[Indications and contraindications for plasma substitutes in operative medicine].
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Biomedical subjects
Publications and source records attributed to J Simon.
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In the present paper the possibilities of scintigraphic diagnosis of experimental pericarditis are discussed. Pericarditis was induced by either talc or formaldehyde intrapericardially. In all animals the administration of talc as well as formaldehyde produced inflammatory changes which were more serious after formaldehyde. The scan of the talc pericarditis was carried out on the 7th day after operation and of the formaldehyde pericarditis on the 3rd, 7th or 14th days. No positive scintigraphic finding was made in any of the experimental animals, apart from a massive incorporation in the operation scars. The counting of radioactive impulses after the exstirpation of the tissue samples confirmed the scintigraphic findings. Statistical evaluation did not reveal any essential difference between the accumulation of the radiopharmaceutical into the pericarditis as well as into the pericardial bag in comparison with the control animals. Although our model does not exactly reflect the situation of patients suffering from pericarditis it may be assumed that pyrophosphate scintigraphy is not suitable for the diagnosis of acute pericarditis in clinical practice.
The respiratory minute volume was determined in 144 normal persons during anaesthesia i a semi-closed system. The measured volumes were related to the bodyweight of the individual person: Quotient Q = Minute volume (ml/min.) over Bodyweight (kilogramme). For adults Q was found to be clearly dependent on bodyweight and sex; extreme weight groups required correction by a factor q which differed for men and women. A table for the calculated minute volumes is available for routine purposes.
Effects of atmospheric ammonia on performance and respiratory tract health of young pigs experimentally infected with Bordetella bronchiseptica were studied. Treatments were: (1) control, (2) Bordetella inoculation (approx 10(9) bacteria/naris) alone, (3) Bordetella inoculation plus exposure to atmospheric ammonia at 34.7 mg/m3 (50 ppm), and (4) Bordetella inoculation plus exposure to atmospheric ammonia at 69.4 mg/m3 (100 ppm). Pigs weighted 8.01 kg (av) at start of treatment. Body weight and feed disappearance were measured weekly. After 4 weeks, all pigs were killed and examined grossly, and appropriate specimens were obtained for histopathologic examination. Regression models were fitted to growth, feed disappearance, and gain-to-feed data. The growth model indicated that Bordetella-inoculated pigs gained 26% less body weight than did controls, regardless of atmospheric ammonia concentration. Bordetella inoculation, regardless of ammonia exposure, reduced feed disappearance 12% below the control rate. Treatment difference was not noted in gain/feed data. Shrunken turbinates were observed in Bordetella-inoculated pigs. Shrinkage also appeared to be related directly to ammonia concentration. Rhinitis was confirmed histopathologically, and its severity was related with atmospheric ammonia concentration, but no difference was seen in the osseous core of the turbinates.
Effects of atmospheric ammonia at 69.4 mg/m3 (100 ppm) on productive performance and respiratory tract health of young pigs (starting body weight averaged 7.5 kg) experimentally infected with Ascaris suum (50,000 embryonated ova administered by gavage when pigs were 5 weeks of age) were studied in 5 trials of 4 weeks each (when pigs were 5 to 9 weeks of age). Effects of atmospheric-ammonia exposure and ascarid infection on growth were additive. Compared with controls, percentage reductions in average daily gain were 32%, 28%, and 61% for ammonia-exposed, ascarid-infected, and combined ammonia plus ascarid groups, respectively. Ammonia exposure or ascarid infection alone depressed feed disappearance by 18%. Effects of the 2 factors were additive, resulting in a 35% reduction in feed disappearance. Pigs exposed to the combined factors had an average gain/feed ratio of 0.518, which was less than that of control pigs (0.546), but was greater than that of pigs exposed to atmospheric ammonia (0.489) or pigs infected with ascarids (0.501) alone. Liver scarring, due to larval migration, was not affected by ammonia exposure. Larval migration through the respiratory tract was not confirmed histopathologically in pigs killed 4 weeks after inoculation. A supplementary experiment was conducted which demonstrated that residual evidence of previous pulmonary larval migration was present 2 weeks after inoculation.
Adult female beagles were given oral HCB for 21 days. Subdividing the dose resulted in greater accumulation of HCB in fat and seemed to enhance toxic effects. Subjecting the animals to a 10-day period of food restriction immediately following 21 days of dosing further increased residues, but obscured any differences due to dosing regimen. Liver and hepatocyte enlargement, as well as physiologic changes in the central nervous system, were HCB-induced. Weight loss and various hematological changes were equivocal, with dietary stress and HCB probably contributing to the changes to varying degrees. A dose of 50 mg/kg/day of HCB for 21 days must be considered at least minimally toxic to female beagles.
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The kidneys and the bladder are regularly visible when bone scintiscans are performed during 99mTc-labelled phosphorus compounds, and abnormalities in the distribution of local activities within these organs are not uncommonly detected. The authors were able to compare such abnormalities with clinical, laboratory and X-ray data in 139 out of 1980 cases of bone scintiscan. In 84% of the cases the pathological image was associated with an established renal or urinary disease and was indeed often responsible for its unexpected discovery. Urinary tract abnormalities detected on bone scintigrams therefore deserve to be taken into consideration and should be confirmed by appropriate investigations.
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Experimental vaccinia infection in immunosuppressed and immunocompetent Rhesus monkeys has been studied for two years. The results show that vaccinia virus induces two forms of infection in the central nervous system, i.e. choriomeningitis and demyelination disease. The first form occurs in immunologically competent animals; the latter can develop in animals with defective immune response associated with an incomplete clearance of virus. These animals exhibit a noncytocidal persistent infection of glial cells, inducing a complex of potentially pathogenic immune mechanisms. Their direct, or by mediators mediated action is capable of damaging myelin sheaths.
If rabbits were given total body irradiation and infected wih vaccinia virus (strain Elstree) a severe disease developed with a viraemia lasting up to 12 days. The clearance of the virus from the peripheral blood was severely impaired by x-ray doses above 800 R. The attenuated vaccinia virus strain MV did not turn virulent, if it was injected to irradiated rabbits. With caution it can be assumed that live vaccines, containing attenuated viruses, may be given to immunosuppressed persons. Rats are not susceptible to ectromelia-virus (mouse-poxvirus); overt clinical sympatoms, however, with a mortality of 30 per cent developed in irradiated rats. This proofs that specific poxviruses can be transferred to another species. As the experimental conditions are unnatural, this may occur only rarely in immunosuppressed persons. After intracerebral infection of Balb-C-mice with low doses of vaccinia virus two types of infection were seen: 1. a severe cytocidal infection of leptomeninges, chorioid plexus and vessels; 2. a noncytocidal, latent infection of glial cells and neurons. Several animals developed a picture resembling experimental allergic encephalomyelitis. It seems that irradiation altered the antigenic conditions of the cytoplasmic membranes in non-cytocidally infected cells. The model might explain some processes in the pathogenesis of demylinating diseases.
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We report on an 8-year-old girl who presented clinically with an acute abdomen. Examination revealed a left hypoplastic kidney with its ureter draining into the lower segment of the vagina, which was closed by an imperforate hymen. Initially, we thought that pressure by the urometrocolpos on the right ureter caused right hydronephrosis. Subsequently, it was found that the right ureter followed a retroiliac course and was compressed by a U-shaped iliac artery loop at the ureteral crossing. The iliac artery extended to the level of the second lumbar vertebra.
The effects of acute and chronic ingestion of tolbutamide were studied in the growing chicken. After an oral load of 100 or 25 mg tolbutamide/kg b.w., plasma insulin levels increased in a dose-dependent manner but to relatively low levels for about 10 min, while 10-20 min following tolbutamide, plasma glucose levels were markedly decreased and remained so for 2--5 hr. After 100 mg tolbutamide/kg, the profound hypoglycaemia which developed, was generally accompanied by symptoms resembling an hypoglycaemic coma: panting, muscular flacidity and convulsion. Body temperature and plasma calcium levels were not changed during and after tolbutamide-induced insulin release. In the chicken, tolbutamide response is therefore characterized by a fugitive insulin release and a profound and prolonged hypoglycaemia which suggest that the action of insulin is potentiated by other factors. Chronic ingestion of tolbutamide in the diet transiently (for one week) increased the live body weight of a dose of 400 mg tolbutamide/kg of diet. Long term (5 weeks) fasting plasma glucose levels were unchanged and fasting plasma insulin levels were decreased in the chronic tolbutamide treated chickens.
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1. A possible relationship between glucose tolerance and body-fat content was examined in broilers selected at 2 and 4 weeks of age for fast or slow glucose disposal. 2. At 8 weeks of age, selected chickens were different in glucose tolerance but similar in body weight, food conversion efficiency, carcass composition and glucose-induced insulin release. 3. Therefore, variations in glucose regulation and insulin sensitivity which are detectable at an early age, do not appear to be related to body composition in 8-week-old broilers.
In an attempt to determine if alterations in intraneuronal Ca2+ may regulate tyrosine hydroxylase activity, brain slices were subjected to experimental manipulations known to increase the intraneuronal concentration of free Ca2+ ions. Incubation of either striatal or olfactory tubercle slices in a Na+-free medium for 15 min at 37 degrees resulted in a marked increase in the activity of tyrosine hydroxylase present in the 20,000 g supernatant fraction of homogenates prepared from the slices. Tyrosine hydroxylase isolated from slices previously incubated in a Na+-free, choline-enriched medium or in a Na+-free, sucrose-enriched medium exhibited maximal activities when assayed at pH 6.0 and 7.0, respectively. However, the percentage stimulation of enzyme activity induced by incubation of the slices in a Na+-free medium was maximal when the enzyme assays were performed at pH 7.0. The observed increase in enzyme activity seems to be mediated by a decrease in the apparent Km of the enzyme for pteridine cofactor, regardless of whether the kinetic enzyme analyses were conducted at pH 6.0 or 7.0, and by an increase in the Ki of the enzyme for end-product inhibitor dopamine. The apparent kinetic changes in the enzyme do not seem to result from alterations in the endogenous dopamine content of the slices, and they are independent of any increase in dopamine release that might have occurred as a response to the augmented intraneuronal Ca2+ concentration. Furthermore, the activation of tyrosine hydroxylase produced by incubating slices in a Na+-free medium is observed even in slices depleted of dopamine by pretreatment of rats with reserpine 90 min before preparation of brain slices. The activation of tyrosine hydroxylase observed under these experimental conditions does not seem to be mediated by cAMP or by a cAMP-dependent phosphorylation process. It is suggested that the changes in tyrosine hydroxylase reported are mediated primarily by a rise in the free Ca2+ concentration within the nerve tissue. These observations are consistent with the hypothesis that the kinetic activation of tyrosine hydroxylase produced after depolarization of central dopaminergic neurons may occur through a Ca2+-dependent even other than transmitter release.