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PubMed1993

Effects of mexiletine on formalin-induced nociceptive responses in mice.

We investigated the effect of mexiletine on the formalin-induced nociceptive response and its modulation by diabetes. We also investigated the effects of mexiletine on intrathecally-administered substance P- and somatostatin-induced nociceptive responses in both non-diabetic and diabetic mice. Intraperitoneal injection of mexiletine (30 mg/kg) significantly reduced the duration of the formalin-induced nociceptive response in both non-diabetic and diabetic mice. When mexiletine (30 mg/kg, i.p.) was injected 30 min before injection of substance P (SP), it significantly inhibited SP-induced nociceptive responses in both non-diabetic and diabetic mice. Furthermore, mexiletine also significantly inhibited the intensity of somatostatin (SST)-induced antinociceptive effect of mexiletine in diabetic mice involves the inhibition of SP- and SST-mediated nociceptive transmission in the spinal cord.

Animals↗
PubMed1995

Metabolism of [14C]- and [35S]S-(1,2-dichlorovinyl)-L-cysteine in the male Fischer 344 rat.

The metabolic fate, tissue distribution, and elimination profile of [35S]- and [cysteine-U-14C]S-(1,2-dichlorovinyl)-L-cysteine (DCVC)--given either intravenously or intraperitoneally to male Fischer 344 rats--was investigated. Blood samples were collected periodically from 5 min to 96 hr after administration. More than 99% of the DCVC was cleared from plasma within 2.5 hr after either intravenous or intraperitoneal injection. The initial half-lives of both [35S]- and [14C]DCVC were 2.0 and 2.8 hr, respectively, and the mercapturate S-(1,2-dichlorovinyl)-N-acetyl-L-cysteine was detected in plasma within 5 min of giving DCVC. The major plasma metabolite detected after giving [35S]DCVC was inorganic sulfate, and S-(1,2-dichlorovinyl)-N-acetyl-L-cysteine and pyruvate were also detected in plasma after giving [14C]DCVC. S-(1,2-Dichlorovinyl)-N-acetyl-L-cysteine was the major urinary metabolite detected after giving [14C]DCVC, and inorganic sulfate was excreted in the urine after giving [35S]DCVC. Administration of the cysteine conjugate beta-lyase inhibitor aminooxyacetic acid led to a significant increase in the urinary excretion of radioactivity, mostly in the form of the mercapturate. The kidney contained the highest amount of radioactivity after administration of [35S]DCVC. In addition, similar amounts of radioactivity were present in brain, heart, kidney, and liver after administration of [14C]DCVC, but the 14C content of the liver was decreased in aminooxyacetic acid-treated rats. This study shows that DCVC is rapidly metabolized to inorganic sulfate and S-(1,2-dichlorovinyl)-N-acetyl-L-cysteine, which are eliminated in the urine.

Aminooxyacetic Acid↗
PubMed1994

Immunocytochemical localization of desferrioxamine in the kidney, liver and brain of the developing and adult mouse: implications for drug processing and therapeutic mechanisms.

The iron chelator, desferrioxamine, has been shown to interfere with hydroxyl radical formation, which mediates tissue damage in several disease states. In this study, young and adult mice were given intraperitoneal injections of desferrioxamine and sacrificed after 1, 24 or 72 hr, and adult rats were given intraventricular injections and sacrificed after 24 or 72 hr. Immunohistochemical experiments, that utilized an anti-desferrioxamine antiserum, were performed to localize the cellular distribution of the drug in the kidney, liver and brain. In the kidney, the findings were as follows: 1) at 0 days, there was heterogeneous distribution of desferrioxamine, which suggests that there are functional differences between nephrons in the immature kidney; 2) with increasing age, the degree of staining decreased, which suggests that the efficiency of renal clearance of desferrioxamine increases with maturity; 3) punctate staining was superimposed onto diffuse staining, which suggests that the drug can get taken up in pinocytotic vesicles during tubular reabsorption; and 4) staining was present at 72 hr, which suggests a prolonged clearance period. In the liver, there was an absence of staining at 24 and 72 hr and only diffuse staining at 1 hr, which suggests a rapid processing of the drug by the liver. In the normal mouse brain, the drug was found localized to the choroid plexus and ependymal cells at all ages, and the staining decreased with increasing time following injection. These results indicate that there are differences in the way that desferrioxamine is processed by cells in different tissues and indicate possible therapeutic mechanisms.

Aging↗
PubMedDate not supplied

In vivo stimulation of insulin release by succinic acid methyl esters.

Both the monomethyl and dimethyl esters of succinic acid, administered intravenously to fasted and anesthetized rats, caused a rapid increase in plasma insulin. A positive insulin secretory response to succinic acid monomethyl ester was also observed after intraperitoneal injection to fed and conscious rats. On a molar basis, stimulation of the insulin release, evoked by succinic acid esters, represented about twice that caused by D-glucose. It is speculated that succinic acid esters may be efficient insulin secretagogues even in those models of noninsulin-dependent diabetes characterized by a site-specific defect in the transport of D-glucose or in the early steps of its catabolism in the pancreatic B-cell.

Anesthesia↗
PubMedDate not supplied

Protection by gonadal steroid hormones against procarbazine-induced damage to spermatogenic function in LBNF1 hybrid rats.

Some anti-cancer drugs, such as procarbazine (PCZ), are associated with irreversible damage to spermatogenic function and cause sterility in men. In the present study, protection of spermatogenesis by gonadal steroid hormones during PCZ treatment was investigated in male rats. LBNF1 hybrid rats were chosen for these studies because the response of the testis to PCZ was more uniform than in a stock of Sprague-Dawley outbred rats. Mature male LBNF1 rats were subcutaneously implanted with cholesterol (C)-, testosterone (T)-, and/or estradiol-17 beta (E)-containing capsules, and 5-10 weeks later given one or four weekly intraperitoneal injections of PCZ at a dose of 200-250 mg/kg of body weight. Hormone capsules were removed 24 hours after the last PCZ injection and the animals were killed 10-12 weeks later. Testicular weights, sonication-resistant sperm head counts, and quantitative testicular histology revealed protection of the spermatogenic epithelium from PCZ toxicity by gonadal steroid hormones when compared with the C controls. Protection was observed against both single and multiple injections of PCZ. A combination of T and E capsules provided better protection than T alone. This model system is suitable for studies of the mechanism of protection of spermatogenesis from chemotherapy-induced damage.

Animals↗
PubMed1998

Evaluation of oral, subcutaneous, and nasal administration of Salmonella enteritidis-immune lymphokines on the potentiation of a protective heterophilic inflammatory response to Salmonella enteritidis in day-old chickens.

We have previously reported that the prophylactic administration of factor(s) from T-cell supernatants derived from Salmonella enteritidis-immune chickens (ILK) have a favorable effect in controlling or eliminating salmonellosis in neonatal poultry. Experimentally, we have used the intraperitoneal injection as the standard method of administering ILK to neonatal poultry. However, this method is neither easy, practical, nor economical for the poultry industry. In the present study, we evaluated the effectiveness of oral (p.o.), intranasal (i.n.), and subcutaneous (s.c.) administration of ILK for ease of delivery, induction of protective resistance against Salmonella enteritidis (Se) organ invasion, and the ability to activate peripheral blood heterophils in day-old chickens. In the first experiments, delivery of ILK p.o., i.n., and s.c. significantly (P < 0.01) increased the resistance of day-old chickens to Se organ invasion. The level of protection was equivalent to that induced by the i.p. route. Administration of a comparable protein control (bovine serum albumin, BSA) by the 3 routes induced no protective effect against Se organ invasion. Likewise, a significant increase was found in the number of circulating heterophils within 4 h of administration of the ILK by all routes. In the 2nd experiment, the function of the heterophils from ILK-treated birds was compared with that of the control cells in adherence, chemotaxis, and phagocytosis assays. The heterophils from birds given ILK i.p., s.c., p.o., or i.n. had significantly (P < 0.01) increased functional activities when compared to the activities of the heterophils from the control birds. These studies indicate that the delivery of ILK either orally or parenterally, routes which can be used by the poultry industry, can confer protection to chickens against a localized enteric Se organ invasion by potentiating the systemic heterophilic innate response.

Administration, Intranasal↗
PubMed1998

[Dynamics of interferon induction in albino mice by interferon inducer ridostin administered by various routes].

The time dependence of interferon production in blood, tissues of the respiratory tract, brain and olfactory tract of mice BALB/c was investigated after administration of the interferon inductor ridostin by various routes. Intraperitoneal injection of ridostin in a dose of 5 mg/kg induced intensive accumulation of interferon in the blood serum with the peak in 8 hours (2560 U/0.2 ml) while no interferon was detected in the tissues of the respiratory tract and brain of the animals. Intracerebral injection of ridostin in the same dose induced accumulation of interferon in both the tissues of the brain (maximum 160 U/0.2 ml in 24 hours) and the blood serum (maximum 1280 U/0.2 ml in 8 hours). After respiratory administration of ridostin interferon was detected only in the site of the administration in the tissues of the upper respiratory tract and lungs of the mice.

Administration, Inhalation↗
PubMed1976

[Experimental heart tumours in rats (author's transl)].

In continuation of previous own investigations 68 heart tumours including 46 early stages were found in the heart of 590 BD IX rats systematically examined after treatment with methylnitrosourea (MNU) or ethylnitrosourea (ENU). The tumour incidence was about 40% in animals treated by repeated intravenous or intraperitoneal injections of 20 mg per kg body weight MNU. These experiments are suitable for the study of early stages and the histogenetic origin of heart tumours. At present MNU in addition to triazenes (table 5) belongs to the most powerful carcinogens which affect the heart in rats.

Animals↗
PubMed1976

Studies on the metabolism of 5-hydroxytryptamine (serotonin). VII. Effects of haloindoles on cerebral 5-HT in various species.

In a comparative study, the effective of intraventricularly or intraperitoneally injected p-chloroamphetamine (p-CA) and some chloroindoles on cerebral levels of serotonin was evaluated. 5-Chloroindole depressed 5-HT levels in the brainstem and telencephalon for three days, 6-chloro-2-methylindole (6-CMI) only during the first day. 5-Chloroindazole had no effect at all. p-CA was more toxic to guinea pigs than to rats. p-CA and 5-chloro-2-methylindole (5-CMI) had no effect on cerebral 5-HT in chicks. Apparently, none of these compounds represented or was converted to a metabolite possibly responsible for the neurotoxic effects of p-CA.

Animals↗
PubMed1992

Effects of verapamil on the acute toxicity of doxorubicin in vivo.

BACKGROUND: Studies indicating that verapamil substantially enhances doxorubicin levels in certain drug-resistant tumor cells have led to the use of verapamil in combination with doxorubicin in animal and clinical studies of multidrug-resistant tumors. These studies have shown this drug combination to be associated with severe toxic effects. It is important to determine whether verapamil modulates the dose-limiting and potentially lethal cardiotoxicity of doxorubicin and to elucidate possible mechanisms. PURPOSE: The aims of this study were to evaluate the in vivo effects of verapamil on (a) doxorubicin-stimulated cardiac lipid peroxidation and cardiac damage, (b) doxorubicin-induced animal mortality, and (c) biodistribution of doxorubicin to the heart. METHODS: Male (BALB/c x DBA/2)F1 mice were treated with a high dose of doxorubicin (15 mg/kg, injected intraperitoneally), verapamil (25 mg/kg, injected intraperitoneally), or combinations of the two. Lipid peroxidation was determined using the 2-thiobarbituric acid assay for malonaldehyde. Light microscopy was used for histopathologic examination of cardiac tissue. A fluorometric assay procedure was employed to determine doxorubicin levels in the heart. RESULTS: Verapamil was an effective inhibitor of peroxidative damage to myocardial lipids following a high dose of doxorubicin (15 mg/kg, injected intraperitoneally). However, mice treated with verapamil and doxorubicin had a lower survival rate and a higher initial peak concentration of doxorubicin in the heart than those treated with doxorubicin alone. They also demonstrated a higher incidence and severity of degenerative changes in cardiac tissue. CONCLUSIONS: Our findings suggest that verapamil effectively inhibits doxorubicin-mediated lipid peroxidation in vivo but that cardiac lipid peroxidation is not the major limiting mechanism underlying doxorubicin-induced toxicity. A possible explanation for the excess mortality and cardiac injury in mice treated with verapamil plus doxorubicin is that verapamil alters the pharmacokinetics of doxorubicin. IMPLICATIONS: Further studies are necessary for development of safer protocols and/or drug combinations to treat multidrug-resistant tumors. We are currently studying treatment of tumor-bearing animals with a cumulative dosage regimen of doxorubicin in the presence and absence of verapamil.

Animals↗
PubMed2006

[Effects of midazolam on muscarinic receptor of brain in healthy and scopolamine-treated rats].

OBJECTIVE: To investigate the recent and permanent effects of pretreatment with midazolam on muscarinic receptor of brain in healthy and scopolamine-treated rats. METHODS: (1) In recent effect group, thirty-eight male SD rats were randomly divided into 4 groups: control group (Con, n=9), midazolam group (Mid, n=9), scopolamine group (Sco, n=10), midazolam+scopolamine group (Mid+sco, n=10). On the 1st, 2nd, and 3rd days, Mid group and Mid+sco groups were treated with intraperitoneal injection of 50 mg/kg midazolam per day while Con group and Sco group were treated with intraperitoneal injection of the same voluminal physiological saline per day. On the 4th, 5th, and 6th days, Scopolamine 0.8 mg/kg intraperitoneal injection per day was administered in Sco group and Mid+sco group while same voluminal physiological saline was administered in Con group and Mid group. (2) In permanent effect group, thirty-six male SD rats were randomly divided into 4 groups: control group (Con, n=9), midazolam group (Mid, n=9), scopolamine group (Sco, n=9), midazolam+scopolamine group (Mid+sco, n=9). On the 1st, 2nd, and 3rd days, Mid group and Mid+sco group were treated with intraperitoneal injection of 50 mg/kg midazolam per day while Con group and Sco group were treated with intraperitoneal injection of the same voluminal physiological saline per day. On the 10th, 11th, and 12th days, Scopolamine 0.8 mg/kg intraperitoneal injection per day was administered in Sco group and Mid+sco group while the same voluminal physiological saline was administered in Con group and Mid group. (3)Then the rats was decapitated and the cerebra cortex and hippocampus were removed. The binding capacity of muscarinic receptor with [3H] QNB were determined. Bmax and Kd of muscarinic receptor in hippocampus were determined by Scatchard analysis in recent effect group. RESULTS: (1) In recent effect group: the binding capacity of muscarinic receptor in hippocampus was significantly higher in Con group than in Mid group, Sco group and Mid+sco group (P<0.01), which was also higher in Mid group than in Sco group (P<0.05) and Mid+sco group (P<0.01), higher in sco group than in Mid+sco group (P<0.01). Kd of muscarinic receptor in hippocampus in Sco group and Mid group were higher than in Con group and Mid+sco group (P<0.01). Bmax of muscarinic receptor in hippocampus was significantly higher in Con group than in Mid group (P<0.05), Sco group and Mid+sco group (P<0.01), which was also higher in Mid group than in Sco group and Mid+sco group (P<0.01), higher in sco group than in Mid+sco group (P<0.05). There was no significant difference of the binding capacity of muscarinic receptor in cortex. (2) In permanent effect group: the binding capacity of muscarinic receptor in hippocampus was significantly higher in Con group and Mid group than in Sco group and Mid+sco group (P<0.01). There was no significant difference of the binding capacity of muscarinic receptor in cortex. CONCLUSION: Pretreatment with intraperitoneal injection of 50 mg/kg midazolam for three days had no effect on muscarinic receptor of cortex, but could induce the binding capacity of muscarinic receptor with [3H] QNB and change the density and affinity of muscarinic receptor in hippocampus in healthy and scopolamine-treated rats, yet the changes were not permanent.

Animals↗
PubMed2002

[Liposome and complete Freund's adjuvant for the prevention of insulitis in non-obese diabetic mice].

OBJECTIVE: To explore the effects of complete Freund's adjuvant (CFA), incomplete Freund's adjuvant(IFA), large multilamellar liposome (LML) and small cationic liposome (DOTAP) on insulitis and diabetes. METHODS: 1. 3-week-old non-obese diabetic(NOD) female mice were randomly divided into 3 groups: CFA group (injected subcutaneously in the hind footpad, n = 16), IFA group (injected intraperitoneally, n = 16) and PBS group (injected subcutaneously in the hind footpad, n = 16). Three mice from each group (9 in total) were killed at the age of 12 weeks for the analysis of pancreatic pathology, and the others were not killed until they were 30 weeks old for diabetes incidence. 2. 3-week-old NOD female mice were randomly divided into 3 groups and injected intraperitoneally with LML (n = 13), DOTAP (n = 13) and PBS (n = 13), respectively. The insulitis score and diabetes incidence were estimated in the same way. RESULTS: 1. CFA injected subcutaneously in the hind footpad could significantly reduce the insulitis score and decrease diabetes incidence in NOD mice. At the age of 30 weeks, the incidence of diabetes in the CFA group was lower than that in the PBS group (injected subcutaneously in the hind footpad) (9.2% vs 81.8%, P = 0.001). At the age of 12 weeks, the insulitis score in the CFA group was lower than that in the control group [(0.05 +/- 0.02) vs (0.54 +/- 0.11), P < 0.001]. 2. LML injected intraperitoneally could significantly reduce the insulitis score in NOD mice. At the age of 12 weeks, the insulitis score in the LML group was lower than that in the PBS control group (injected intraperitoneally) [(0.16 +/- 0.02) vs (0.58 +/- 0.06), P < 0.001]. At the age of 30 weeks, there were no significant differences in the diabetes incidence between the LML group and the PBS group (60% vs 90%). 3. The protective effect of CFA was better than that of LML in NOD mice. CONCLUSION: CFA injected subcutaneously in the hind footpad may prevent NOD mice from developing diabetes and reduce the insulitis severity. Although the protective effect of CFA is better than that of LML, LML can lessen the insulitis severity and may become a new preventive strategy in NOD mice.

Animals↗
PubMed1997

Transient emotional changes elicited by intraperitoneal saline injection: effect of naloxone and flumazenil.

The effect of the intraperitoneal (i.p.) saline injection was assessed by using the defensive burying (DB) and the elevated plus-maze (EPM) anxiety paradigms in rats. Animals were handled gently by the body, injected i.p. with saline solution, 2 ml/kg, and tested independently in the defensive burying as well as in the elevated plus-maze test at different times after the i.p. injection: 1.5, 3, 5, 10, 15, and 30 min. A transient effect of i.p. saline injection was observed (i.e., increased DB in animals tested 1.5 min after injection) and a decrease in this parameter when studied 3 min after the injection. No changes at 5, 10, 15, and 30 min after the injection were found. To discriminate the putative participation of the opiate peptide and benzodiazepine receptors in the actions of the i.p. injection, flumazenil (5 mg/kg) and nalozone (1 mg/kg) were administered. The increase in DB at 1.5 min was masked by double injection, an effect blocked by naloxone, but not by flumazenil, while both of them reverted the decrease in DB response in animals tested 3 min after injection. A partial action of the i.p. in the animals tested in the elevated plus-maze test was found. Present results are discussed on the basis of behavioral and pharmacological evidence.

Animals↗
PubMed1983

Biotransformation of nitric oxide, nitrite and nitrate.

Biotransformation of NO, nitrite and nitrate was investigated in rats and mice in a 15NO inhalation experiment and intraperitoneal injection experiments of 15N-nitrite and 15N-nitrate, and the following results were obtained: (1) Rats were forced to inhale 15NO (145 ppm, 123 minutes) or were given an intraperitoneal injection of 15N-nitrite (2 mg animal-1 as 15N) or 15N-nitrate (2mg animal-1 as 15N), and determination of 15N recovery in urine was made up to 48 h later. The results were 55, 53 and 78% of the inhaled or injected 15N, respectively. (2) 15N-nitrate in the urine was converted into a 6-nitro derivative of 3,4-xylenol and its identification and quantitative determination were made by the GC-MS method. As to 15N-urea in the urine, identification and quantitative determination were made by the urease method. 15N was present in the urine of rats after 15NO inhalation in the form of NO3- and urea. 75 and 24% respectively. In the urine of rats injected with 15N-nitrite, about 20% of unidentified 15N-compounds not discovered in the inhalation experiment was found. The content of 15N-urea in the urine after injection with 15N-nitrate was lower than that after injection with 15N-nitrite. (3) When 15N-nitrite (0.617 mg animal-1 as 15N) was injected intraperitoneally in mice, 60.7, 7.8 and 0.3% of the injected 15N were found in the urine, feces and exhaled gas (NO, NO2 and NH3 in the gas were caught) up to 48 h after injection respectively, and 1.6% was found in the body 48 h after injection, but the remaining 30% of 15N could not be recovered.

Animals↗
PubMed1996

Migratory responses of PMN after intraperitoneal and intratracheal administration of lipopolysaccharide.

The present study was undertaken primarily to investigate accumulation of polymorphonuclear leukocytes (PMN) within the lung vasculature after intraperitoneal injection of lipopolysaccharide (LPS) and migratory responses of those intravascular PMN to intratracheally instilled LPS in mice. Intraperitoneally injected LPS was absorbed into the blood rapidly, and the concentration of circulating LPS peaked at 1 h postinjection. Tumor necrosis factor concentration in blood began to increase at 0.5 h and also peaked at 1 h postinjection. The number of lung vascular-associated PMN was increased 7.5-fold at 0.5 h post-intraperitoneal injection. However, neither diapedesis of PMN nor injury was observed in the lung, while mixed cell infiltration was observed in the liver. Although intraperitoneally injected LPS caused a significant PMN accumulation within the lung vasculature, pre-intraperitoneal injection of LPS dramatically and dose dependently abolished both intratracheal LPS-inducible PMN infiltration and apparent plasma protein leakage into the alveolar space. On the other hand, pre-intratracheal instillation of LPS enhanced rather than reduced intraperitoneal LPS-inducible PMN infiltration into the peritoneal cavity. In rats, a sublethal dose of intraperitoneally injected LPS caused a modest increase in alveolar PMN and yet reduced intratracheal LPS-inducible robust transpulmonary PMN infiltration. Although mechanisms of different migratory responses of the lung vasculature-associated PMN are unknown, the inhibitory effects of intraperitoneally injected LPS on transpulmonary PMN infiltration may be applicable to treatments for septic lung diseases.

Animals↗
PubMed1998

Influence of Route of Injection on Efficacy and Side Effects of Immunisation.

Immunisation experiments are performed on a large scale in laboratory animals e.g. for the production of antibodies. Depending on the immunisation protocol, severe discomfort may be induced. In several countries, guidelines for the immunisation of laboratory animals were drafted to refine immunisation protocols. One of the aspects that effects the immune response as well as the side effects is the route of injection. Careful selection of the route of injection is therefore crucial to refine immunisation protocols. In several papers the influence of the route of injection on the immune response is studied but generally the induced discomfort in the animals is not evaluated.In several comparative experiments we studied the influence of the route of injection on efficacy and side effects. The most widely used routes of injection were compared in rabbits (subcutaneous and intramuscular injection) and in mice (subcutaneous and intraperitoneal injection). After the injection of several adjuvant- (Freund's adjuvant, TiterMax, RIBI, Specol, or Montanide ISA50) and antigen- (synthetic peptide, glycolipid, or particulate antigen) combinations by different routes, we studied antibody production to evaluate efficacy of the injection and clinical-, physiological- and behavioural parameters and pathology (macroscopy/microscopy) to compare the induced side effects. In both rabbits and mice minimal differences in antibody titers were found between the two routes under study. However, differences in the severity of the induced side effects did occur. In rabbits, no significant differences were found in clinical, physiological and behavioural parameters but severe pathological changes were found depending on the route of injection. In mice, the intraperitoneal injection induces significant discomfort as compared to subcutaneous injection as shown by the severity of the pathological changes in the peritoneum and by the decreased activity of the animals. Important disadvantages of intramuscular and intraperitoneal injections are that these injections are difficult to perform properly and that the injection site is hard to monitor. Since minimal differences in antibody production were found between the two routes of injection, we concluded that the subcutaneous route of injection is preferred for the induction of polyclonal antibodies in rabbits and mice when an adjuvant is applied.

Journal Article↗
PubMed1984

Concomitant induction of an inflammatory response and immunosuppression by an extract from Listeria monocytogenes.

An immunosuppressive agent (ISA) present in an aqueous extract from Listeria monocytogenes diminished the immune response in vivo to subsequently injected heterologous antigen. Intraperitoneal injection of ISA induced an inflammatory response and activation of the reticuloendothelial system, both of which coincided with the period of immune hyporesponsiveness. Mice treated with ISA exhibited increased accumulation of labelled antigen to phagocytic peritoneal cells but decreased delivery of labelled antigen to the spleen. Both delivery of antigen to spleen and the immune response could be improved by injecting either ISA or antigen or both intravenously, or by increasing the dose of antigen. The response of ISA-treated animals could also be improved by intraperitoneal injection of latex beads, colloidal carbon, or carrageenan shortly (60 min) before immunization. Spleen cells from ISA-treated mice adoptively transferred to irradiated syngeneic recipients were able to mount a normal immune response. These results suggest that ingestion of antigen by the enlarged population of phagocytes in peritoneal cavities of ISA-treated mice prevented antigen delivery to the spleen and was partly responsible for the observed immunosuppression.

Antibody Formation↗
PubMedDate not supplied

Effect of glutamine-supplemented intravenous nutrition on survival after Escherichia coli-induced peritonitis.

Current solution formulations for total parenteral nutrition (TPN) do not contain glutamine (GLN). The purpose of this study was to examine whether GLN supplementation of TPN would improve survival in experimental Escherichia coli peritonitis in Fischer 344 rats (190-210 g). Initial experiments were performed to determine the degree of stress and to evaluate survival after intraperitoneal E coli injection. The E coli colony used was isolated from a culture of human blood. Graded doses were injected intraperitoneally in Fischer 344 rats (190-210 g). The response of white blood cell count, plasma insulin, glucagon, and corticosterone levels, and urinary excretion of vanillylmandelic acid reflected a significant stress response for at least 3 days. Survival was dose-dependent, with 60% mortality at 3 days after injection of 5 x 10(5) colony forming units of E coli/200 g body weight. To determine whether GLN supplementation of TPN would alter survival in this E coli peritonitis model, Fischer 344 rats were randomized to receive TPN containing 4.25% standard amino acids (group STD, n = 38) or the same solution with 1.5% of the amino acid content replaced with L-GLN (group GLN, n = 38). After 7 days of TPN, 5 x 10(5) colony forming units of E coli/200 g body weight were injected intraperitoneally under direct vision through a small laparotomy. Survival was monitored for 3 days. Surviving rats were killed to determine various nutritional parameters including plasma albumin and GLN concentration, the weight and nitrogen content of the gastrocnemius muscle, and biochemical and histological composition of the small intestine.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗