperitoneal injection of thioperamide reduced food intake in a dose-dependent manner with maximal inhibition (35%, P<0.01 vs saline) at 3 mg/kg. (R)alpha-MeHA (0.3-3 mg/kg i.p.), an H3-receptor agonist alone had no effect on feeding but reversed the thioperamide-induced inhibition of food intake in a dose-dependent manner. The maximal feeding inhibitory dose of thioperamide (3 mg.kg i.p) increased by 40% and 22 % (P<0.01 vs saline) brain and stomach histamine contents, respectively. Histamine (0.3 - 6 mg/kg i.p.) and CCK-8 (3 - 30 microg/kg i.p) also inhibited food intake in a dose-dependent manner. Inhibition was 20% to 40% for histamine and 40% to 80% (P<0.01 vs saline) for CCK8. CCK-8 inhibition of feeding was increased by thioperamide and prevented by (R)alpha-MeHA in a dose-dependent way. In addition, CCK-8 did not reduce food intake if rats were pretreated with pyrilamine or ranitidine postsynaptic H1- and H2-receptor antagonists respectively. Our data suggest that the H3-receptor is involved in basal feeding. They also suggest that CCK satiety depends upon the release of histamine which acts on the H2- and H1-receptors, the final mediators of this effect.

Animals↗
PubMed2002

In vivo effects of Panax ginseng extracts on the cytochrome P450-dependent monooxygenase system in the liver of 2,3,7,8-tetrachlorodibenzo-p-dioxin-exposed guinea pig.

The effects of the subchronic administration of Panax ginseng extracts were examined on the hepatic cytochrome P450-dependent monooxygenase system of guinea pigs pre-exposed to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). Panax ginseng extracts were intraperitoneally administered to guinea pigs at 100 mg/kg/day for 14 days from 1 week after a single intraperitoneal injection of 1 microg of TCDD/kg of body weight. TCDD treatment increased the total cytochrome P450 content 2.86-fold, and this was remarkably inhibited by the administration of Panax ginseng extracts. Treatment with ginseng extract alone also decreased the contents of cytochrome P450 by 33%, but both TCDD and ginseng extracts had no effect on cytochrome b(5) content. The administration of TCDD resulted in a 1.73-fold increase in microsomal NADPH-cytochrome P450 reductase activity in the guinea pig liver, and this was significantly inhibited by ginseng extracts, but treatment with ginseng extracts alone had no effect on its activity, and no statistical changes in the activity of NADPH-cytochrome b(5) reductase were observed in guinea pig liver due to TCDD and/or ginseng extract administration. Compared to the control, ECOD activity remarkably (1.76-fold) increased after TCDD administration, but this increase was completely inhibited by treatment with ginseng extract. Treatment with ginseng extract alone resulted in a 50% reduction of ECOD activity. TCDD administration remarkably induced benzphetamine demethylation (BPDM) activity, while ginseng extract also slightly increased the enzyme's activity, but the induction attributed to ginseng extracts was not statistically significant. Even though administration of ginseng extracts slightly inhibited TCDD-induced BPDM activity, the inhibition was not statistically significant. These results indicate that ginseng extract exerts different effect on the induction of P450 isozymes. From these results, we suggest that Panax ginseng extracts may act as an inhibitor of CYP1A rather than that of CYP2B.

7-Alkoxycoumarin O-Dealkylase↗
PubMed2003

Transforming growth factor alpha-mediated gastroprotection against stress ulceration in the rat: involvement of capsaicin-sensitive sensory neurons.

Exogenously administered TGF alpha has been shown to protect rodent gastric mucosa against injury caused by acid-dependent and acid-independent injury. The present study examined whether the gastroprotective effects of TGF alpha on stress-induced gastric ulceration in the rat involves activation of capsaicin-sensitive sensory neurons. Fasted male SD rats were subjected to water restraint stress (WRS) for four hours. Thereafter, rats were euthanized; the stomach opened and macroscopic areas of gastric ulceration quantitated (mm(2)). Gastric tissue contents of TGF alpha and the sensory neuropeptide, calcitonin gene-related peptide (CGRP) were determined by radioimmunoassay. Prior to stress rats received TGF alpha 50, 100 or 200 microg/kg by intraperitoneal injection. Sensory denervation was accomplished by high dose capsaicin treatment. WRS caused severe ulceration in the gastric corpus; 46.1 + 6.6 mm(2). Parenteral administration of TGF alpha caused dose-dependent reduction in gastric injury: 34.7 + 4.9 mm(2) with 50 microg/kg (p < 0.05); 25.4 + 3.6 mm(2) with 100 microg/kg (p < 0.001) and 9.4 + 0.8 mm(2) with 200 microg/kg (p < 0.001). The gastroprotective action of TGF alpha (200 microg/kg, i.p.) was abolished by capsaicin-induced sensory denervation. In addition, WRS ulceration was associated with significant reduction in gastric CGRP (-42%) and TGF alpha (-48%) content. Reduction in CGRP content was prevented by TGF alpha pretreatment. We conclude that: 1) TGF alpha caused dose-dependent gastroprotection against WRS ulceration, 2) TGF alpha-mediated gastric mucosal protection was prevented by capsaicin-induced sensory denervation and, 3) stress-induced injury was associated with significant reduction in gastric content of both TGF alpha and CGRP.

Animals↗
PubMed1996

Systemic cocaine challenge after chronic cocaine treatment reveals sensitization of extracellular dopamine levels in nucleus accumbens but direct cocaine perfusion into nucleus accumbens does not: implications for the neural locus of cocaine sensitization.

Rats were treated chronically with 20 mg/kg/day cocaine (by intraperitoneal injection) for 16 days, followed by 7 days of cocaine wash-out. On the next day, rats were challenged with an acute dose of cocaine administered by one of two routes (systemic or intracranial), and extra-cellular dopamine (DA) in the nucleus accumbens (Acb) was measured by in vivo microdialysis. Rats acutely challenged systemically with 20 mg/kg cocaine showed enhanced Acb extracellular DA levels (compared to control rats that had not previously received chronic cocaine). However, rats acutely challenged with intracranial cocaine by perfusion of 10(-5) M cocaine directly into the Acb did not. It is suggested that both the development and triggering of cocaine sensitization, as manifested by enhanced Acb DA content to subsequent acute cocaine challenge, may involve more than just neural mechanisms occurring locally within the Acb.

Analysis of Variance↗
PubMed1999

Mucolytics and antioxidant activity.

We investigated effects of the mucolytics ambroxol and N-acetylcysteine on airways reactivity evoked by histamine in guinea pigs exposed to toluene vapors. We did not find significant changes in reactivity of tracheal smooth muscle from animals treated with mucolytics compared to the control group. However, the administration of ambroxol and N-acetylcysteine caused a significant decrease in lung tissue reactivity. The effect of ambroxol was more pronounced after intraperitoneal injection than after inhalation, while N-acetylcysteine was only effective after inhalation. The protective effects of mucolytics in the lung tissue may be due to their antioxidant activity together with other mechanisms.

Acetylcysteine↗
PubMed1996

Effects of chronic treatment with haloperidol on [3H]PK 11195 binding in the rat brain and peripheral tissues.

The effects of chronic treatment with haloperidol on [3H]PK 11195 binding and labelling of the peripheral-type benzodiazepine receptor (PBR) in the rat brain and peripheral tissues were investigated using an in vitro receptor binding technique. The intraperitoneal injection with haloperidol (0.3 or 1.0 mg/kg) for 21 days produced a significant increase in the specific [3H]PK 11195 binding only in the olfactory bulb, but not in the other brain areas or peripheral tissues, while single or subchronic (4 days or 7 days) administration with the drug (0.3 mg/kg, i.p.) failed to increase the binding in the olfactory bulb. Scatchard analysis revealed a significant increase in the maximum number of [3H]PK 11195 binding sites in the olfactory bulb after chronic treatment with haloperidol, showing no change in the affinity of the binding. These results suggest that there is an interaction between PBR and the pharmacological actions of haloperidol in the brain area, and that some compensatory mechanism may be involved in the PBR changes.

Animals↗
PubMed2000

The effect of dehydroepiandrosterone on Zucker rats selected for fat food preference.

When allowed to select between macronutrients in a 1-h-a-day meal paradigm, Zucker rats consume 20-80% of their total caloric intake as fat. If they receive an intraperitoneal injection of DHEA 2 h before such a test meal, they consume fewer total calories. The magnitude of this effect on each macronutrient depends upon the animal's initial preference for fat; the higher the initial fat preference, the more profound is the decrease in caloric intake and the more pronounced the effect on fat consumption. Doses as low as 25 mg DHEA/kg body weight are effective. Lean Zucker rats that prefer to consume a high-fat diet have higher epinephrine and dopamine levels in select regions of the hypothalamus known to control food intake. Administration of DHEA to such animals 2 h before decapitation reduces the content of norepinephrine and these monoamines to levels that mimic the values found in the low-fat-preferring animals. It is hypothesized that exogenous DHEA causes the acute release of norepinephrine, epinephrine, and dopamine in select regions of the hypothalamus, and this release causes a decrease in food intake, particularly fat.

Animals↗
PubMed2002

Inhibition of nitric oxide synthase delays the development of tolerance to LPS in rats.

The role of nitric oxide (NO) was investigated in endotoxin (lipopolysaccharide, LPS) tolerance in freely moving biotelemetered rats. We monitored changes in febrile response and feeding behavior (food intake, water intake) during the development of tolerance to repeated intraperitoneal injections of LPS (50 microg/kg) along with injections of N(omega)-nitro-L-arginine methyl ester (L-NAME; 50 mg/kg), an inhibitor of NO synthase. Rats were treated with LPS and L-NAME for three consecutive days. On the fourth day, all rats were injected with LPS alone. Control rats were injected with saline along with saline or with L-NAME for four consecutive days. Rats repeatedly injected with LPS became tolerant to pyrogenic and hypophagic/cachexic effects of LPS as early as on the second day of experiment. The treatment with L-NAME prevented the attenuation of febrile response following the second LPS injection. Moreover, the depressive effects of LPS on body weight as well as on water and food intake were prolonged in rats treated with a combination of L-NAME and LPS. Injection of LPS caused a 3.5-fold increase in plasma nitrite within 3 h and nitrite levels remained significantly elevated 6 and 24 h after LPS. Rats injected secondly with LPS did have still 2.5- to 3-fold increase in plasma nitrite levels 3 and 6 h, but not 24 h, after injection. Third injection of LPS did not elevate nitrite level in plasma. Taken together, presented data provide clear evidence that NO formation is involved in mechanisms responsible for development of early-stage tolerance to endotoxin.

Animals↗
PubMed1997

Behavioral and physiological sex differences observed in an animal model of fulminant hepatic encephalopathy in the rat.

Hepatic encephalopathy is characterized by a number of neuropsychiatric and motor disturbances observed in patients with liver dysfunction. The purpose of this study is to fully characterize behavioral and physiological sex differences in an animal model of fulminant hepatic encephalopathy (FHE). Male and female rats were administered thioacetamide (600 mg/kg) via i.p. (intraperitoneal) injection at Hours 0 and 24 and allowed to progress into the four stages of FHE. Male rats reached all four stages of FHE significantly earlier than female rats (p < 0.05). The performance of the male rats deteriorated more quickly (p < 0.05) than that of the females in all of the sensory and motor behavioral tests. Sex differences were observed in the liver enzymes of the FHE rats. The levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), and alkaline phosphatase were significantly greater (p < 0.05) in male rats in all four stages of FHE. Significant increases were also observed in the levels of direct and total bilirubin (p < 0.05). Neuronal damage was observed in the CA1 and CA2 regions of the hippocampus. In the CA1 region, male rats displayed greater pathological changes in Stages III and IV (p < 0.05) than female rats. The damage in the CA2 region was only observed in Stage IV male rats. Our data indicate that observable behavioral and physiological sex differences occur in thioacetamide-induced FHE in the rat.

Animals↗
PubMed1998

Inhibitors of fatty acid oxidation (mercaptoacetate, R-3-amino-4-trimethylaminobutyric acid) stimulate feeding in mice.

Several lines of evidence indicate that fatty acid oxidation contributes to control of eating. We examined the effect of inhibitors of fatty acid oxidation (mercaptoacetate, R-3-amino-4-trimethylaminobutyric acid = emeriamine) on food intake in mice because fatty acid oxidation has been shown recently to increase the hepatic membrane potential in mouse liver, and this potential has been proposed to represent a signal for control of food intake. The effect of intraperitoneal injection of mercaptoacetate (200, 400, or 600 micromol/kg body weight) and emeriamine dihydrochloride (8.7, 17.4, 34.8, or 69.6 micromol/kg body weight) was investigated in mice fed a fat-enriched diet (18% fat). Both mercaptoacetate (400 or 600 micromol/kg) and emeriamine (34.8 or 69.6 micromol/kg) significantly increased food intake. These results suggest that fatty acid oxidation is also involved in feeding control in mice. Therefore, the pertinent mechanisms can be studied in mice.

Animals↗
PubMed1999

Dehydroepiandrosterone (DHEA) decreases open-field spontaneous activity of Zucker rats.

The behavioral endpoint of open-field spontaneous activity was used to characterize further the central nervous system actions of dehydroepiandrosterone. DHEA, administered by intraperitoneal injection, causes a dose-dependent decrease in the spontaneous activity of lean and obese Zucker rats when exposed to a novel environment. The midpoint of DHEA's effect is around 50 mg/kg, a dose similar to that which reduces caloric intake of the rat by nearly 50%. d-Fenfluramine, a known anorectic agent, decreases spontaneous activity under the same conditions. Administration of either DHEA or d-fenfluramine leads to changes in serotonin or its metabolite, 5-hydroxyindole acetic acid, in select regions of the brain. These results emphasize that DHEA given peripherally can affect both the level of neurotransimitters and central nervous system function.

Animals↗