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Biomedical subjects

D Sauer

Publications and source records attributed to D Sauer.

At least 19 recordsLinked to original sources
PubMed1992

Differing effects of alpha-difluoromethylornithine and CGP 40116 on polyamine levels and infarct volume in a rat model of focal cerebral ischaemia.

Focal cerebral ischaemia was induced in rats by occlusion of the left middle cerebral artery. Two days later, infarct volume was determined by magnetic resonance imaging and the concentrations of the polyamines putrescine (PU), spermine and spermidine by HPLC. In control (occluded) animals, PU levels were elevated in infarcted and non-infarcted areas of the left hemisphere. Treatment with the ornithine decarboxylase (ODC) inhibitor alpha-difluoromethylornithine, prevented the ischaemia-induced increase in tissue PU without affecting infarct volume. Conversely, administration of the N-methyl-D-aspartate (NMDA) receptor antagonist CGP 40116 decreased cortical infarction without changing the tissue content of PU. We conclude that there is no direct link between NMDA receptor activation and brain PU, or PU and post-ischaemic tissue damage, and that inhibitors of ODC are not cerebroprotective in this animal model of stroke.

2-Amino-5-phosphonovalerate↗
PubMed1992

Evaluation of quinolinic acid induced excitotoxic neurodegeneration in rat striatum by quantitative magnetic resonance imaging in vivo.

Excitotoxic neurodegeneration in the rat striatum was induced by direct injection of quinolinic acid. The degree of damage was evaluated in vivo 1 day later by quantitative magnetic resonance imaging (MRI) and 7 days later in the same animals by measuring the activities of the neuronal marker enzymes choline acetyltransferase and glutamic acid decarboxylase. Striatal damage assessed using the two approaches was highly correlated. Moreover the cerebroprotective efficacy of the N-methyl-D-aspartate receptor antagonist CGP 40116 was indistinguishable based on all analytical parameters. MRI, however, was more reproducible than the enzymatic methods and was faster and simpler for routine analyses of excitotoxic damage and cerebroprotection in vivo.

2-Amino-5-phosphonovalerate↗
PubMed1992

Application of magnetic resonance imaging to the measurement of neurodegeneration in rat brain: MRI data correlate strongly with histology and enzymatic analysis.

Focal brain ischemia was induced by middle cerebral artery occlusion in the rat. The volume of cerebral damage was determined 2 days later by MRI in vivo and in the same animals histologically. The edema volume as measured by MRI and the histologically determined infarction was highly correlated. As a consequence, the neuroprotective effect of the N-methyl-D-aspartate (NMDA) receptor antagonists CGP 40116 and MK 801 were similar with both methods. Excitotoxic neurodegeneration in the rat striatum was induced by direct injection of quinolinic acid. The degree of damage was evaluated in vivo 1 day later by quantitative MRI, and 7 days later by measuring the activities of neuronal marker enzymes choline acetyltransferase and glutamic acid decarboxylase. Striatal damage assessed using the three approaches was highly correlated. Cerebroprotective efficacy of the NMDA receptor antagonist CGP 40116 was indistinguishable based on all methods. MRI was more reproducible than the enzymatic methods and was faster and simpler than histologic examination for routine analysis of excitotoxic damage and cerebroprotection in vivo in a pharmaceutical research environment.

2-Amino-5-phosphonovalerate↗
PubMed1992

[Activated circulating lymphocytes as a parameter for clinical activity in patients with Crohn disease].

Patients with Crohn's disease exhibit peripheral lymphocytes during exacerbation which express activation associated epitopes on their cell surface. We have therefore enumerated circulating lymphocytes in 36 patients with Crohn's disease by immunofluorescent staining using monoclonal antibodies directed against activation associated antigens (CD 25, CD 71, CD 38 and MHC-class II-antigens, respectively). We found a highly significant correlation between the percentage of activated lymphocytes and the clinical activity. Thus in our experience measuring of activated peripheral lymphocytes proved as a valuable parameter in assessing the clinical activity of Crohn's disease for a well-timed medication.

Adult↗
PubMed1991

[Circulating lymphocyte subpopulations in patients with Crohn's disease].

Circulating lymphocytes were enumerated in 25 patients with Crohn's disease and in 43 healthy donors by immunofluorescent staining using monoclonal antibodies for T cell surface phenotypic markers (CD 3, CD 4, CD 8) or for surface immunoglobulin of B cells (mu-chain). Proportions of peripheral T cells and percentages of T cell subsets in Crohn's disease were not significantly different from those in controls. For analyzing the lymphocytes for the expression of activation associated antigens (HLA-DR, CD 25) we found increased numbers of activated lymphocytes during acute exacerbation, whereas, in remission, the population of activated lymphocytes was in the upper normal range. The results leads to the conclusion that the assessment of activated lymphocytes may serve as a parameter in the evaluation of the activity of Crohn's disease.

Adolescent↗
PubMed1990

PAF antagonist ginkgolide B reduces postischemic neuronal damage in rat brain hippocampus.

We investigated the effect of the known antagonist of platelet-activating factor (PAF), ginkgolide B, on postischemic neuronal damage in the rat. Neuronal necroses were evaluated in the hippocampus 7 days after a 10-min forebrain ischemia. Preischemic application of ginkgolide B (50 mg/kg p.o.) significantly reduced neuronal damage. It is suggested that the antagonism of PAF is responsible for this beneficial effect of ginkgolide B.

Animals↗
PubMed1989

Naftidrofuryl protects neurons against ischemic damage.

The effects of naftidrofuryl on postischemic neuronal damage and on local cerebral blood flow (LCBF) were examined in a rat model of forebrain ischemia (occlusion of carotid arteries and hypotension). Ischemia was induced for 10 min. LCBF was measured after 2 and 10 min of recirculation. A histological evaluation of cell loss in the hippocampal areas was performed 7 days after ischemia. Naftidrofuryl (10 mg/kg) was administered intraperitoneally 15 min before ischemia. The drug reduced the percentage of necrotic neurons in the CA1 and CA4 sector of the hippocampus, while the LCBF of these hippocampal sections was not significantly altered. Thus, naftidrofuryl is suggested to protect hippocampal neurons against ischemic damage mainly by a direct effect on brain parenchyma.

Animals↗
PubMed1989

[Under the thigh amputation according to Bruckner].

Knee joints of 24 in 28 patients were successfully preserved by below-knee amputation according to Brückner, at the Surgical Department of Karl-Marx University in Leipzig in 1987. The above patients had been in advanced age and in multimorbid conditions. Surgical technique and postoperative care are described and discussed in some detail.

Aged↗
PubMed1988

Effects of flunarizine on postischemic blood flow, energy metabolism and neuronal damage in the rat brain.

The effects of flunarizine on local cerebral blood flow, cortical energy metabolism and neuronal necrosis were evaluated in a rat model of forebrain ischemia. The application of flunarizine (2 X 40 mg/kg p.o.) at 24 and 4 h before ischemia accelerated the restoration of cortical high-energy phosphates during early post-ischemic recirculation and also increased the flow in cortical but not in hippocampal areas. Neuronal necrosis was reduced in the hippocampal CA 1 sector but unchanged in the cortex. It is concluded that flunarizine reduces ischemic damage mainly via a direct effect on brain tissue.

Animals↗
PubMed1988

Phencyclidine reduces postischemic neuronal necrosis in rat hippocampus without changing blood flow.

In this report the effects of phencyclidine (PCP) on physiologic variables, local cerebral blood flow (LCBF), and on hippocampal cell damage were measured in a rat model of forebrain ischemia (2-vessel occlusion and hypotension). Ischemia was induced for 10 min. LCBF was determined after 2 min of recirculation, using the [14C]iodoantipyrine technique. Hippocampal cell loss was quantified histologically 7 days postischemia as the percentage of acidic stainable neurons. Intravenous application of PCP (2 mg/kg) at 15 min prior to ischemia left postischemic LCBF unchanged, but neuronal damage was significantly reduced in hippocampal CA1 sector from 46 to 15.7%. PCP is concluded to reduce ischemic damage of neurons mainly via a direct effect on brain tissue.

Animals↗
PubMed1988

Vinpocetine prevents ischemic cell damage in rat hippocampus.

The effects of vinpocetine on hippocampal cell damage and local cerebral blood flow (LCBF) were measured in a rat model of forebrain ischemia (2-vessel occlusion and hypotension). Duration of ischemia was 10 min. LCBF was determined after 2 min of recirculation using the 14C-iodoantipyrine technique. Hippocampal cell loss was quantified histologically 7 days post-ischemia. Intraperitoneal application of vinpocetine (10 mg/kg) 15 min prior to ischemia significantly reduced neuronal cell loss in hippocampal CA 1 sector from 60% to 28%. The drug led to a marked increase in blood flow in cortical areas, whereas LCBF remained unchanged in hippocampus and all other structures measured. It is suggested that the protective effect of vinpocetine does not depend on increased postischemic blood flow.

Animals↗
PubMed1988

Morphology of tissue damage due to experimental cerebral ischemia in rats.

Two models of experimental cerebral ischemia in rats were developed and used. The first model was permanent occlusion of both carotids up to 3 weeks, the second model the temporal occlusion of both carotids and systemic hypotension for 10 min. Rats treated by the first experimental set were investigated after one, 2 and 3 weeks. In all groups, about 40% of so treated animals had territorial infarcts, often more than one in the animal in question. These infarcts developed from necrotic, pale areas to ischemic cysts and this copied the evolution of human territorial infarction. Astroglial reaction was only seen in the border zone. In the second model, rats preferentially developed, as known, the so called delayed ganglion cell necrosis in the field CA 1 of the hippocampus. Cells were not altered on the second, but damaged on the sixth day after experimental ischemia. In both models the hippocampus was damaged, however in the first the damages were morphologically distinct from the damage in carotid occlusion in systemic hypotension. The first experimental model suits better for human territorial infarction, the second is highly reproducible and thus provides a much better experimental tool.

Animals↗
PubMed1987

Effects of cerebroprotective agents on cerebral blood flow and on postischemic energy metabolism in the rat brain.

Male Wistar rats were subjected to forebrain ischemia of 10 min duration by clamping both common carotid arteries and simultaneously lowering systemic blood pressure to 40 mm Hg by exsanguination. Recovery was achieved by removing the arterial clamps and reinfusing the blood. Cortical levels of high-energy phosphates and glycolytic substrates were determined enzymatically. Naftidrofuryl (10 or 20 mg/kg i.p.) or ketamine (5 mg/kg i.v.) were applied 30 min prior to the induction of ischemia. S(-)-Emopamil (4 mg/kg) or nimodipine (50 micrograms/kg) were administered by intravenous infusion over 30 min. Nimodipine and emopamil increased the blood glucose level and lowered preischemic blood pressure. Under control conditions, a tendency toward a higher cortical glucose level was observed in treated brains. Brain energy stores were exhausted after ischemia in control and treated animals to the same degree. Lactate levels, however, were higher in emopamil-treated animals. This effect was attributed to the elevated preischemic glucose levels. During the early recovery period, the restoration of high-energy phosphates was accelerated by both calcium entry blockers. Nimodipine and emopamil increased the levels of glucose and glucose-6-phosphate in the early postischemic period. Naftidrofuryl (10 mg/kg) increased the level of creatine-phosphate and ATP after 2 min of recovery. Naftidrofuryl (20 mg/kg) exerted no effect on cerebral energy metabolism, but considerably reduced postischemic blood pressure (possibly thereby masking its ameliorative action). Ketamine accelerated the postischemic restoration of high-energy phosphates. In the conscious rat, local cerebral blood flow (LCBF) was determined with the 14C-iodoantipyrine technique following emopamil (20 mg/kg s.c.) or naftidrofuryl (10 mg/kg i.v.) application.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

[Nutritional status in stomach cancer--a criterion for evaluating operability?].

The nutritional status of 41 male patients with carcinoma of the stomach was recorded, right after admission to hospital, and was related to tumour-specific operability. The nutritional condition of most of the patients was moderately impaired. Significant differences between operable and non-operable patients were recorded from the following parameters: upper-arm circumference, haemoglobin concentration, serum albumin, pseudocholinesterase, intradermal testing, E-rosette count. The findings thus obtained provided some limited information on operability.

Body Weight↗
PubMed1985

One-carbon metabolism in lectin-activated human lymphocytes.

Serine is an essential amino acid for the lectin-mediated transformation of human peripheral blood lymphocytes due to the inability of this cell to synthesize sufficient quantities via either the phosphorylated pathway or by reversal of the serine hydroxymethyltransferase reaction to meet the metabolic demands. The level of intracellular serine is tightly regulated, and the culture medium concentration for optimum cellular transformation falls within a relatively narrow range. The three-carbon atom of serine is the major source of one-carbon units required for purine and pyrimidine nucleotide biosynthesis, but the key effect of both serine deprivation and of high medium serine levels would appear to be on protein synthesis. Although an alternative source of one-carbon units, as provided by high levels of formate in the culture medium, can partially reverse the effects of serine deprivation, the only other demonstrable source of one-carbon units, tryptophan, requires serine for its incorporation and subsequent metabolism. Methionine is also essential for lymphocyte transformation and is involved in the synthesis of a small amount of phosphatidylcholine, although most of this phospholipid is provided by choline and lysophosphatidylcholine from the serum-supplemented culture medium.

Blood Proteins↗
PubMed1985

[The antigen-specific rosette test--its value for clinically relevant problems].

The antigen specific rosette test was used for the evaluation of the sensibilization in animal models and in patients to antigens with clinical relevance. The corresponding antigens were coupled to sheep- and guinea pig-erythrocytes respectively or to a synthetical carrier and we have determined the frequency of antigen binding lymphocytes in patients or animals by rosette formation. The suitability of this test we have studied for following problems: Evaluation of a sensitization against a cutaneous burn toxin in mice following thermic injury, against the transplantation antigens in pigs following allogenic renal transplantation, against TAA from breast carcinoma in patients with breast cancer.

Animals↗