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Biomedical subjects

R Pohle

Publications and source records attributed to R Pohle.

At least 19 recordsLinked to original sources
PubMed2000

[Computer-supported tissue characterization in musculoskeletal ultrasonography].

A new diagnostic system combining conventional gray-scale ultrasonography (US) and computer-assisted texture analysis of sonograms makes it possible to differentiate more easily between specific neuromuscular diseases. The first step involves myosonography with strictly standardized US. In a group of 72 patients with histologically and molecular-genetically confirmed diagnosis 63 patients (88%) were diagnosed by conventional US as having Duchenne's muscular dystrophy, spinal muscular atrophy, hereditary sensomotor neuropathy or inflammatory myopathy. Secondly, in a double blind setting computer-assisted texture analysis was used on the same sample of subjects. Tissue Texture can be characterized by the brightness as well as the micro- and macro-structure of the tissue. The use of these parameters leads to a sensitivity of 77 to 94% and a specificity of 81 to 98%. In conclusion, the combination of both techniques allows us to avoid invasive diagnostic procedures in a substantial group of patients.

Diagnosis, Computer-Assisted↗
PubMed1990

[Enzyme immunoassays for the quantification of human gamma-gamma-enolase (NSE)].

A direct two-site binding assay on the basis of antibodies from sheep for the quantification of human gamma-gamma enolase is described. The antibody was produced by immunization with human NSE coupled to horse spleen ferritin. The assay shows two feature: a decreased reactivity with NSE from rat and NSE from human serum in spite of 100% recovery of purified human brain NSE. The sheep antibody seems to react with epitopes less accessible on the rat NSE and on the NSE of human serum. The assay is characterized by gamma-gamma enolase specificity, a high sensitivity (2 pg) and a precision of CV = 3-7%.

Animals↗
PubMed1988

Concentration of hypoxanthine in both cerebrospinal fluid and brain tissue increases under intensive hypoxia only.

The relationships between the concentrations of glycogen, glucose, lactate, adenosine triphosphate (ATP) and hypoxanthine in the brain tissue, and the hypoxanthine and lactate concentration in cerebrospinal fluid and blood were examined after exposure of rats to hypoxia. The animals (1 and 10 days old) were exposed to hypobaric hypoxia for 1-12 h, pO2 11.3 kPa (mild), pO2 8.6 kPa (moderate), pO2 6.4 (strong) and pO2 4.7 kPa (severe) in inspired air. The concentration of hypoxanthine in both cerebrospinal fluid and brain tissue increases in severe hypoxia. This severe hypoxia was related to a decrease of ATP level in brain tissue. This study showed that the level of hypoxanthine in blood did not closely correlate to the level of hypoxanthine in brain tissue and cerebrospinal fluid. Extremely high hypoxanthine values in the blood might indicate a decrease in ATP content in brain tissue.

Adenosine Triphosphate↗
PubMed1988

The relationship of hypoxia to hypoxanthine concentration during pregnancy and delivery.

The concentration of hypoxanthine in plasma was suggested as an indicator of hypoxic conditions in newborns. We examined the concentration of hypoxanthine in maternal venous as well as in umbilical cord blood during pregnancy and during and after labor. The concentration of hypoxanthine in the cubital venous blood of nonpregnant healthy women and in healthy pregnant women and in women with complicated pregnancies was the similar. During birth there is an increase of the hypoxanthine concentration in maternal blood. This could be caused by the muscular work involved in giving birth (contraction, pushing, breathing). The values increased from 2.0-4.1 mumol/l in normal and abnormal pregnancy up to values of 9.4-11.8 mumol/l immediately after delivery. At the end of delivery the level of hypoxanthine is higher in the venous blood of the mother than in the umbilical blood. The concentration of hypoxanthine in umbilical venous blood and umbilical arterial blood did not show any significant differences. When clinical symptoms of hypoxia (depressed state of the neonate, high Thiringer asphyxia score, low Apgar score) were observed in the neonate, the hypoxanthine concentration in the umbilical vessels was increased (normal 4.7 mumol(l; slightly depressed 7.6 mumol/l, severely depressed 10 mumol/l).

Cardiotocography↗
PubMed1986

Influence of a perinatal hypoxia on the carbonic anhydrase activity in different brain regions of the rat.

Homogenates of striatum, hippocampus and cerebral cortex of the rat brain were investigated for carbonic anhydrase activities. During ontogeny the enzyme activities increase with proceeding gliogenesis. At the 5th postnatal day (PD) prenatal hypoxia (17th day of gestation (GD)--birth) is followed by a 4-fold increase of carbonic anhydrase (CA) activity in the hippocampus. After postnatal hypoxia (2nd-10th day of life) CA activity in all investigated brain regions rise. At the 11th PD the values were 190 (cerebral cortex), 242 (striatum) and 176 (hippocampus) per cent of control. Noradrenaline (10(-6)M) enhanced CA activity in cerebral cortex and hippocampus about 2-fold. Dopamine (10(-6)M) caused an increase in the striatum up to 210% of control. The increased CA activity after hypoxia is assumed to be a functional response to activation of the glia by catecholamines.

Aging↗
PubMed1985

The relations between erythrocytic and CNS parameters following postnatal hypobaric hypoxia of the rat.

In the present paper the relations between selected erythrocytic criteria and alterations of biochemical brain parameters following hypoxia were investigated in order to find out the relevance of erythrocytic criteria for the diagnosis of hypoxia-induced alterations of the CNS during development. Newborn Wistar rats (n = 80) with their mother were exposed to hypobaric hypoxia, pO2 = 11.3 kPa, from day 2-10 of life, daily for 11 h. On the 11th day of life the animals had a lower body (38%), liver (33%) and brain (17%) weight, an increased number of reticulocytes, a lower median density of peripheral red blood cells (rbc) and an increased packed cell volume (PCV) indicating stimulation of erythropoiesis. Hypoxia caused a decrease of protein concentration, of AChE activity and of the amount of DNA in the brain tissue. In addition to these parameters the cholesterol level and the protein/DNA ratio are diminished and the carboanhydrase activity is increased in the cortex. In order to quantify the changes of various brain parameters in each animal in the sense of altered development a score of these results was calculated. It can be concluded that the hypoxia-induced changes of erythrocytic parameters correlate with those of the neurochemical indices.

Animals↗
PubMed1984

Effects of piracetam on brain development in newborn rats exposed to hypoxia.

Perinatal hypoxia is one of the main causes of disturbances of the function of the CNS during childhood. In this study the protective effect of the nootropic drug piracetam (oxo-2-pyrrolidinyl-1)-2-acetamide was tested. One-day-old Wistar rats were exposed together with their mothers to hypoxia up to the 10th day of life (11 h daily, pO2 = 9.86 kPa). On the 11th day a 48% decrease of body weight and a 30% decrease of brain weight was found in the hypoxic animals. The protein/DNA ratio and the AChE activity in the brain cortex were decreased indicating retarded brain development. Piracetam (daily 100 mg/kg, s. c., before hypoxic exposure) did not affect the mortality rate, the somatic development of the animals, or the estimated basic neurochemical markers in the cortex of the brain. At the age of 3 months the fractional efflux rate (FER) of dopamine (DA) evoked chemically or electrically as a characteristic functional feature of chemical synaptic transmission, was examined. It was found that postnatal hypoxia induces a long lasting increase of FER of DA of striatum slices. Animals exposed postnatally to hypoxia and treated with piracetam showed an increased FER of DA (potassium as stimulus) by comparison with those animals also exposed postnatally to hypoxia but left untreated with piracetam.

Animals↗
PubMed1982

Hypoxanthine levels in amniotic fluid: an indicator of fetal hypoxia?

During hypoxia there is an increased formation of hypoxanthine from the consumption of ATP; simultaneously the oxidation into uric acid is decreased. The purpose of this study was to determine possible correlations between hypoxanthine concentrations in the amniotic fluid and states of fetal hypoxia. We obtained 83 amniotic fluid samples from 68 patients during pregnancy or delivery. Hypoxanthine was assayed fluorimetrically according to GARDINER [4]. In the course of pregnancy, hypoxanthine levels in the amniotic fluid rise slightly. A marked increase occurs during delivery (without labor mean = 3.4 +/- 0.9 mumol/l, with labor mean = 7.0 +/- 5.4 mumol/l, p less than 0.02). There is no significant difference in the levels obtained from the first and second stages of labor. In intrauterine fetal death (Fig. 1) and in depressed newborns (Tab. I) there were increased hypoxanthine levels in the amniotic fluid, this was not seen in other complications of pregnancy. Independently from the fetal state increased hypoxanthine concentrations may occur in the amniotic fluid evidently as a consequence of labor activity. Thus the determination of hypoxanthine levels in the amniotic fluid cannot be used for the diagnosis of fetal hypoxia.

Adenosine Triphosphate↗
PubMed1982

[Relation between the density and maturity of red blood cells in the perinatal period in the rat].

Relations between 59Fe incorporation into red blood cells (rbc) and their density was examined in rats during ontogenesis (20th, 21st, 22nd gestational day, 1st, 21st day of life, adults). The incorporation of 59Fe in rbc of different density was measured 24 or 96 h after application. The density separation was carried out by centrifugation of rbc in phthalate esters of known density. The density of rbc increased during ontogenesis (median density 1.093 kg/l on the 20th gestational day and 1.102 kg/l in adult rats). The erythropoietic activity, in terms of 59Fe-incorporation into peripheral rbc, is higher in newborn rats (60-70%) than in adults (30-50%). 59Fe incorporation into pregnant rats and their fetuses is similar to adult nonpregnant rats. In fetuses a relatively high incorporation of 59Fe was found in comparison to their mother. The relationship between density and maturity of rbc is postnatally more evident than in the prenatal period. (59Fe enrichment in cells of low density prenatally: 2.6 +/- 0.5, postnatally: 8.4 +/- 0.5 (1st day of life), 5.8 +/- 0.8 (21st day of life) 28.5 +/- 5.6 (adult male rats). These findings may reflect a simultaneous formation of rbc at different sites or different clonal origin during prenatal period of ontogenesis.

Age Factors↗
PubMed1982

[Effect of hypoxia on the relationship of density and maturity of erythrocytes of newborn, young and adult rats].

Adult male, juvenile and pregnant rats were exposed to repeated hypoxia 8 h daily for 3-9 days in a low pressure chamber (altitude of 5000 m, pO2 = 11.3 kPa and 6000 m, respectively, pO2 = 9.89 kPa). The density distribution curves of the red blood cells (RBC) and the incorporation of 59Fe into cells of different density were determined. In the ontogenesis the density of RBC increases (median density on the first day of life 1.100 kg/l; on the 21st day of life 1.102 kg/l, adult rats 1.103 kg/l). The density difference between the 1st and 4th quartile in which 50% of the cells range was 0.010 kg/l for newborn and juvenile animals and 0.004 kg/l for adult ones. Exposure to hypoxia led iN the animals of the investigated age groups to a rise of the proporborns, 0.004 for juveniles, and 0.002 kg/l for adult rats. The cumulative distribution curves of 59Fe incorporation and density of RBC can be described by the equation (formula: see text). The value alpha characterizes the relation between density, on the one hand, and the maturity and age of cells, on the other. For control and hypoxic animals the following values for alpha have been calculated: for newborns 0.515 and 0.520, for juveniles 0.829 and 0.596 (p less than or equal to 0.01), and for adult rats 0.875 and 0.823. Juvenile animals from in regard to density similar heterogenic cells as newborns after hypoxia. It may be that ontogenetically older cell forming sites or clones are reactivated.

Aging↗
PubMed1980

Increased creatine kinase BB activity in rat plasma induced by hypoxia.

Rats show an elevated creatine kinase (CK) activity in plasma after a 20-hour exposure to hypoxia. The increase of CK activity is essentially caused by CK-BB activity attaining its maximum at the 3rd day after exposure to hypoxia. The possibility of establishing a potential brain damage by determining CK-BB activity in plasma is discussed.

Animals↗
PubMed1980

[Behavior of creatine in red blood cells and blood plasma of adult rats following exposure to hypoxia].

Adults rats exposed to hypoxia showed a definite increase of creatine concentration in red cells and plasma. The rise in cell creatine 37 h after the beginning of hypoxia had disappeared 2 days after the end of hypoxia. It is explained by the expulsion of preformed reticulocytes from the bone marrow. The increase of plasma creatine is supposed to be due to hypoxic damage to the muscles, which release creatine into the blood stream.

Animals↗
PubMed1978

[Influence of hypoxia and hyperoxia on the 2,3-diphosphoglycerate concentration in rat red blood cells].

The influence of hypoxia (pO2 = 85 mmHg) lasting 5 h, a strong single bleeding of the animals, and the effect of hyperoxia (pO2 = 745 and 1520 mmHg) lasting 24 and 5 h, respectively, on the 2.3-DPG concentration of red cells from rat has been studied. A distinct increase in 2.3-DPG concentration at hypoxia and bleedig, but no reliable alteration in hyperoxia were found. When bled and anemic animals are exposed to hyperoxia (24 h, pO2 = 745 mmHg, normal air pressure) there is also observed a rise of 2.3-DPG concentration, which is much less than in normoxia. A non-linear relationship was established between the change of 2.3-DPG concentration and the percentage of deoxyhemoglobin in the centralvenous blood.

Anemia↗