Biomedical subjects

N G Ilbäck

Publications and source records attributed to N G Ilbäck.

At least 19 recordsLinked to original sources

PubMed2003

Cardiovascular effects of xylazine recorded with telemetry in the dog.

Cardiovascular effects of xylazine have not been studied with telemetry in dogs. In the present study, the effects on cardiovascular parameters after intramuscular (i.m.) administration of 2.0 mg/kg xylazine were studied via telemetry in unrestrained dogs. Telemetry transmitters were implanted subcutaneously (s.c.) with a pressure catheter in the femoral artery. Cardiovascular effects and body temperature effects were assessed after i.m. administration of xylazine. Heart rate decreased for about 10 min and was continuously depressed during 60 min. Thereafter, heart rate slowly increased but had not fully reached pre-dose values 4 h after treatment. Both systolic and diastolic blood pressure increased immediately after administration of xylazine. The systolic blood pressure showed a peak increase for about 5-10 min and then decreased below the baseline value not normalizing within 90 min. The diastolic blood pressure peaked 5-10 min after xylazine administration but did not return to baseline level until 50 min after administration. Body temperature decreased continuously for about 90 min and remained low for more than 4 h after treatment. An additional administration of xylazine to the same individuals after a recovery period of 4 weeks induced exactly the same response in systolic and diastolic blood pressure and in heart rate. By using the telemetric recording system it was possible to continuously evaluate xylazine-induced cardiovascular responses in a way that is not possible with conventional techniques.

Adrenergic alpha-Agonists↗

PubMed2000

Relation between trace element levels in plasma and myocardium during coxsackievirus B3 myocarditis in the mouse.

During most infections the plasma levels of trace elements change, but it is not clear if this reflects changes in the infected tissues. Coxsackievirus B3 (CB3) infection may result in viral replication, subsequent inflammation and changed trace element levels in the myocardium. In the present study, the trace element levels in the plasma and heart of adult male A/J mice were determined during the pre-inflammatory stage (day 4) of CB3 myocarditis for the following trace elements: aluminium (Al), arsenic (As), calcium (Ca), cobalt (Co), copper (Cu), iron (Fe), magnesium (Mg), manganese (Mn), selenium (Se), silver (Ag), vanadium (V) and zinc (Zn). The severity of the infection was assessed through clinical signs of disease and trace element levels were measured through inductively-coupled plasma mass-spectrometry (ICP-MS). In the heart, the levels decreased for V (59%; p < 0.01), Co (38%; p < 0.01), Al (81%; p < 0.01), As (66%; p < 0.01) and Se (16%; p < 0.01). Increased levels were detected for Mn (13%; p < 0.05), Fe (48%; p < 0.01), Cu (34%; p < 0.01) and Ag (46%; p < 0.01). In the plasma, decreases were detected in the level of Zn (32%; p < 0.05), whereas increases were seen in Mn (362%; p < 0.05), Fe (272%; p < 0.01), Co (71%; p < 0.05), Cu (25%; n.s.) and Mg (43%; p < 0.01) levels. A correlation was found between the levels in plasma and myocardium for Co (r(s) = -0.636; p < 0.05), Fe (r(s) = 0.764; p < 0.05), Mn (r(s) = 0.682; p < 0.05) and Mg (r(s) = -0.791; p < 0.05). Thus, determination of some of these trace elements in the plasma may be useful to indicate target tissue involvement in the early pre- inflammatory stage of an infectious disease. Some of these elements are important nutrients for the immune system, while others may be associated with the development of disease complications, such as cardiac arrhythmias.

Animals↗

PubMed2000

Effects of EDTA on trace elements and cardiovascular function in the anesthetised rabbit.

The present study was undertaken in order to study the effects of the broad-acting chelating agent CaNa2-EDTA on plasma trace elements and cardiovascular function in anesthetised New Zealand White rabbits. Trace elements are important for cardiovascular and immune functions and the rabbit is a well-accepted species in cardiovascular studies. The test compound CaNa2-EDTA was administered intravenously to rabbits at single doses of 4, 20, and 100 mg/kg. In addition, at 20 mg/kg, the effects of a second dose after 3 h were also investigated. Heart rate, blood pressure and body temperature were continuously monitored during a 6-h interval after injection of CaNa2-EDTA. Immediately before administration (-1 min) and at 3 and 6 h over the period of the experiment, the plasma cytokine response (tumor necrosis factor-alpha) and trace elements (Mn, Cu, Zn, Se, Ag, Cd, Hg, Pb) were measured. Regardless of dose, blood pressure was found to decrease, but no corresponding changes in heart rate were observed. Both a repeated administration of 20 mg/kg and a single dose of 100 mg/kg were detrimental and caused severe cardiovascular effects and lethality. alpha-TNF tended to increase, though only at 100 mg/kg. The electrocardiogram and body temperature were not affected by the treatment. The most pronounced trace element change was a dose-dependent increase in Mn that was equally pronounced at all time-points after the dose. There was an initial decrease in Cd at low dose levels (4 and 20 mg/kg) that turned into an increase after 6 h at 20 mg/kg and from 2 h at 100 mg/kg. A similar pattern with pronounced decreases at low dose levels was observed for Zn. Cu decreased similarly at all dose levels. For the other trace elements, no or inconsistent effects were observed. This model allows the study of concomitant cardiovascular and trace element changes during treatment with drugs and chelating agents preceding a possible lethal end point and associated pathophysiologic changes.

Anesthesia↗

PubMed2000

Trace element changes in the myocardium during coxsackievirus B3 myocarditis in the mouse.

During most infections plasma, concentrations of trace elements change, but it is unclear if this reflects changes in infected target tissues. In coxsackievirus B3 (CB3) infection, the myocardium is a target in both humans and mice. The concentrations of 12 trace elements were analyzed by inductively coupled plasma-mass spectrometry (ICP-MS) in the myocardium of sham-inoculated controls and infected A/J mice 4 and 7 d postinoculation. The size of the inflammatory lesion was positively correlated to the virus content of the heart, as estimated by histopathology and in situ hybridization, respectively. Iron, cobalt, vanadium, and selenium showed transient changes, whereas for the other elements, tendencies on d 4 were manifest on d 7. A three-fold increase in calcium on d 7 suggests prestages of calcification, whereas increases in zinc, selenium, and copper may be the result of the accumulation of immune cells. The magnesium decrease may contribute to the increased sensitivity to cardiac arrhythmias in myocarditis.

Animals↗

PubMed2000

Trace element distribution in heart tissue sections studied by nuclear microscopy is changed in Coxsackie virus B3 myocarditis in methyl mercury-exposed mice.

Methyl mercury (MeHg) has been shown to change Coxsackie virus type B3 (CB3) myocarditis in a direction compatible with the development of chronic disease. Murine models of CB3 myocarditis closely mimic the pathogenesis in humans. There are also indications that metals, such as mercury, and trace elements may interact and adversely affect viral replication and development of inflammatory lesions. The effects of low-dose MeHg exposure on myocardial trace element distribution, as determined by means of nuclear microscopy, was studied in CB3 myocarditis. Balb/c mice were fed a MeHg-containing diet (3.9 mg/kg diet) for 12 wk prior to infection. Areas of inflammatory lesions in the myocardium were identified by traditional histologic examination, and serial tissue sections in these selected areas were used for immune histology (macrophages), in situ hybridization of virus genomes, and nuclear microscopy of tissue trace element distribution. Areas with no inflammation or virus were compared with areas of ongoing inflammation and viral replication. In the inflammatory lesions of MeHg-exposed mice as compared to nonexposed mice, the myocardial contents of calcium (Ca), manganese (Mn), and iron (Fe) were significantly increased, whereas the zinc (Zn) content was decreased. The increased Ca and decreased Zn contents in the inflamed heart may partly explain a more severe disease in MeHg-exposed individuals. Although not significant in the present study, with a limited number of mice, the inflammatory and necrotic lesions in the ventricular myocardium on d 7 of the infection was increased by 50% (from 2.2% to 3.3% of the tissue section area) in MeHg-exposed mice and, also, there was a tendency of increased persistence of virus with MeHg exposure. No increased MeHg uptake, either in the inflammatory lesions or in the areas of noninflamed heart tissue in infected mice, could be detected. The present results indicate that a "competition" exists between potentially toxic heavy metals from the environment/diet and important trace elements in the body and that a disturbed trace element balance adversely influences the development of pathophysiologic changes in inflammatory heart disease.

Animals↗

PubMed1999

The lichen rock tripe (Lasallia pustulata) as survival food: effects on growth, metabolism and immune function in Balb/c mice.

The present study was performed to investigate whether the lichen rock tripe (Lasallia pustulata) can be used as food during survival situations. The effects of 30% lichen supplementation given to female Balb/c mice were studied on growth rate, metabolism and immune functions. After 3 weeks on this diet, it was found that the lichen supplementation did not affect the growth rate or the well-being of the animals. The growth rate tended to be higher in the lichen group when compared to control mice. Food consumption was similar in both groups, but with a trend towards slightly higher intake (12%) in the lichen group. The heart, liver, kidney and lymphoid organ (spleen and thymus) weights were not affected by the lichen. Histological hematoxylin eosin staining showed that all these organs were normal. Plasma glucose levels were unchanged, but plasma urea levels decreased by 24% (p < 0.05) with the lichen diet. Red and white blood cells and the number of lymphoid cells in the thymus and spleen were normal. The activity of thymocytes and spleen T-lymphocytes were not affected by the lichen diet, but spontaneous cell-mediated cytotoxicity (NK cells) tended (n.s.) to increase and spleen B-lymphocyte activity increased by 40% (p < 0.05). This study shows that the lichen rock tripe has immune stimulating effects important for host defence reactions and can be used as food in survival situations without any adverse effects on the metabolism.

Animals↗

PubMed1998

The intestinal absorption of cadmium increases during a common viral infection (coxsackie virus B3) in mice.

Murine intestinal absorption, tissue accumulation and redistribution of 109Cd during infection were studied using the common human virus Coxsackie virus B3 (CB3) adapted to the mouse. Female Balb/c mice were infected with CB3 and, on day 4 of the infection, dosed orally with 0.3 or 750 microgram Cd/kg body weight, with 109Cd as a tracer, in order to study intestinal absorption and tissue distribution of Cd during infection (Experiment 1). Other mice were dosed with 0.3 microgram Cd/kg body weight 3 days before being infected and, on day 4 of the infection, Cd redistribution was studied (Experiment 2). In both experiments non-infected control animals received the same treatment as infected animals. Results showed that the infected animals had a higher gastrointestinal absorption of Cd than noninfected animals when Cd was administered during infection. In the infected animals the absorption at the low Cd dosage was increased by 70% and was tripled at the high dosage. The increased absorption enhanced the accumulation of Cd in all organs studied. Moreover, the infection caused a Cd dose-dependent change in the organ distribution of Cd, when Cd was administered during the infection. However, no redistribution of previously accumulated Cd occurred during ongoing disease, indicating that Cd was not mobilised from body stores by the infection. These results show, for the first time, that an invading micro-organism can increase the intestinal absorption and concomitantly alter the tissue distribution of an environmental pollutant (Cd) if exposure occurs during the course of viral infection.

Administration, Oral↗

PubMed1998

Effects of selenium supplementation on virus-induced inflammatory heart disease.

The effects of 10 wk of selenium (Se) supplementation (5 ppm) in drinking water on immune responses and resistance to a myocarditic Coxsackie virus B3 (CB3) infection were studied in female Balb/c mice. Se supplementation reduced CB3-induced mortality: at day 14 postinoculation, survival was 58% in the Se-treated group as compared to 25% in the untreated group. Whole-blood glutathione peroxidase (GSH-Px) activity was elevated by 68% (p < 0.001) and Se content in the liver by 24% (p < 0.001). Red (RBC) and white blood cell (WBC) counts, as well as the number of cells in the spleen and thymus, were unaffected. The cellular counts of T-lymphocytes (CD4+, CD8+) and natural killer (NK+) cells in the blood were not affected. However, the CD4+/CD8+ ratio (5.2) tended to increase after Se supplementation (5.9). The spleen lymphoproliferative response to T- and B-cell mitogens were increased by 9 and 43%, respectively (ns), in the Se-supplemented group. The total NK cell activity in blood and spleen showed minor increases, but when the activity in the blood was expressed per cell, the increase amounted to 35% (ns) with Se supplementation. The inflammatory and necrotic lesions in the ventricular myocardium at 7 and 14 d postinoculation were not significantly reduced by Se treatment, probably owing to the increased survival with Se even of mice with the most pronounced heart damage; comparable untreated mice were estimated to have died at day 14. Results indicate that modest doses of Se can improve immune function, which may increase the general resistance to this viral infection.

Animals↗

PubMed1998

Acute infection: metabolic responses, effects on performance, interaction with exercise, and myocarditis.

Acute infections are associated with multiple host responses that are triggered by cytokines and correlated to fever, malaise and anorexia. The purpose of this systemic acute phase host reaction ("the acute phase response") is to mobilize nutrients for the increased needs of the activated immune system, as well as for energy production and tissue repair. Important effects include wasting of striated muscle, degradation of performance-related metabolic enzymes and, concomitantly, deteriorated central circulatory function. These effects result in decreased muscle and aerobic performance, the full recovery of which may require several weeks to months following week-long febrile infections. Also during early infection and fever, prior to the development of muscle wasting, performance is compromised by other mechanisms. Strenuous exercise may be hazardous during ongoing infection and fever and should always be avoided. In infection, muscle wasting seems to be less pronounced in the conditioned (trained) host than in the unconditioned host. Acute myocarditis most often has a viral etiology but bacteria and their toxins may also be the cause. Furthermore, slow-growing bacteria, previously difficult to diagnose, have emerged as potential "new" causes of subacute to chronic myocarditis. Since myocarditis may or may not be associated with fever, malaise, or catarrhal symptoms, athletes should be taught the symptoms suggestive of myocarditis. Whenever myocarditis is suspected exercise should be avoided.

Acute-Phase Reaction↗

PubMed1997

Genetically engineered superantigens as tolerable antitumor agents.

Superantigens (SAg) are a family of bacterial and viral proteins with strong immunostimulatory properties. SAg bound to major histocompatibility complex (MHC) class II molecules activate a high frequency of T cells and represent the most potent known activators of T cells to date. To explore the use of SAg for T cell-based tumor therapy we have created a tumor-reactive SAg by engineering a fusion protein composed of a tumor-reactive mAb (C215Fab) and the bacterial SAg staphylococcal enterotoxin A (SEA). A point mutation D227A was introduced at the major MHC class II binding site in SEA to reduce systemic toxicity. Treatment of tumor bearing mice with the Fab-SEA D227A fusion protein resulted in profound antitumor effects with a markedly reduced toxicity as compared with the wild-type Fab-SEA fusion protein. The reduced toxicity was probably due to a weak distribution of the SEA D227A fusion protein in tissues with a high MHC class II expression and low systemic cytokine levels as exhibited in mice and rabbits. The data presented demonstrate the efficacy of immunoconjugates containing a mutated SAg in directing a T cell attack against tumor cells with minimal systemic immune activation.

Animals↗

PubMed1996

Antiviral treatment with WIN 54 954 reduces mortality in murine coxsackievirus B3 myocarditis.

BACKGROUND: Coxsackieviruses B (CBVs) are dominant causative agents in myocarditis and are associated with pathogenesis is some cases of dilated cardiomyopathy, a clinical entity with a poor survival without heart transplantation. METHODS AND RESULTS: In vitro, the antiviral agent WIN 54 954 was shown to inhibit replication of CBV3 at a minimal inhibitory concentration value of 0.02 mg/L. Administration of WIN 54 954, 100 mg/kg BID PO, beginning on the day of infection resulted in complete protection from enteroviral mortality (P < .01). WIN 54 954 treatment did not abrogate the inflammatory reaction in the myocardium. No difference was found in the expression of surface lymphocyte subset markers. At 3 weeks, macrophages seemed to dominate the inflammatory reaction, regardless of treatment. There was no difference in CBV3 antibody titers, indicating that WIN 54 954 does not interfere with the development of protective immunity. Complement factors C3 and B were synthesized at a higher level during infection and correlated well with the degree of inflammatory reaction. CONCLUSIONS: The results show that WIN 54 954 is a potent antiviral agent with a highly significant effect on survival in CBV-induced myocarditis in the A/J mouse if treatment is started early. It is suggested that the reduction in mortality seen with WIN 54 954 administration is due to an inhibitory effect on virus replication in affected organs that does not interfere with cellular or humoral immunity.

Animals↗

PubMed1996

Effects of methyl mercury on cytokines, inflammation and virus clearance in a common infection (coxsackie B3 myocarditis).

A myocarditic coxsackievirus B3 (CB3) infection in Balb/c mice was used to investigate the effects of 12 weeks of methyl mercury (MeHg) exposure (3.69 mg/g diet) on inflammatory heart lesions, virus in the heart, the cytokine response, i.e. cachectin/TNF-alpha and gamma-interferon (IFN-gamma) levels in plasma, and on disease complications and mortality. This dose of MeHg did not influence mortality in this infection model. The inflammatory and necrotic lesions in the ventricular myocardium 7 days after the inoculation covered 2.2% of the tissue section area in infected control mice. This damage was increased (n.s.) by 50% (to 3.3% of the tissue section area) in MeHg-treated mice. The response pattern of lymphocyte subsets in situ in myocardial inflammatory lesions was corroborated using an immune histological technique. MeHg treatment tended to increase (2.2-fold, n.s.) the number of Mac 2+ cells (macrophages) in the heart muscle in this infection. Plasma levels of both TNF-alpha and IFN-gamma increased on day 3 of the infection in MeHg-treated as well as in non-MeHg-treated mice, but the mean IFN-gamma response was more pronounced in the MeHg-treated mice. On day 7 of the infection, when most animals still showed clinical signs of disease, cytokine levels were back to normal. MeHg-exposure in non-infected mice did not affect cytokine levels. In situ hybridization of virus RNA in myocardial tissue showed remaining virus in those mice who had the lowest plasma IFN-gamma levels. A 20% increased (P < 0.05) lymphoproliferative response to the T cell mitogen Con A was observed as a result of the MeHg treatment. Even heart tissue lesions and virus persistence tended to be influenced by MeHg in a direction compatible with the development of chronic disease.

Animals↗

PubMed1995

New aspects of murine coxsackie B3 myocarditis--focus on heavy metals.

The magnitude of inflammatory lesions in the hearts of coxsackie B3 (CB3)-virus infected mice can be affected by the potentially toxic heavy metals cadmium (Cd), nickel (Ni) and methyl mercury (MeHg). The infection is associated with a changed distribution, such as Cd accumulation in the spleen and kidneys. New target organs for Ni during the infection were the heart, pancreas and lungs in which inflammatory lesions were present. This increased uptake was correlated with the disturbed function of immune cells and an increased inflammatory reaction. Ni and MeHg appeared to have a direct effect on immune cells that resulted in changed natural killer cell activity and decreased mobilization of macrophages, CD4+ and CD8+ cells into the inflammatory lesions. Although MeHg increased spleen T cell activity and gamma-interferon (IFN-gamma) levels, the inflammatory lesions in the heart increased. Another detrimental effect of MeHg treatment was evident by an increased calcium and decreased zinc content in the inflamed heart, which may partly explain the more severe inflammatory lesion. The host's response, CB3 infection, changed the distribution of each metal in a specific way, a fact which may subsequently result in altered target organ toxicity and resistance to the infection.

Animals↗

PubMed1994

Changed distribution and immune effects of nickel augment viral-induced inflammatory heart lesions in mice.

We have used the myocarditic coxsackievirus B3 (CB3) infection in Balb/c mice to investigate immunotoxic effects of a ten-week low-dose (0.002 M) administration of nickel chloride (NiCl2) prior to infection. This dose did not influence CB3-induced mortality. Whole-body autoradiography of [63Ni] during the disease showed the pancreas, lungs and myocardium to be new target organs in this disease. Seven days after the inoculation, impulse counting of these organs showed the infection-induced increase of [63Ni] to be 5-fold (P < 0.01) in the pancreas, 2.2-fold (P < 0.05) in the lungs and 1.3-fold (P < 0.05) in the heart. Nickel tended to increase spleen B- and T-cell activities, but thymocyte activity was unaffected. The activity of spleen natural killer (NK) cells decreased by 30% (P < 0.05), whereas blood-cell activity in fact increased by 51% (P < 0.05). The inflammatory and necrotic lesions in the ventricular myocardium seven days after the inoculation covered 3.31% of the tissue section area in infected control mice. This damage was increased by 43% (to 4.74% of the tissue section area) in nickel-treated mice. The response pattern of lymphocyte subsets in situ in myocardial inflammatory lesions was elucidated by an immune histochemical staining technique. The number of cytotoxic T-cells, helper T-cells and Mac 2+ cells (macrophages) in these lesions decreased by 46% (P < 0.05), 41% (P < 0.05) and 27% (not significant), respectively, with the nickel treatment. The number of helper T-cells was negatively correlated to the size of the inflammatory area (r = -0.529, P < 0.02). The results indicate that nickel may contribute to the progression of target organ pathology in infection-induced diseases of an autoimmune and/or inflammatory character, such as diabetes and myocarditis.

Administration, Oral↗

PubMed1994

Coxsackievirus B3 infection alters the uptake of 2,3,7,8-tetrachlorodibenzo-p-dioxin into various tissues of the mouse.

The tissue uptake of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) during infection was studied in a mouse model using the common human virus Coxsackievirus B3 (CB3), adapted here to the mouse. Male A/J-mice were infected with the CB3 virus and subsequently, on days 4 and 7 of the infection, injected with 0.5 microCi [14C]TCDD (about 65 micrograms/kg). An uninfected group was injected with [14C]TCDD and served as the control group. Spleen, thymus, heart, pancreas, liver and brain were dissected 24 h after isotope injection, and the [14C]TCDD content of the tissues was determined by standard liquid scintillation techniques. On day 7, whole body autoradiography was also performed, 4 h after the isotope injection. Our results clearly show that there is an increased TCDD uptake in the selected tissues during the CB3 infection and that this increased uptake is most pronounced on day 4 post inoculation, which corresponds to the peak of viraemia. It was found that the total tissue concentrations of TCDD were significantly increased on day 4 in the brain, pancreas, heart, spleen and liver. In the spleen, heart and brain they were still significantly increased on day 7. The considerable metabolic and immunological changes that generally are caused by infections might explain the change in accumulation of TCDD. It is possible that the increased uptake of TCDD affects the immune cells involved in repair of inflammatory tissue lesions, thereby affecting the progression of the disease.

Animals↗

PubMed1994

Immune responses and resistance to viral-induced myocarditis in mice exposed to cadmium.

The effects of 10 weeks of treatment with cadmium (Cd) on the immune function and resistance to coxsackievirus B3 (CB3)-induced myocarditis in female Balb/c mice were investigated. A 2mM dose of Cd in the drinking water did not influence mortality due to the CB3 infection. The inflammatory and necrotic lesions in the ventricular myocardium seven days after inoculation (2.94% of tissue section area) were not increased by Cd (2.82% of tissue section area). The response pattern of lymphocyte subsets in situ in myocardial inflammatory lesions was elucidated by an immune histochemical staining technique. With Cd treatment the number of cytotoxic T cells and B cells in these lesions decreased by 22% (n.s.) and 21% (p < 0.05), respectively. Spleen weight and the lymphoproliferative response to the B-lymphocyte mitogen increased by 19% (p < 0.05) and 23% (n.s.), respectively. The titers of neutralizing antibodies increased by 22% (n.s.) with Cd treatment. However, the activity of spleen T lymphocytes and spontaneous cell-mediated cytotoxicity (NK-cell) was unchanged. Thymus weight and WBC count in peripheral blood tended to decrease. Thus, Cd exposure seems to result in a decreased maturation and mobilization of T and B lymphocytes, but increased humoral immune host responses.

Animals↗

PubMed1993

Influence of sodium selenite on 203Hg absorption, distribution, and elimination in male mice exposed to methyl203Hg.

To study the effects of long-term selenium supplementation on absorption, distribution, and elimination of methylmercury (MeHg) in mice, three groups of male mice (Balb/c CA) were exposed for 7 wk to 0, 0.6, and 3 ppm sodium selenite in tap water. They were then given a single oral dose of Me203Hg (2 mumol/kg) by gastric intubation, and elimination of 203Hg was followed by whole-body counting for 49 d at the same Se exposure as previously. Twenty-four hours and 49 d after dosage, 6-7 animals/group were sampled for analysis of 203Hg distribution in the body. Glutathione peroxidase (GSH-PX) activity in blood and selenium levels in the liver were used as measures of selenium status. Gastrointestinal absorption of Me203Hg was not influenced by the Se status of the animals. Selenium supplementation of MeHg-exposed mice caused an enhanced whole-body elimination of Hg, but selenium-supplemented animals did not have lower Hg levels in the brain and kidney than nonsupplemented animals. The effect of selenium on the accumulation of Hg in the brain was dose-dependent, a high dose (3 ppm Se) causing a higher initial accumulation of Hg. The intracellular distribution of 203Hg in the liver and kidney was not affected by Se. The results indicate that selenium treatment of MeHg-exposed mice may have a positive effect on the health of the animals by decreasing the total body burden of MeHg.

Absorption↗

PubMed1993

Coxsackie B3 myocarditis induces a decrease in energy charge and accumulation of hyaluronan in the mouse heart.

Interstitial oedema in chronic inflammation and ischaemia is related to an accumulation of hyaluronan (hyaluronic acid; HA) in the interstitium. As interstitial oedema will affect the oxygen transport in the interstitium we have evaluated whether accumulation of HA is related to signs of myocardial energy depletion in virus induced myocarditis. Myocarditis was induced in Balb/c mice by inoculation of Coxsackie B3 virus. The extractable HA content of the myocardium increased progressively from a baseline value of 153 +/- 26 micrograms g-1 dry weight to a maximum of 286 +/- 78 micrograms g-1 dry weight at day 7, whereafter there was a slight decline. Affinity histochemistry visualized HA in the endo-perimysium in healthy myocardium. At day 5 after Coxsackie B3 inoculation there was a general widening of the endomysium, which exhibited a positive staining for HA. In conjunction with focal inflammatory infiltrates the staining for HA was even more pronounced. The energy rich adenylates were reversibly affected by the Coxsackie B3 infection. There was a slight, but significant decline in EC from 0.74 +/- 0.05 in the control group to a minimum value of 0.64 +/- 0.10 at day 5, whereafter a restitution was observed at days 7 and 10. The total adenine nucleotide pool was similarly decreased from 27.8 +/- 2.9 mumol g-1 dry weight in controls to 24.6 +/- 2.1 micrograms g-1 dry weight at day 5, and normalized at days 7 and 10. The data suggest that virus induced myocarditis is associated with a local accumulation of HA in the myocardium.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗