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PubMed1979

Effects of drugs on the acute inflammation following intraperitoneal injection of antigen into actively sensitised rats.

When actively sensitised rats were injected intraperitoneally with antigen, the local reaction that ensued can be divided into two phases: an immediate reaction characterised by histamine and SRS-A release with an associated extravasation of plasma proteins, and a later reaction involving infiltration of neutrophilic polymorphonuclear leucocytes. When the immediate reaction was modified by BRL 10833 (which inhibits histamine release from rat mast cells and reduces extravasation of plasma proteins), there was no reduction in neutrophil infiltration. FPL 55712, an SRS-A antagonist, also failed to inhibit neutrophil infiltration. The beta-adrenoreceptor stimulants isoprenaline and salbutamol reduced neutrophil infiltration. Isoprenaline inhibited the extravasation of plasma proteins when given before antigen, but even when administered to rats after antigen, when extravasation was complete, it still inhibited neutrophil infiltration. Propranolol reversed isoprenaline-induced inhibition of neutrophil infiltration.

Adrenergic beta-Agonists↗
PubMed1982

Effect of intraperitoneally injected cadmium on renal and hepatic gluconeogenic enzymes in rats.

Male Sprague-Dawley rats were injected intraperitoneally with 0, 0.25, 0.75 and 1.25 mg/kg/day for 14 days. At the end of 7 and 14 days treatment period, body weight gain, serum protein, serum glucose, serum glutamic oxaloacetic transaminase (SGOT) and serum glutamic pyruvic transaminase (SGPT) were measured. Glucose-6-phosphatase (G6-Pase), fructose-1, 6-di-phosphatase (FD-Pase), phosphoenol pyruvate carboxykinase (PEPCK) and pyruvate carboxylase (PC) in kidney and liver were determined. A significant decrease in body weight gain in rats treated with 1.25 mg cadmium for 7 and 14 days was observed. Serum glucose, serum protein, SGOT and SGPT were increased in cadmium treated rats. A significant increase in all four key gluconeogenic enzymes were observed in both kidney and liver tissues of rats treated with cadmium. The results of this study suggest that cadmium induces gluconeogenesis which is dose and time dependent.

Alanine Transaminase↗
PubMed1977

[Comparative transmission and scanning electron microscopy studies of liver changes in mice followed sublethal skin burns and intraperitoneal injection of a specific skin burn toxin].

Ultrastructural alterations of the liver were examined on the 1st, 2nd, 3rd, 5th, 7th and 14th day after a standard burn in mice. Our results can be divided pathogenetically into two groups: 1. Alterations explained by the primary thermal injury including electron-optically empty vacuoles and sinusendothelium destruction. 2. Alteration due to the influence of a specific burn toxin including mitochondrial changes and the formation of autophagic vacuoles. Evidence of this distinction was produced by a second investigation. Burn toxin isolated from the serum of severely burned patients was injected intraperitoneally (15 mg) into 4 mice. The livers were examined by electron microscopy on the 2nd, 4th, 7th and 14th day. Alterations described in 2 above were not observed in any case of this investigation series. The nature and timing of liver alterations were similar to those described in 2 above. In none of the cases were changes similar to those in 1 above observed.

Animals↗
PubMed1984

Distribution of intraperitoneally injected [125I] BSA in cytoplasm, nucleoplasm and chromatin of lymphocyte-like and macrophage-like rat spleen cells.

[125I] BSA injected intraperitoneally penetrated into the cytoplasm and nucleoplasm of rat spleen cells, being rapidly and very tightly bound with chromatin. Distribution in lymphocyte-like and macrophage-like cells was quite similar, but in lymphocyte--like cells between the 4th and 8th day [125I] BSA was totally degraded, while in macrophage-like cells it was still present, being degraded between the 8th and 14th day.

Animals↗
PubMed1989

Repeated intraperitoneal injections of saline attenuate the antibody response to a subsequent intraperitoneal injection of antigen.

The results of two experiments with male C3H/HeJ mice indicated that repeated intraperitoneal (ip) injections of sterile saline over a 2-week period resulted in an attenuated antibody response to the subsequent ip injection of a soluble protein antigen, keyhole limpet hemocyanin. There were no differences among experimental groups that received a different number of preimmunization injections of saline, and comparable effects were obtained simply by the daily handling of mice. Neither repeated ip injections nor handling altered preimmunization (baseline) corticosterone levels, and only previously unmanipulated mice showed an elevation in corticosterone levels 30 min after ip immunization. These latter results suggest that the depressed IgM and IgG responses were not due to the immunosuppressive effects of endogenously elevated adrenocortical steroids.

Animals↗
PubMed1988

Behavioral and neurochemical effects of intraperitoneally injected dendrotoxin.

Intraperitoneal administration of dendrotoxin, a polypeptide isolated from Dendroaspis angusticeps venom, provoked in mice the appearance of a complex stereotyped behavior including biting, head nodding, 'wet-dog' shakes and rearing. Signs of autonomic hyperactivity as well as hyperreactivity to sound and touch were prominent. Neurochemical analyses of monoamines and monoamine metabolites showed no change 90 min after dendrotoxin, with a decrease in dopamine concentrations and an increase in their metabolites in the striatum starting 3 hr later. Moreover, at this time, dendrotoxin also produced a significant increase of 5-hydroxytryptamine metabolites. These data are interpreted as indicating that dendrotoxin crosses the blood-brain barrier and provokes an increase of the activity at monoaminergic terminals.

Animals↗
PubMed1987

The role of prostaglandins in the nociceptive response induced by intraperitoneal injection of zymosan in mice.

Intraperitoneal injection of zymosan (1 mg in 0.5 ml saline) in mice induces a transient writhing response accompanied by the synthesis of small amounts of prostaglandin E2(PGE2, less than 2 ng) and larger amounts of PGI2 (200 ng per mouse), measured as its non-enzymatic breakdown product, 6-keto-PGF1 alpha. Although both centrally-acting analgesics (morphine, clonidine) and prostaglandin biosynthesis inhibitors (aspirin, indomethacin, ibuprofen) blocked the writhing response to intraperitoneal injection of zymosan, only the latter reduced prostaglandin levels in the peritoneal cavity. The writhing response correlated equally well with PGE2 levels and 6-keto-PGF1 alpha levels when data from mice treated with centrally-acting analgesics were excluded. However, intraperitoneal injection of PGI2, but not PGE2, reversed the analgesia induced by indomethacin in zymosan-injected mice. Centrally-acting agents, but not ibuprofen, blocked the ability of PGI2 to reverse the analgesic activity of indomethacin. PGI2 (2 micrograms per mouse), injected intraperitoneally in otherwise untreated mice, induced writhing. These data indicate that PGI2 is the prostaglandin involved in mediation of the writhing response to zymosan and that prostaglandin biosynthesis inhibitors, but not centrally-acting analgesics, exert their analgesic activity by reducing the peritoneal level of PGI2. It is possible that PGI2 may have the ability to stimulate pain receptors directly in the mouse peritoneal cavity, in addition to its previously recognized ability to sensitize pain receptors to other pain-producing stimuli.

Animals↗
PubMed1990

Labeling of the neurons of origin of zinc-containing pathways by intraperitoneal injections of sodium selenite.

Intraperitoneal injections of sodium selenite result in the formation of zinc-selenium complexes in zinc-containing axonal boutons ("Timm stainable boutons"), and the zinc-selenium precipitate can be rendered visible in histological sections by silver enhancement. In this work we present evidence, in the rat, that zinc-selenium precipitates formed in vivo after intraperitoneal injections of sodium selenite are translocated by colchicine-sensitive retrograde transport to neural perikarya when animals are allowed to survive 12-24 h after the selenite administration. Silver enhancement renders the perikaryal precipitates visible and thus demonstrates the perikarya of all zinc-containing neurons in the CNS simultaneously. Large populations of zinc-containing neurons identified by the method are found in layers II, III, and VI of all neocortical areas, in the superficial and deep layers of the prepyriform areas and, with a high degree of regional differentiation, in the retrosplenial, entorhinal, para- and presubicular cortices, the hippocampal formation and the amygdaloid complex. Zinc-containing cells were absent from the caudate-putamen, nucleus accumbens and septal complex. Labeled zinc-containing cells are absent in non-telencephalic parts of the brain. The findings indicate that the zinc-containing circuitry of the brain mainly serves in telencephalic information processing.

Animals↗
PubMedDate not supplied

Poloxamer 407-mediated changes in plasma cholesterol and triglycerides following intraperitoneal injection to rats.

Poloxamer (Pluronic) nonionic surfactant vehicles are a series of chemically-related block copolymers finding widespread use in parenteral formulations as solubilizing and wetting agents for traditional, low-molecular weight organic drug molecules, as well as stabilizing agents for proteins and polypeptide drugs. We report the effects of poloxamer 407 (Pluronic F-127) on plasma cholesterol and triglyceride concentrations in rats. Poloxamer 407 injected into rats by intraperitoneal injection (dose = 1.5 gm/kg) resulted in sustained (greater than 96 hour) hypercholesterolemia and hypertriglyceridemia. A larger dose of poloxamer 407 was required to elevate plasma triglyceride relative to total cholesterol. Ingestion of commercial rat chow had a negligible effect on plasma cholesterol and triglycerides levels in control (no poloxamer injection) animals, but consumption of food by animals that received an intraperitoneal injection of poloxamer 407 (30% w/w) resulted in significantly (p < .05) greater elevations in plasma cholesterol and triglycerides than in fasted animals administered poloxamer 407. The route of poloxamer 407 administration, namely intramuscular vs. intraperitoneal injection, was observed to be a more important factor for poloxamer-induced elevations in plasma cholesterol than poloxamer-mediated elevations in plasma triglycerides. Our results also provide suggestive evidence that the mechanism responsible for the elevation of plasma cholesterol following intraperitoneal injection of a poloxamer 407 solution (30% w/w) to rats may be due to stimulation of 3-hydroxy-3-methylglutaryl-co-enzyme A (HMG-CoA) reductase activity in the liver by the poloxamer vehicle.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Biodistribution of indium-111-labeled OC 125 monoclonal antibody after intraperitoneal injection in nude mice intraperitoneally grafted with ovarian carcinoma.

The purpose of this work was to study the biodistribution of 111In-labeled OC 125 monoclonal antibody (MAb) with known affinity for ovarian carcinomas in a nude mouse model grafted i.p. with a human ovarian cancer (NIH:OVCAR-3). Tumor uptake 24 h after i.p. injection was higher with intact 111In-labeled OC 125 MAb (28 +/- 7.44%ID/g) than with 111In-nonspecific immunoglobulin (6.86 +/- 1.35%ID/g). The kinetics of tumor uptake also differed, showing a plateau followed by a drop at Day 7 with 111In-OC 125 MAb and a decrease beginning at 24 h with 111In-nonspecific immunoglobulin. Tumor-to-normal tissue ratios ranged between 29.91 +/- 11.85 and 0.68 +/- 0.15 with 111In-OC 125 MAb and between 4.50 +/- 1.06 and 0.53 +/- 0.04 with 111In-nonspecific immunoglobulin according to the normal tissues and the time points considered. Tumor uptake 2 h after injection was the same for F(ab')2 fragments as for intact MAb, whereas maximum uptake at 24 h (18.76 +/- 4.62%ID/g) was lower and was followed by a decrease at Day 4. Tumor-to-normal tissue ratios were in the same range, except for the tumor to blood ratio which was higher and the tumor to kidney ratio which was lower at 24 and 96 h. Maximum tumor uptake was higher after i.p. (30.77 +/- 4.76%ID/g) than i.v. (14.59 +/- 2.70%ID/g) injection. Instead of attaining the plateau noted after i.p. injection, tumor uptake after i.v. injection remained low at 2 h (2.11 +/- 1.66%ID/g), reaching its peak only after 96 h. 131I-OC 125 injected i.p., which reached maximum tumor uptake at 2 h (13.53 +/- 4.25%ID/g), showed tumor-to-tissue ratios ranging between 15.98 +/- 2.63 and 0.96 +/- 0.86, i.e., not very different from those with 111In. After i.p. injection of a radiolabeled colloid solution, maximum tumor uptake was reached at 96 h (20.22 +/- 5.35%ID/g), but with very high nonspecific uptake in liver (31.06 +/- 6.22%ID/g) and spleen (55.23 +/- 14.11%ID/g). These results indicate high, selective tumor uptake of 111In-OC 125 after i.p. injection and demonstrate the feasibility of i.p. radioimmunotherapy of ovarian carcinomas.

Animals↗
PubMed1994

Features of the Guillain-Barré syndrome in mice following intraperitoneal injection of patient serum.

Intraperitoneal injection of serum from a patient with the Guillain-Barré syndrome (GBS) produced GBS-like signs in mice: inadequate respiration and weakness in the legs. We studied the clinical, electrophysiological and pathological features of these mice. Three groups of three mice were injected with patient serum from days 6, 10 and 15 after onset of neurological symptoms. GBS-like signs in mice were observed only with serum from day 6 and improved within 48 h. When serum was frozen and thawed more than once no signs were seen. Electrophysiological measurements of the sciatic nerves of injected and control mice were done before and after serum injection. Five days after injection of patient serum of day 6, the mice showed a significant decrease in the ratio between CMAP amplitude from proximal and distal stimulation and increase in H-M interval from proximal stimulation. These electrophysiological changes returned to normal within 12 days. The sciatic nerve showed no morphological abnormalities. Our results indicate that the observed GBS-like signs in mice are caused by peripheral nerve dysfunction.

Adult↗
PubMed1994

Induction of lupus-associated autoantibodies in BALB/c mice by intraperitoneal injection of pristane.

Intraperitoneal injection of pristane (2,6,10,14 tetramethylpentadecane) is a standard technique for obtaining monoclonal antibody-enriched ascitic fluid. However, pristane also induces plasmacytomas and an erosive arthritis resembling rheumatoid arthritis in BALB/c mice, probably as a consequence of enhanced interleukin 6 production. We report here that the production of autoantibodies characteristic of systemic lupus erythematosus (SLE) is a further consequence of injecting pristane in BALB/c mice. Anti-Su antibodies appeared as early as 1-2 mo after a single injection of 0.5 ml pristane, followed by anti-U1RNP and anti-Sm antibodies after 2-4 mo. Within 6 mo of pristane injection, 9 of 11 BALB/c mice had developed anti-Su, anti-U1RNP, anti-U2RNP, anti-Sm, and possibly anti-U5RNP antibodies. Autoantibodies were not produced by 20 BALB/c mice of the same age and sex that were not injected with pristane. Thus, autoantibodies characteristic of lupus were induced in mice that are not usually considered to be genetically susceptible to the disease. The induction of autoantibodies associated with SLE by pristane may be relevant to understanding the role of abnormal cytokine production in autoantibody production and the pathogenesis of autoimmune disease. Furthermore, the induction of high titer autoantibodies by pristane dictates caution in the use of ascitic fluid as a source of monoclonal antibodies, since the polyclonal antibodies induced by pristane may copurify with the monoclonal antibody secreted by an injected hybridoma.

Animals↗
PubMed1967

Retrograde amnesia produced by intraperitoneal injection of physostigmine.

Intraperitoneal injection of physostigmine in rats produced a retrograde amnesia of a trained task of escaping shock. This amnesic effect was a U-shaped function of the length of the interval between initial training and injection. In all cases, retraining Occurred 30 minutes after injection. A substantial effect was produced by physostigmine if its application was made 30 minutes after training; there was no effect if application and tests were made 1, 2, or 3 days after the original training. When the substance was injected and the rats were retrained 5, 7, or 14 days after the original training, a substantial effect again appeared. These results are similar to those reported in experiments in which another anticholinesterase, diisopropyl fluorophosphate, was applied intracerebrally. The data demonstrate a similar pattern of change of the amnesia with time, and they substantiate the view that neither the place of application nor the brain lesions caused the reported amnesia.

Amnesia↗
PubMed1991

[Inhibition of the high-threshold calcium current in hippocampal neurons of rats subjected to intraperitoneal injection of phenylalanine].

Effect of intraperitoneal injection of phenylalanine on the calcium current of hippocampal neurons of rats has been studied by the voltage clamp method of the whole-cell recordings. Calcium currents in hippocampal neurons of control animals after 5-7 days in culture can be separated into two components: low and high voltage-activated ones. The value of high voltage-activated calcium current was 69 +/- 13% at Vt = -10 mV from total calcium inward current in these neurons. High voltage-activated Ica in neurons of phenylalaninemic rats was significantly depressed and its value was 32 +/- 14%, the Vt value being the same. Low voltage-activated calcium current was resistant to intraperitoneal injection of L-phenylalanine.

Animals↗
PubMed1993

Transmigration routes and a delayed systemic hypotension in rats after intraperitoneal injection of endotoxin from Escherichia coli.

An intraperitoneal injection of endotoxin (ETX; 3 mg/kg) to rats caused gradual decrease in the systemic arterial blood pressure for up to 3 hr, together with decrease in heart rate, increase in hematocrit, and changes in the core temperature (an initial increase and a subsequent decrease). Pretreatment of rats with indomethacin (10 mg/kg, p.o.) prevented the decrease in the systemic blood pressure and the changes in other three parameters. The intraperitoneal injection of ETX also induced a gradual increase in exudation of plasma for up to 3 hr, with increased levels of prostaglandin (PG) E2 and 6-keto-PGF1 alpha in the peritoneal exudate. Indomethacin inhibited the exudation of plasma. The levels of ETX in the arterial and portal venous plasmas began to increase 5 min after the intraperitoneal injection of ETX, and reached levels on the order of micrograms per milliliter plasma 10-20 min after the injection. The levels of ETX in the right and left thoracic lymph nodes, but not in the mesenteric lymph nodes, increased in parallel with those in the systemic arterial plasma. In conclusion, the delayed hypotension may be attributable to the mesenteric vasodilatation induced by PGs generated in the peritoneal cavity, and the ETX injected entered the systemic circulation mainly through lymphatic vessels, but in the initial stage, a part of ETX may be transmigrated into portal vein through damaged intestine.

Animals↗
PubMed1986

Stimulation of hepatic polyamine metabolism following intraperitoneal injection of some dietary oils.

Intraperitoneal injection of partially hydrogenated marine oil into rats is shown to cause marked stimulation of hepatic polyamine metabolism, as characterized by increased activity of ornithine decarboxylase (EC 4.1.1.17), and corresponding increase in tissue levels of putrescine. A maximal effect was observed about 5 hours after injection. An effect on the hepatic activity of S-adenosyl-methionine decarboxylase (EC 4.1.1.50) was also observed. Of the various dietary oils examined only partially hydrogenated marine oil gave significant stimulation of polyamine metabolism. A single oral dose of partially hydrogenated marine oil gave a small increase in hepatic ornithine decarboxylase activity.

Animals↗
PubMedDate not supplied

Ultrastructure in the stria vascularis of the guinea pig following intraperitoneal injection of ethacrynic acid.

Following intraperitoneal injection of ethacrynic acid, progressive, mainly reversible changes occurred in the stria vascularis, affecting all three cell types and the capillary basal laminae. Both marginal and intermediate cells showed abnormalities early, at a time when EP was just beginning to decline. Progressive changes in marginal cells culminated in apical bulging followed by recession of the swelling and stretching of the cells concomitant with gross interstitial oedema. Marginal cell mitochondria showed damage and the transcellular tubule system was dilated. Intermediate cells also showed a progression of changes, culminating in a marked, but reversible, shrinkage. The time of appearance of severe strial derangement correlated with the time of maximal depression of EP. The ability of the stria to regain rapidly an almost normal morphology appeared to be due partly to the distribution and orientation of microtubules in marginal and intermediate cells preventing major disruption of stria vascularis architecture.

Animals↗
PubMed1994

Intraperitoneal injections of Fluorogold reliably labels all sympathetic preganglionic neurons in the rat.

The ability of intraperitoneal injections of a retrograde neuronal tracer, Fluorogold, to label the entire population of sympathetic preganglionic neurones was tested with a double-labelling strategy. Animals were injected intraperitoneally (i.p.) with Fluorogold, while Fast Blue or subunit B of cholera toxin were injected into a peripheral autonomic ganglion or into the adrenal gland. Sympathetic preganglionic neurones were then examined for retrogradely transported tracers. In all cases, preganglionic neurones labelled with Fast Blue or cholera toxin also contained Fluorogold, indicating that i.p. injections of Fluorogold do reliably label the entire population of sympathetic preganglionic neurones.

Adrenal Glands↗