Showing papers on "Intraperitoneal injection published in 1983"
TL;DR: It is concluded that soluble factors generated by cultured cells in vitro or intrasplenically transplanted cells improve survival either by a direct hepatotrophic effect, by stimulation of the reticulo-endothelial system or by an unspecific humoral mechanism.
Abstract: Intraperitoneal injection of 0.5 g/kg D-galactosamine results in 95% lethal acute acute liver failure in male Fisher 344 rats. Intrasplenic injection of viable syngeneic hepatocytes 20-28 h after poisoning improves survival in a dose-dependent fashion, 10(7) cells being the optimal dose with a survival rate of 47.1%. While nonviable cells and hepatocyte fragments are totally ineffective, 42.9% of rats survive after injection of 28-hour liver cell culture supernatant. It is concluded that soluble factors generated by cultured cells in vitro or intrasplenically transplanted cells improve survival either by a direct hepatotrophic effect, by stimulation of the reticulo-endothelial system or by an unspecific humoral mechanism.
96 citations
TL;DR: The relative distribution of verapamil and its demethylated metabolite, norverpamil, was studied in rats at intervals after intraperitoneal injection of the parent drug.
Abstract: The relative distribution of verapamil and its demethylated metabolite, norverapamil, was studied in rats at intervals after intraperitoneal injection of the parent drug (30 mg/kg). This route of drug
89 citations
TL;DR: It is postulated that HFDA exercise their inhibitory effects on the DTH response by interfering with the migration of cells into the challenge site.
85 citations
TL;DR: It is suggested that this reaction results from cellular proliferation and could reflect a regenerative process after focal necrosis induced by gentamicin at low doses, and could be a useful tool to measure kidney cortex alterations caused by various aminoglycosides at low, therapeutic doses.
Abstract: Kidney cortex DNA synthesis was studied in female rats treated with a low dose of gentamicin (10 mg/kg) up to 14 days. Synthesis was measured by incorporation of [3H]thymidine into DNA 1 h after intraperitoneal injection of the labeled precursor (200 muCi per animal). Gentamicin given in one injection per day resulted in a greater incorporation of [3H]thymidine into DNA after both 7 and 14 days of treatment as compared with control animals. When the daily dose was divided into three equal injections given at 8-h intervals, a statistically significant increase in thymidine incorporation was observed as early as 4 days after starting gentamicin administration. Excellent agreement was found between DNA specific radioactivity and kidney cortex nuclear labeling, as measured by histoautoradiography. The greatest amount of [3H]thymidine incorporation occurred within proximal tubular cells and interstitial cells. We conclude that a finite duration of gentamicin treatment at low dosage induces an increased DNA synthesis in vivo in rat kidney cortex. We suggest that this reaction results from cellular proliferation and could reflect a regenerative process after focal necrosis induced by gentamicin at low doses. The demonstrated early increase in DNA synthesis could be a useful tool to measure kidney cortex alterations caused by various aminoglycosides at low, therapeutic doses.
81 citations
TL;DR: It is concluded that /S-endorphin acting on opiate receptors in the brainstem is involved in the antihypertensive action of central a2-adrenergic receptor activation, and that this depressor endorphinergic system is distinct from and its effects are opposite to those of other endogenous opioids that appear to tonically inhibit baroreflex sensitivity in spontaneously hypertensive rats.
Abstract: The possible involvement of 0-endorphin in the antihypertensive action of clonidine and a-methyldopa, drugs acting on central a2-adrenergic receptors, has been examined in rats with spontaneous, steroid-salt, or one-kidney, one-clip renal hypertension. In all three groups of rats, the hypotensive effect of a single intraperitoneal injection of 100 mg/kg of a-methyldopa was partially reversed by naloxone (2 mg/kg, ip) or reduced by pretreatment with naltrexone (2 mg/kg, ip). In matched normotensive control rats, a-methyldopa caused a slight reduction or no change in blood pressure, and subsequently administered naloxone had no significant effect on blood pressure. Administration of an antiserum to j3-endorphin into the 4th cerebral ventricle of awake rats inhibited the hypotension and bradycardia produced by intravenous or intracerebroventricular injection of clonidine in all three groups of hypertensive animals. Intracerebroventricular injection of /9-endorphin caused hypotension and bradycardia in spontaneously hypertensive rats. Baroreflex sensitivity was assessed in normotensive Wistar-Kyoto rats and in spontaneously hypertensive rats from the bradycardic response to systemic administration of graded doses of phenylephrine. Naltrexone, 2 mg/kg, ip, did not influence baroreflex sensitivity in Wistar-Kyoto rats but increased it in spontaneously hypertensive rats, as indicated by a progressively greater bradycardia in response to increasing pressure rise. It is concluded that /S-endorphin acting on opiate receptors in the brainstem is involved in the antihypertensive action of central a2-adrenergic receptor activation, that the absence of this mechanism in normotensive animals and its presence in animals with different forms of hypertension indicates that it is activated by the hypertensive process itself, and that this depressor endorphinergic system is distinct from and its effects are opposite to those of other endogenous opioids that appear to tonically inhibit baroreflex sensitivity in spontaneously hypertensive rats. (Circ Res 53: 150-157, 1983)
63 citations
TL;DR: AFP and E2 incubated for 1 hr thus produce a potent inhibitor of estrogen-stimulated mitotic activity and growth, which might act upon estrogen-responsive cells at specific sites at which competition by an inactive component of AFP can block the process.
Abstract: The binding of estrogen to alpha-fetoprotein (AFP) in the plasma cannot account for the impaired estrogen response seen in immature rodents because estradiol (E2) doses that far exceed the total body burden of AFP will stimulate only modest uterine growth. We investigated this phenomenon in immature female mice by determining their uterine weights 23 hr after intraperitoneal injection of estrogens or AFP or both. Administration of either 0.5 micrograms of E2 or 10 ng of moxestrol (MOX) approximately doubled the uterine weight. Giving 1 microgram of AFP 1 hr before injection of either estrogen did not alter that response. Combining the E2 and AFP just prior to injection resulted in decreased uterine growth (34% inhibition). Preincubating the estrogens with purified AFP (0.1-50 micrograms) did not affect the growth response to moxestrol but markedly decreased the response to E2. This was not due to sequestering of hormone because maximal reduction of the E2 response (ca. 65% inhibition) required only 1.0 microgram of AFP (AFP/E2 molar ratio, 1:130), and higher AFP doses inhibited less. About 40% of the growth elicited by injection of either 0.5 micrograms of E2 or 10 ng of MOX was inhibited when these doses were preceded by injection of the preincubated AFP/E2 mixture but not when preceded by either of the components. In each experiment, the mitotic index of luminal epithelium was affected to the same degree as uterine weight. AFP and E2 incubated for 1 hr thus produce a potent inhibitor of estrogen-stimulated mitotic activity and growth. This inhibitor might act upon estrogen-responsive cells at specific sites at which competition by an inactive component of AFP can block the process.
63 citations
TL;DR: The data suggest that in severe gentamicin nephrotoxicity, many cortical nephrons may be contributing very little to excretory function, presumably because of intratubular obstruction.
52 citations
TL;DR: The intraperitoneal route of injection for DS was more effective for liver blockade than the intravenous route and maximal liver blockade occurred at 12 hr after DS injection.
Abstract: The effect of dextran sulfate (DS, 500,000 Mr) and multilamellar vesicles (MLV) as liver blockade agents has been investigated in mice. Intravenous injection of unlabeled MLV prior to radioactive MLV caused moderate reduction in the liver uptake and increased tibia, lung, and spleen uptake. More drastic differences were observed with intraperitoneal injection of DS. When tested in the range of 0-50 mg of DS per kg of body weight, maximal liver blockade occurred at a dose of 50 mg. By using 50 mg of DS per kg, maximal liver blockade occurred at 12 hr after DS injection. The liver blockade was temporary, ending within 48 hr. The intraperitoneal route of injection for DS was more effective for liver blockade than the intravenous route.
47 citations
TL;DR: 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.
Abstract: 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 GGMS 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 N03− 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, N02 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.
47 citations
TL;DR: It was found that OK-432 induced a time-dependent multi-step alteration of motility, adhesiveness, IL1 production, and inhibition of tumor cell growth in vitro were examined in murine peritoneal macrophages obtained after intraperitoneal injection of a streptococcal preparation, heat-inactivated OK- 432, and thioglycollate medium.
46 citations
TL;DR: This pattern of fluid compartmental and electrolyte changes suggests that brain volume regulation during acute DH occurs via reduction of extracellular volume as cells swell, which may result from bulk flow ofextracellular fluid to CSF or from ion and water movement across the blood-brain barrier.
Abstract: Dilutional (DH) and isosmotic (IH) hyponatremia (plasma [Na+] = 103-109 meq/l) were produced in conscious rats over 3-6 h by intraperitoneal injection of water or mannitol Ringer solution. During D...
TL;DR: W-7, a calmodulin antagonist may inhibit the growth of solid Sarcoma-180 by modulation of the Ca2+-calmodulin-dependent processes.
TL;DR: It is suggested that the IFN induced by VSV or poly(rI):(rC), rather than those agents themselves, causes the observed lymphopenia as well as some of the changes observed in the spleen.
TL;DR: An extract vaccine against Vibrio anguillarum was compared with other vaccine preparations when administered to rainbow trout intraperitoneally or orally on food and the addition of alum as adjuvant enhanced the response to antigen administered by both routes.
Abstract: . An extract vaccine against Vibrio anguillarum was compared with other vaccine preparations when administered to rainbow trout intraperitoneally or orally on food. Intraperitoneal vaccination resulted in virtually 100% protection within two weeks whereas oral vaccination gave a maximum protection of 50–70% after eight weeks. When administered intraperitoneally the extract performed better than formalin killed cells but when administered orally formalin killed cells were better. The addition of alum as adjuvant enhanced the response to antigen administered by both routes. Serum agglutinin litres after oral vaccination were low and variable but after intraperitoneal injection they reached a consistent peak of 64. As the response to oral vaccination was so low it was not possible to relate agglutinin titre to protection in a quantitative relationship.
TL;DR: The time course of radioactivity in plasma, liver and brain is described following the intraperitoneal injection of 2-amino-7-phosphono-[4,5-3H]heptanoic acid in mice, with a peak concentration at 30 min, declining markedly between 90 and 180 min, corresponds to the anticonvulsant action.
TL;DR: A technique permitting the serial determination of plasma ethanol concentration (PEC) in mice is described and it was demonstrated that this source reflects the rapid dynamics of absorption and clearance after an intraperitoneal injection of ethanol.
TL;DR: Nicotine did not alter the plasma levels of either of the thyroid hormones but did produce a significant increase in plasma corticosterone, an effect which peaked at 20 min post-injection and lasted for 45 min.
Abstract: The effects of a single intraperitoneal injection of nicotine hydrogen tartrate (200 micrograms/kg) on the plasma levels of thyroxine, triiodothyronine and corticosterone were monitored over a 24 hour period. Nicotine did not alter the plasma levels of either of the thyroid hormones but did produce a significant increase in plasma corticosterone, an effect which peaked at 20 min post-injection and lasted for 45 min.
TL;DR: The results are tentatively interpreted as evidence that C-H bond cleavage is not a rate limiting feature of overall metabolism, but that the complex between NDMA and the principal enzyme(s) metabolizing it in vivo freely equilibrates with unbound substrate.
Abstract: The maximal rates of metabolic oxidation of N-nitrosodimethylamine (NDMA) and N-nitrosodimethylamine-d6 (NDMA-d6) in vivo (VH and VD, respectively) have been measured by following 14CO2 exhalation in rats after intraperitoneal injection of the two 14C-labelled carcinogens at high doses (20 or 40 mg/kg). Complete deuteration of NDMA reduced only slightly the maximal rate of metabolism when the two substrates were administered separately (VH/VD approximately 1.2). However, much larger (approximately 4-fold) deuterium isotope effects were observed when mixtures of NDMA with NDMA-d6 were injected. These results are tentatively interpreted as evidence that C-H bond cleavage is not a rate limiting feature of overall metabolism, but that the complex between NDMA and the principal enzyme(s) metabolizing it in vivo freely equilibrates with unbound substrate. Single, large, intraperitoneal doses of NDMA and NDMA-d6 produced a similar alkylation of rat liver DNA and also of kidney DNA. However, a small oral dose (54 micrograms/kg) of NDMA-d6 produced 1/3 less alkylation of liver DNA and 3 times as much alkylation of kidney DNA as did an equimolar dose of NDMA. The reduction in alkylation of liver DNA correlates well with, and possibly explains, the decreased ability of NDMA-d6 to induce liver tumors in rats. The associated increase in the alkylation of kidney DNA suggests that this change is due to a decrease in the amount of nitrosamine removed from the portal blood on the first pass through the liver.
TL;DR: Significant increases in micronuclei were seen in circulating erythrocytes only at 48 h in C57Bl/6J mice with both test chemicals and in C3H/C57 mice only with cyclophosphamide.
TL;DR: The data suggest that CrCl3 may affect embryos directly and cause neural tube defects and that pyknotic cells on the neural plate may be an early pathological finding in cases of developing exencephaly.
TL;DR: The present study supports the notion that the LS mice are more sensitive to the peripherally mediated concentration-dependent effects of ethanol than are the SS mice, and the systemic toxic effects of high ethanol concentrations may be more important in determining narcosis than previously suspected.
Abstract: It has been observed that responses to ethanol may be altered by varying the injection concentration while keeping the dose constant, but these concentration-dependent effects have not been well characterized. The results of the study reported here indicate that the long-sleep (LS) and short-sleep (SS) mice, selectively bred for ethanol-induced narcosis at a concentration of 30% v/v, may have been selected in large part for the concentration-dependent peripheral toxic effects of ethanol rather than ethanol's direct effects on the central nervous system. The study was designed to assess sleep time and waking blood ethanol concentration (BEC), hypothermia, and the linear decline in BEC in LS mice following an intraperitoneal injection of 3.8 g/kg of ethanol in concentrations of 190.0, 237.5, 292.3, or 380.0 mg/ml, and in SS mice following an intraperitoneal injection of 4.1 g/kg of ethanol in concentrations of 205.0, 256.2, 315.4, or 410.0 mg/ml. LS sleep time increased as a function of concentration, and mice injected with 380.0 mg/ml never regained the righting reflex. Waking BECs were significantly different for LS mice injected with the 190.0 and 292.3 mg/ml concentrations. For the SS mice, marginally significant differences were found among sleep times, and none of the animals injected with the 410.0 mg/ml regained the righting reflex. The lack of significant concentration-dependent differences in SS waking BECs is attributable to extreme variability in the BECs of mice injected with the 315.4 mg/ml concentration. Both the LS and SS mice showed a concentration-dependent decrease in body temperature, with the greatest temperature change observed at the highest concentrations. Maximum temperature depression occurred at 120 to 150 min postinjection in the LS mice and at 60 to 90 min postinjection in the SS. Only SS mice injected with the 205.0 or 256.2 mg/ml concentrations reethanolgained control temperature levels. The linear decline in BEC was faster at lower concentrations than at higher concentrations for LS mice. The declines in BEC for SS mice were not found to vary as a function of concentration. Concentration-dependent differences in sleep time and hypothermia may not be due to differences in circulating levels of ethanol, but rather to slower elimination rates and/or enhanced depressant effects on peripheral organ systems. The present study supports the notion that the LS mice are more sensitive to the peripherally mediated concentration-dependent effects of ethanol than are the SS mice. The systemic toxic effects of high ethanol concentrations may be more important in determining narcosis than previously suspected.
TL;DR: Elevation of plasma levels of cholesterol and triglyceride was reduced by the intramuscular injection of ginseng principles fraction 4 and the elimination of intraperitoneally injected 4-[14C]-cholesterol from plasma was accelerated by fraction 4 administration.
Abstract: Elevation of plasma levels of cholesterol and triglyceride was reduced by the intramuscular injection ginseng principles fraction 4 (saponin content, ca. ½). The elimination of intraperitoneally injected 4-[14C]-cholesterol from plasma was accelerated by fraction 4 administration. Fecal excretion [14C] bile acids and [14C] sterols after intraperitoneal injection of 4-[14C]-cholesterol was significantly increased by fraction 4 administration.
TL;DR: In these experiments, the lower-isoelectric-point endogenous pyrogens were produced by macrophages from the peritoneal cavity of rabbits that had been injected 4 days earlier with 50 ml of light mineral oil, and were found to have leukocytic endogenous mediator activity in mice but to be completely inactive in rats.
Abstract: It was recently shown (Murphy et al., Infect. Immun. 34:177-183), that rabbit macrophages produce two biochemically and immunologically distinct endogenous pyrogens. One of these has or copurifies with substances having a molecular weight of 13,000 and a pI of 7.3. This protein was produced by blood monocytes or inflammatory cells elicited in 16-h rabbit peritoneal exudates. These acute peritoneal exudates were produced by the intraperitoneal injection of large volumes of saline containing shellfish glycogen. When the leukocytes in these exudates were washed and incubated at 37 degrees C in saline, they released an endogenous pyrogen. The injection of this pyrogen into rabbits, rats, or mice caused the biological manifestations which have been attributed to leukocytic endogenous mediator. These effects were increases in blood neutrophils, the lowering of plasma iron and zinc levels, and the increased synthesis of the acute-phase proteins. The other rabbit endogenous pyrogen seems to be a family of proteins with isoelectric points between 4.5 and 5.0. These proteins are produced by macrophages in the lung, liver, or in chronic peritoneal exudates. In these experiments, the lower-isoelectric-point endogenous pyrogens were produced by macrophages from the peritoneal cavity of rabbits that had been injected 4 days earlier with 50 ml of light mineral oil. These rabbit pyrogens were found to have leukocytic endogenous mediator activity in mice but to be completely inactive in rats. When injected into rabbits, these proteins produced fever, lowered plasma iron, increased blood neutrophils, but failed to elevate plasma fibrinogen.
Journal Article•
TL;DR: A correlation between immunocytotoxicity of PAH compounds on T-cell subsets and the responsiveness of mouse strains to these carcinogens is suggested.
Abstract: The in-vivo effects of a polycyclic aromatic hydrocarbon (PAH), 3-methylcholanthrene (MCA), on in-vitro mitogen activation, cell-mediated lympholysis (CML) and T-cell subset distribution in mouse splenic lymphocyte populations were measured. Three inbred mouse strains were treated with a single intraperitoneal injection of corn oil alone or with different doses of MCA in oil (0.5-50 mg kg -1). One to ninety days after injection, splenic lymphocytes were isolated, and assayed for blastogenesis, CML and the percent T-helper and T-suppressor cells using monoclonal antibodies. High doses of MCA suppressed mitogen activation (15.2-53.6%) and CML (69-90%) within 24 hr in lymphocytes from PAH-responsive mice (C57 and C3H). Blastogenesis was stimulated and CML was suppressed to a lesser degree (5-45%) in lymphocytes from non-responsive mice (DBA). MCA induced an increase in T-suppressor cells in responsive mice, but there was no change in DBA mice. These studies suggest a correlation between immunocytotoxicity of PAH compounds on T-cell subsets and the responsiveness of mouse strains to these carcinogens.
TL;DR: A single, intraperitoneal injection of diethyldithiocarbamate (DDTC) to adult, male Sprague-Dawley rats decreased hepatic cytochrome P- 450 (P-450) concentrations, suggesting that diminished P-450 concentrations are related to the metabolic activation of DDTC.
TL;DR: In naturally exposed fish high concentrations were also found in the gut and gills while in injected fish high levels were demonstrated in the gall bladder and kidney.
TL;DR: Findings suggest that 17α, 20β-diOHprog is the major ovarian mediator of LH-RH-induced oocyte maturation in ayu and the changes in serum levels of these steroids during final maturation and ovulation are medizted through the secretion of pituitary GtH.
Abstract: The time course changes in serum concentrations of gonadotropin (GtH), 17α-hydroxypro-gestrone and 17α, 20β-dihydroxy-4-pregnen-3-one (17α, 20β-diOHprog) during LH-RH-induced final oocyte maturation and ovulation in gravid ayu Plecoglossus altivelis were examined. The fish underwent GVBD one day following a single intraperitoneal injection of emulsified LH-RH and ovulated in 2 days. A slow and moderate increase in serum levels of GtH occurred 1-3 days after injection. The LH-RH treatment caused a prompt increase in hte serum levels of 17α-hydroxypro-geterone and 17α, 20β-diOHprog concomitant with final oocyte maturation and ovulation. The levels of 17α, 20β-diOHprog remained high for 1-3 day after injection, followed by a sharp decrease at 5-7 days. The elevation of 17-hydroxyprogesterone, which is a precursor for 17α, 20β-diOHprog occurred earlier and persisted longer than the changes in 17α, 20β-diOHprog. Thus, the changes in serum levels of these steroids during final maturation and ovulation are medizted through the secretion of pituitary GtH. These findings suggest that 17α, 20β-diOHprog is the major ovarian mediator of LH-RH-induced oocyte maturation in ayu.
TL;DR: The combined effect of copper and insulin significantly decreased peak blood glucose at 30 min and increased the incorporation of [14C]glucose into lipid in the epididymal fat pad when compared to either copper or insulin alone.
Abstract: The effects of copper and insulin on lipogenesis and glucose tolerance were studied using diabetic, copper-deficient rats. Diabetes was induced by intraperitoneal injection of 50 mg streptozotocin/kg body weight to rats fed a sucrose-copper deficient diet for 7 weeks. Five days later the rats were injected intraperitoneally with [14C]glucose with either saline, insulin, copper, or copper plus insulin. The disappearance of serum [14C]glucose at 30, 60, and 120 min postinjection and the incorporation of [14C]glucose into lipid of epididymal fat 2 hr after administration were determined. The combined effect of copper and insulin significantly decreased peak blood glucose at 30 min and increased the incorporation of [14C]glucose into lipid in the epididymal fat pad when compared to either copper or insulin alone. The enhancement of glucose utilization may be due to a formation of a more stable complex which will increase insulin binding and/or decrease its degradation.
Journal Article•
TL;DR: The data support the efficacy of early glucocorticoid treatment in endotoxemia, which prevents the deterioration of brain and kidney mitochondrial function.
Abstract: Endotoxemia was induced in rats and guinea pigs by an intraperitoneal injection of E coli endotoxin In the rat, the dose used (3 mg/100 g body weight) resulted in a 60% mortality in 24 h The same dose in the guinea pig resulted in a similar mortality at 24 h, and a 100% mortality by 3 days Methylprednisolone Na-succinate, a glucocorticoid, given simultaneously with the endotoxin, prevented mortality in the rats No animals died during the observation period In the guinea pigs the same treatment protected all animals for 24 h, and resulted in an 80% survival rate over a 6-day observation period Administration of glucocorticoids 1 or 2 h after endotoxin showed diminished efficacy About 60% of the guinea pigs died during the 6-day observation period Rat kidney and guinea pig brain and kidney mitochondria were isolated and analyzed for their function in untreated and treated animals 24 h after the injection of endotoxin Rat kidney mitochondrial O2 utilization and ATP synthesis function, as well as Ca++ transport activity, were significantly below normal in the untreated animals, but did not differ from normal in glucocorticoid-treated animals In untreated and at zero time treated guinea pigs similar results were found in brain and kidney mitochondrial functions If treatment was delayed for 1 or 2 h, however, brain mitochondrial O2 utilization and ATP synthesis rates were significantly below normal, and both brain and kidney mitochondrial Ca++ transport capacities remained significantly lowered The data support the efficacy of early glucocorticoid treatment in endotoxemia Early glucocorticoid treatment prevents the deterioration of brain and kidney mitochondrial function
TL;DR: It is observed that generation of LPS-induced CSF in mice tolerant to LPS could be restored by an intraperitoneal injection of spleen cells 24 h before the challenging injection of L PS, and data suggest that the spleen Cells are active in generating CSF, provided that macrophages are present and can interact with the splenic lymphocytes to generate L PS-inducedCSF in the serum.
Abstract: Injection of lipopolysaccharide (LPS) into mice was followed by a rapid elevation of colony-stimulating factor (CSF) in the serum. A second, challenging injection of LPS given 3 to 4 days later failed to induce elevated levels of CSF in the serum. Such mice tolerant to LPS were used as an experimental tool to identify the CSF-producing cells which respond to LPS. We observed that generation of LPS-induced CSF in mice tolerant to LPS could be restored by an intraperitoneal injection of spleen cells 24 h before the challenging injection of LPS. Depletion of the adherent cells from the spleen cells reduced the ability of the splenic lymphocytes to restore the capacity of the mice tolerant to LPS to generate serum CSF. Reconstitution of the splenic lymphocytes with 5% thioglycolate-elicited peritoneal macrophages, however, reestablished the restorative capacity of these cells, whereas almost no restoration was observed after direct injection of elicited peritoneal macrophages. These data suggest that the spleen cells are active in generating CSF, provided that macrophages are present and can interact with the splenic lymphocytes to generate LPS-induced CSF in the serum.