Induction of Fos protein in neonatal rat hypothalami following intraperitoneal endotoxin injection.
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Age Factors↗
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Hypothalamic PGE2 and cAMP production and adrenocortical activation following intraperitoneal endotoxin injection: in vivo microdialysis studies in Lewis and Fischer rats.
Inflammatory disease-susceptible Lewis (LEW) rats exhibit reduced glucocorticoid release in response to inflammatory and neurotransmitter stimuli, compared to histocompatible Fischer (F/344) rats. This compromised hypothalamo-pituitary-adrenal (HPA) axis activity has been ascribed to a primary defect in hypothalamic corticotrophin-releasing factor-41 (CRF) secretion, possibly caused by abnormal signal transduction in the CRF neuron. In the present study, we have used in vivo microdialysis to asses the role of hypothalamic prostaglandin E2 (PGE2) and cyclic adenosine monophosphate (cAMP) in endotoxin-mediated HPA axis activation in adult hyporesponsive LEW and hyperresponsive F/344 rats. Basal plasma corticosterone concentration was significantly higher in F/344 relative to LEW rats; however, the basal levels of PGE2 and cAMP, recovered from microdialysis probes in the anterior hypothalamus, were significantly greater in the LEW rat. Lipopolysaccharide (LPS) (200 micrograms/kg) caused a time-dependent increase in corticosterone secretion, the magnitude of which was markedly greater in the F/344 rat. Both LEW and F/344 rats displayed a similar PGE2 profile in response to LPS, although in absolute terms the response was more pronounced in LEW rats. LPS caused a dose-related increase in cAMP production in the LEW rat and comparison with F/344 animals, following the 200 micrograms/kg dose of LPS, revealed a larger and more prolonged cAMP response in the LEW strain. Simultaneous administration of indomethacin (50 mg/kg) with LPS (200 micrograms/kg) in the LEW rat completely blocked the PGE2 and cAMP responses to the toxin and whilst the corticosterone response to LPS was significantly attenuated at 140 min, no difference was apparent by 240 min. Hence, PGE2 and cAMP participate in the hypothalamic response to endotoxin-mediated adrenocortical activation in both LEW and F/344 adult rats but the steroid and second messenger profiles are strain-specific. The cAMP response to LPS appears to depend on products of arachidonic acid metabolism, such as PGE2, and hence basal and stimulated production of these mediators may be effected by the steroid milieu.
Adrenal Cortex↗
[Comparative study of metabolic disturbances provoked in rat liver by the administration of ethanol or other compounds. V. Intraperitoneal pyruvate injection].
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Acetoacetates↗
[Response of the epiploon in guinea pig to intraperitoneal BCG injection; quantitative interpretation of results].
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BCG Vaccine↗
[Effects of sex hormones on experimental asthma induced by intraperitoneal ovalbumin injections in female albino rats].
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Animals↗
Regulation of early peritoneal neutrophil migration by macrophage inflammatory protein-2 and mast cells in experimental peritonitis.
Neutrophil (PMN) migration into the peritoneal cavity in response to fecal peritonitis is an important mechanism of host defense against bacterial invasion. We show that the murine C-X-C (PMN-specific) chemokine, macrophage inflammatory protein-2 (MIP-2), on intraperitoneal injection in mice, causes PMN migration into the peritoneum. MIP-2 mRNA and protein were expressed by peritoneal leukocytes after cecal ligation and puncture (CLP) in mice and neutralization of MIP-2 reduced peritoneal PMN migration. A prerequisite for neutrophil-endothelial adhesion and subsequent migration from the circulation is selectin-mediated rolling. Pretreatment of mice with an anti-P-selectin antibody before intraperitoneal injection of MIP-2 significantly reduced peritoneal PMN migration. However, there are no reports that a C-X-C chemokine can up-regulate endothelial selectins. We postulated that MIP-2, when injected intraperitoneally, interacts with a cell that is known to release factors that up-regulate endothelial selectins. A likely candidate is the mast cell, which contains histamine and tumor necrosis factor alpha (TNF-alpha), and both of these factors induce selectins. Intraperitoneally injected MIP-2 caused an early significant increase in peritoneal TNF-alpha, whereas histamine levels were unaffected. In a subsequent experiment, mast cell-deficient mice and their normal controls were then injected intraperitoneally with MIP-2 or underwent CLP. Significantly fewer PMNs migrated into the peritoneal cavity in the mast cell-deficient mice after MIP-2 injection or CLP. Thus, our findings indicate that mast cells and MIP-2 are necessary for PMN migration into the peritoneum in response to intra-abdominal infection, and that MIP-2 appears to facilitate this through an increase in TNF-alpha release.
Animals↗
The cellular reaction in normal and tumour-bearing mice following intraperitoneal glucan injection.
The effect of a single intraperitoneal injection of yeast glucain in C3D2 mice was studied. The optimal dose for the induction of a cellular exudate was 0.4 mg/kg, producing 17.6 x 10(6) cells on day 7 after injection. The number of T-cells, B-cells and macrophages in this exudate was analysed by the use of morphology, immunofluorescence and the non-specific esterase staining. An increase in both T-cells, B-cells and macrophages was found after glucain injection. There was an 8-fold increase in macrophages, but the increase lasted only 14 days. The increase in T-cells was smaller, but lasted at least 35 days. The effect of pretreatment with glucan on the development of an inoculated syngeneic methyl cholanthrene induced sarcoma was studied. No effect on tumour take could be demonstrated, but differences in T-cell, B-cell and macrophage content of the developing tumour were found. A strinking feature was a prolonged increase in tumour T-cell content.
Animals↗
Behavior disruption in Cebus monkeys as a function of injected substances.
Intraperitoneal injections of blood substances from schizophrenic or stressed normal human donors into primates trained to perform a precision timing task resulted in significant prolongation of time taken to complete the task as compared with injections of blood substances from normal donors.
Animals↗
CCK/gastrin-like immunoreactivity in brain and gut, and CCK suppression of feeding in goldfish.
The presence and distribution of cholecystokinin (CCK)/gastrin-like immunoreactive (IR) material were examined in the goldfish brain and gut. In the forebrain, CCK/gastrin-like IR fibers and perikarya were localized to nuclei of predominantly the ventral telencephalon and diencephalon; more dorsal forebrain regions contained only few, thin-beaded, sparsely distributed IR fibers. CCK/gastrin-like IR was specifically detected in the preoptic hypothalamus, including the nucleus entopeduncularis, nucleus preopticus periventricularis, and nucleus preopticus. Of all brain regions examined, the highest concentration of CCK/gastrin-like IR staining was consistently observed in nuclei of the ventroposterior and inferior lobes of the hypothalamus. Within the gut, both nerve fibers and endocrine cells contained CCK/gastrin-like IR. The abundance of CCK/gastrin-like IR material within brain areas known to represent the feeding center of fish, as well as the presence of IR material within the gut, suggests that CCK may influence feeding behavior in fish. When injected either intraperitoneally or into the third brain ventricle into goldfish, sulfated CCK-8 (CCK-8s) suppressed food intake. The nonsulfated form of CCK-8 was not as effective as CCK-8s in suppressing feeding after intraperitoneal injection. No consistent changes were observed in circulating serum growth hormone or gonadotropin levels after either intraperitoneal or intracerebroventricular injection of CCK-8s. These studies demonstrate for the first time that CCK-8s is effective in acutely suppressing feeding behavior in fish when administered either peripherally or centrally into the third brain ventricle.
Animals↗
The effects of intranasal infusion of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) upon catecholamine concentrations within olfactory bulbs and corpus striatum of male mice.
Male C57/B1 mice received bilateral intranasal infusions of saline, MPTP or an intraperitoneal injection of MPTP. Infusions were performed using a peristaltic pump at a setting of 100 microliters/min. The MPTP, diluted in saline at concentrations of 2 mg/ml, was infused over 15 (0.1 mg) or 30 (0.2 mg) s, while the saline (control) infusions were of 30 s duration. In a separate group of mice, MPTP was injected via the intraperitoneal route at a dose equivalent to that of the 30-s intranasal concentration (0.2 mg). At 7 days post-treatment, catecholamine concentrations were determined from the olfactory bulbs and corpus striatum. Concentrations of norepinephrine within both the olfactory bulbs and corpus striatum of mice receiving the intranasal infusion of MPTP were significantly lower than those of the intranasal saline and intraperitoneal MPTP-treated mice. No significant differences in olfactory bulb or corpus striatal dopamine concentrations were obtained as a function of these treatments. These results demonstrate that intranasal infusion of MPTP at low concentrations (approximately 7.0 mg/kg) can significantly reduce noradrenergic, but not dopaminergic, concentrations within the olfactory bulbs and corpus striatum. By contrast, equivalent concentrations of MPTP administered through intraperitoneal injection were without effect. It appears that the olfactory system may represent a particularly sensitive route for the receipt and transport of the neurotoxin MPTP into the brain.
1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
The effects of somatostatin on serum growth hormone levels in the goldfish, Carassius auratus.
In the present study the effects of somatostatin on serum growth hormone (GH) levels in the goldfish, Carassius auratus, were investigated. A single intraperitoneal injection of either 0.1 or 1.0 micrograms somatostatin/g body wt caused a significant decrease in serum GH levels at 1 h postinjection compared to vehicle-injected controls. Two intraperitoneal injections of somatostatin (1.0 micrograms/g body wt), given 12 hr apart, caused a significant decrease in serum GH levels, compared to both presample and vehicle-injected control groups at 1.5 and 6 hr following the second injection. In fish given two injections of somatostatin, a post inhibitory rebound in serum GH levels occurred by 24 hr following the second injection. Thyrotropin-releasing hormone (1 micrograms/g body wt), given as a control peptide, caused a significant increase in serum GH levels at 24 hr, but no significant changes were found at 1.5 or 6 hr following the second of two intraperitoneal injections given 12 hr apart. The increases in serum GH at 24 hr may be due to stress. The results demonstrate that somatostatin causes a transient decrease in blood GH levels in goldfish.
Animals↗
The influence of anesthetic concentrations of enflurane and ethanol on caffeine metabolism in mice.
Enflurane is a fluorinated volatile anesthetic, mostly eliminated unchanged in exhaled air. About 10% of inhaled enflurane undergoes oxidative metabolism in liver via mixed function oxidase. We examined the influence of ethanol and subchronical exposition (6 hours a day, during five consecutive days) to subanesthetic and anesthetic concentrations of enflurane on liver function in BALB/c mice. Specially designed chamber for inhalatory application of anesthetics was constructed for this study. Animals were divided in six groups of twenty. The ethanol treated group was injected with ethanol intraperitoneally (1 g/kg). Two enflurane treated groups were intraperitoneally injected with 0.9% solution of sodium chloride (10 ml/kg) and one of them exposed to subanesthetic (0.5 Vol%) and the other one to anesthetic (2.75 Vol%) concentrations of enflurane. Following two groups received ethanol (1 g/kg) and each of them inhaled enflurane at previously mentioned doses. The control group was intraperitoneally injected with 0.9 % solution of sodium chloride (10 ml/kg) and did not receive any anesthetic. On the day following the last day of exposure half of the animals from each group were sacrificed for determination of glucose levels, erythrocyte glutathion levels, haematocrit, alanine aminotransferase (ALT), aspartate aminotransferase (AST), lactate dehydrogenase (LDH), liver protein and glutathion levels, and total cytochrome P-450 (CYP P-450). The other half of animals from each group were injected intraperitoneally with caffeine (20 mg/kg). Caffeine and its metabolites in 8 hour urine were analyzed by high performance liquid chromatography (HPLC) method. Excretion of caffeine and its metabolites was different among the groups. We followed two caffeine metabolic ratios - 1,3-dimethyl uric acid and 3,7-xanthine (1,3-U/3,7-X) and 3,7-dimethyl xanthine + 7-xanthine and 1-xanthine + 1,7-dimethyl uric acid (3,7-X + 7-X/1-X + 1,7-U). The difference in caffeine metabolites ratios suggests that enflurane changes oxidative metabolism in liver via certain subtypes of mixed function oxidase, probably via CYP-4502E1. This effect is more expressed when ethanol and enflurane are applied together. Ethanol is well known inductor of CYP-4502E1 and the registrated enzyme induction could be explained by both influences - of ethanol and enflurane.
Alanine Transaminase↗
[Induced tolerance to cardiac allografts with multiple intravenous injection of donor spleen cells].
OBJECTIVE: To study the methods and mechanisms of immune tolerance in cardiac transplantation. METHODS: Male DA rat hearts were transplanted to male Lewis rats using Ono's model and randomly divided into five groups: untreated, intravenous injection of 1 x 10(8) DA splenocytes to Lewis rat, intraperitoneal injection of cyclophosphamide (100 mg/kg) to Lewis rat, intravenous injection of 1 x 10(8) DA splenocytes combined with intraperitoneal injection of cyclophosphamide (100 mg/kg) to Lewis rat, multiple injection of DA rat splenocytes with intraperitoneal injection of cyclophosphamide, 11 days later heart transplantation was performed. Mean survival time (MST), histological changes, mixed lymphocyte reaction (MLR), the role of interleukin-2 (IL-2) to MLR and the role of tolerant rat splenocytes to MLR were measured after operation. RESULTS: The survival time of heart allografts in the group of multiple injection of DA rat splenocytes with intraperitoneal injection of cyclophosphamide [MST: (85.3 +/- 7.5) d, t = 0, P < 0.01] was significantly longer than in the groups of untreated [MST: (7.3 +/- 1.0) d], intravenous injection of 1 x 10(8) DA splenocytes to Lewis rat [MST: (7.9 +/- 0.9) d], intraperitoneal injection of cyclophosphamide (100 mg/kg) to Lewis rat [MST: (8.1 +/- 1.2) d], intravenous injection of 1 x 10(8) DA splenocytes combined with intraperitoneal injection of cyclophosphamide (100 mg/kg) to Lewis rat [MST: (25.8 +/- 3.5) d]. Only a few inflammatory cells infiltrated in cardiac allografts in the group of multiple injection of DA rat splenocytes with intraperitoneal injection of cyclophosphamide. MLR in the group of multiple injection of DA rat splenocytes with intraperitoneal injection of cyclophosphamide were significantly decreased compared with those of normal control (t = 0, P < 0.01). IL-2 could partly reversed the hyporesponsiveness of MLR in tolerant rats, the tolerance could be transferred in vitro. CONCLUSIONS: Multiple injection of donor splenocytes combined with intraperitoneal injection of cyclophosphamide to recipients could induce immune tolerance to cardiac allografts.
Adoptive Transfer↗
Hormone dependence of mammary tumors induced in rats by intraperitoneal NMU injection.
The purpose of this work was to determine the hormone dependence of mammary tumors induced in Sprague-Dawley rats by three intraperitoneal injections of N-nitroso-N-methylurea at 50, 80, and 110 days of age. Two experimental designs were carried out: (a) Ten days before the first NMU injection, 130 rats were divided into 13 batches and randomly assigned to the following treatments: control, ovariectomy (OVX), tamoxifen (TAM), bromocriptine (BROM), haloperidol (HAL), estradiol (E2), progesterone (Pg), OVX + BROM, TAM + BROM, OVX + HAL, TAM + HAL, OVX + TAM, and E2 + BROM. After 150 days of treatment the following growth parameters were determined: latency period (LP), mean tumor number per rat (n/t), and tumor incidence (TI). LP was significantly increased (p < 0.05) only by Pg and TAM + BROM. The n/t was significantly decreased (p < 0.05) by all treatments except HAL. TI was significantly reduced by OVX, TAM, BROM, and their combinations, (b) Rats bearing ip-NMU-induced mammary tumors were divided into 7 batches and assigned to the following treatments: control, OVX, TAM, BROM, HAL, OVX + BROM, and TAM + BROM. Tumor growth was assessed up to 60 days of treatment; only OVX, TAM and their combination with BROM were able to produce tumor regression. These results support the essential role of E2 and prolactin in the promotion stage of carcinogenesis. However, for established tumors, growth becomes more independent from hormone influence, in particular from prolactin deprivation. We conclude that this model seems suitable for studying the mechanisms underlying the evasion of hormonal control of tumor growth.
Animals↗
Suppression effects of human recombinant tissue inhibitor of metalloproteinases-1(TIMP-1) on tumor proliferation using in vivo treatment model of well-differentiated colon cancer cell line, HT29.
To investigate the suppressive effect of human recombinant TIMP-1 (rh-TIMP-1) on tumor proliferation using an in vivo xenograft system, HT29 was suspended in 0.1 ml phosphate buffered saline (PBS) and then subcutaneously injected in the back of female mice (BALB/C nu/nu). The mice were divided into 2 groups an and the tumor diameter was measured after rh-TIMP-1 (2 mg/kg) (rh-TIMP-1 group) or PBS (control group) was administered injections according to the following schedules. Schedule 1 : Beginning 2 weeks after the subcutaneous injection of HT29, an intraperitoneal injection of rh-TIMP-1 or PBS were performed twice a day (every 12 h) for 14 consecutive days. Schedule 2 : Beginning 1 week after the subcutaneous injection of HT29, an intraperitoneal injection was performed twice a day for 14 consecutive days. Schedule 3 : Intraperitoneal injections were started simultaneously with the subcutaneous injection of HT29, and then performed twice a day for 21 consecutive days. The mice were sacrificed and the tumors extirpated for immunohistochemical investigation. In addition, gelatin zymography and a cell proliferation assay were performed. With Schedule 1, the changes in the tumor diameter in the rh-TIMP-1 group followed the same course as those in the control group, and no suppressive effect on tumor proliferation was observed. However, with Schedule 3, a remarkable suppressive effect was observed throughout the treatment period. In immunostaining, more cases negative for MMP-9 were observed in the rh-TIMP-1 group than in the control group. Cases negative for CD34 were significantly more observed in the rh-TIMP-1 group than in the control group with Schedule 3. All of the results were obtained through the suppressive effect of rh-TIMP-1 on angiogenesis.
Animals↗
Some observations on the mechanism of benzodiazepine-barbiturate interactions in the mouse.
1 The prolongation of pentobarbitone sleeping by five benzodiazepines, administered by prior intraperitoneal injection, was measured in mice. The pentobarbitone was injected either intraperitoneally or intracerebroventricularly. For each benzodiazepine, the prolongation was dose-related and differences in potency between benzodiazepines were not marked. 2 The percentage prolongation of sleeping times produced by most of the benzodiazepines was greater when the pentobarbitone was given intracerebroventricularly and was explained by a preferential addition of CNS depressant effects associated with this route. 3 To test whether the action of intraperitoneally administered pentobarbitone had been influenced by a metabolic component, the effects of nitrazepam on drug metabolism, measured by changes in plasma phenazone levels in the mouse, were studied. Nitrazepam (32 mg/kg, i.p.) produced a 23% reduction in the rate of phenazone metabolism. 4 Nitrazepam was also shown to have produced a transient fall in body temperature. Calculations based on Q10 values suggested that this hypothermia accounted, at most, for half the metabolic change measured.
Animals↗
Acute and subacute toxicity study of water-soluble polyalkylsulfonated C60 in rats.
Polyalkylsulfonated C60, or FC4S, a highly water-soluble caged fullerene derivative, is believed to be a free radical remover or an antioxidant in biological systems. A 50 mg/ml aqueous solution was prepared as a master solution and administered to female Sprague-Dawley CD(Crl:CD(SD)BR) rats in a single-dose acute toxicity study or a 12-day subacute toxicity study where rats were given the solution daily. In a study of the median lethal dose (LD50), no rats died after oral administration, and thus FC4S was considered to be nontoxic if administered orally. In an LD50 intraperitoneal injection study, rats died within 30 hr after injection; the LD50 was determined to be approximately 600 mg per kilogram of body weight. Rats injected with the compound intraperitoneally or intravenously immediately eliminated the compound through the kidney; the kidney appeared to be the primary target organ. The compound induced a distinct lysosome-overload nephrosis, a phagolysosomal nephropathy characterized by a tinctorial difference between the outer cortex and the inner cortex and the medulla. The affected outer cortex showed a diffuse degeneration, with the presence of numerous large vacuoles and cytoplasmic aggregates in the tubular epithelium. The phagolysosomal nephropathy was detected in rats after acute exposure as well as in the surviving rats following 1 intraperitoneal injection of 500 mg/kg or intravenous injection of 100 mg/kg. Ultrastructural investigation revealed numerous membranous conglomerates characteristic of phagolysosomal and/or lysosomal inclusions in the cytoplasm of the renal tubular epithelium. These conglomerates were confined to the vacuole, electron-dense, and unevenly stained. They varied in size and shape and were fused or aggregated. Occasional phagolysosomes were also observed in the endothelial cells of the peritubular plexus. A preliminary study of microsomal enzyme activity analysis revealed a suppression effect of liver cytochrome P-450-dependent monooxygenase activities, including cytochrome P-450, cytochrome b5, and benzo(a)pyrene hydroxylase, but an increased level of kidney cytochrome P-450-dependent monooxygenase activities, including NADPH-cytochrome P-450 reductase. The significance of these enzyme alterations was not well determined. Further study is needed to clarify the correlation between the alterations of microsomal enzyme activity and the nephropathy of lysosomal overload-induced changes. These changes may serve as a biological marker in toxicity screening tests for this class of compound.
Administration, Oral↗
Anti-muscarinic drug effects in a swim-to-platform test: dose-response relations.
Rats were given subcutaneous or intraperitoneal injections of scopolamine, intraperitoneal injections of atropine, or control injections, and trained on a simple swim-to-platform task. Errors were proportional to dose for both drugs over a wide range. No difference was found in the effects of intraperitoneal or subcutaneous scopolamine but scopolamine was 25 times more potent than atropine. The potency of both drugs in impairing swim-to-platform behavior was similar to their potency in abolishing the cholinergic component of neocortical low voltage fast activity. The electrocortical effect of anticholinergic drugs may be a major factor in the behavioral impairment they produce.
Animals↗