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Biomedical subjects

T Beck

Publications and source records attributed to T Beck.

At least 127 records · Page 7Linked to original sources
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

Loss of heterozygosity at the c-raf locus in small cell lung carcinoma.

The c-raf-1 oncogene is located at chromosome 3p25, near a region known to be specifically deleted in patients with renal cell carcinoma and small cell lung carcinoma (SCLC). From cytogenetic analyses of SCLC cell lines, we have estimated that one c-raf-1 allele was deleted in approximately 80% of the cases. However, c-raf-1 was generally thought to be distal to the most common deletion in SCLC, 3p14-23. Using restriction site polymorphisms (RFLPs) located within the c-raf-1 locus, we have examined DNA from 84 human lung carcinomas. In an analysis of 11 paired (normal versus tumor) SCLC DNA samples, all five informative cases showed loss of heterozygosity at this locus in the corresponding tumor sample. Analysis of 73 unpaired lung carcinoma DNAs showed that out of 31 non-SCLC samples, 19% were heterozygous for the BglI polymorphism and 25% showed heterozygosity with TaqI. However, all of the 42 SCLC samples were homozygous for both of these RFLPs. This striking loss of heterozygosity at the c-raf-1 locus in SCLC indicates that one allele of c-raf-1 is deleted in SCLC. The kinase activity of the c-raf protein appears to be constitutively activated in these cells. Whether this apparent activation results from genetic or epigenetic events is under investigation.

Carcinoma, Small Cell↗
PubMed1989

[Sterilization failures following fibrectomy].

Four of 272 patients with bilateral fimbriectomy became pregnant. In each of the four cases the distal end of the Fallopian tubes was closed but a tubo-peritoneal fistula could be observed in the antimesenterial part of the tube - immediately proximal of the former ligatures. These failures of sterilization were all found in a group of 16 patients, in which VICRYL 2/0 was used for ligation after resection of the fimbriated end. In all the other cases of fimbriectomy Chromcatgut 2/0 was used.

Adult↗
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

Uncoupling of cerebral blood flow and glucose utilization by dihydroergocristine in the conscious rat.

Dose-dependent effects of the dihydrogenated ergot alkaloid dihydroergocristine on physiological variables, local cerebral blood flow (LCBF) and local cerebral glucose utilization (LCGU) were evaluated in the conscious rat after intravenous injection. Heart rate was reduced with 2.5 mg/kg and 20 mg/kg dihydroergocristine. LCBF and LCGU were determined autoradiographically by employing the 14C-iodoantipyrine or 14C-2-deoxyglucose technique, respectively. At a dose of 0.5 mg/kg, dihydroergocristine neither changed LCGU nor LCBF, while at 2.5 mg/kg a slight decrease in LCGU was measured, which was more pronounced at 20 mg/kg. LCBF was significantly increased in several structures at 2.5 mg/kg, but it was markedly reduced at 20 mg/kg. The divergent effects on LCBF and LCGU at a dose of 2.5 mg/kg suggest a potential capacity of dihydroergocristine to uncouple the close interrelation of cerebral blood flow and cerebral energy metabolism.

Animals↗
PubMed1988

Local cerebral glucose utilization in the Ammon's horn and dentate gyrus of the rat brain.

The local cerebral glucose utilization (LCGU) was measured in different regions and layers of the Ammon's horn and dentate gyrus in the conscious rat. The LCGU was determined by quantitative [14C]2-deoxyglucose autoradiography using a computerized image processing system. In the hippocampus, the various regions and layers exhibited different glucose consumptions, the lowest values being found in the alveus and the highest ones in the lacunosum-molecular layers of the sectors of the Ammon's horn and the molecular layer of the dentate gyrus' external limb. Additionally, in many layers, the LCGU values of the left hemispheres were found to be higher compared with the right hemispheres. The analysis of LCGU changes in rostrocaudal direction revealed, that in sector 1 of Ammon's horn and in the dentate gyrus the glucose consumption decreased from rostral to caudal levels, whereas in sector 3 of Ammon's horn an increase was found.

Afferent Pathways↗
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

Effects of Ginkgo biloba constituents related to protection against brain damage caused by hypoxia.

The purpose of the present study was to approach the compound(s) responsible for the beneficial effects of an extract of Ginkgo biloba leaves (EGB) on animals subjected to hypoxia. In this first approach we compared the effects of the flavone and the non-flavone fraction of EGB with those of the whole extract on mice in lethal hypoxia (3.5% O2), on brain energy metabolism of artificially ventilated rats inspiring 7% O2, and on local cerebral blood flow (LCBF) of normoxic rats. The latter two experimental settings should also extend the knowledge about the underlying mechanisms of the antihypoxidotic actions. EGB as well as its non-flavone fraction considerably prolonged the survival time of mice under lethal hypoxia. EGB retarded the breakdown of brain energy metabolism in the hypoxic artificially ventilated rat. A corresponding effect was exerted by the non-flavone fraction while the flavone fraction even worsened the metabolic state. The non-flavone fraction increased LCBF in the majority of 35 examined brain regions; a similar effect could be seen after EGB-treatment, while the flavone fraction caused only minor alterations of LCBF. We conclude that the non-flavone fraction of EGB carries the antihypoxidotic activity. Metabolic effects are suggested to cause this activity. Further studies are necessary to elucidate the effective compound within this fraction.

Animals↗
PubMed1988

[Magnetic resonance tomography in the diagnosis of cervix cancer. Computed tomographic and histological correlations].

The value of magnetic resonance tomography in the diagnosis of carcinoma of the cervix was studied in a prospective series of 20 patients. The results were compared with those of computed tomography and with the clinical findings. The diagnosis depended on the postoperative histology. Gynaecological examination proved superior to imaging methods in determining the extent of local tumour spread. Tumour involvement of the regional lymphatic system was better demonstrated by MRT than by CT. Exact staging proved inadequate with both these methods and the new imaging methods have not produced any changes in operative planning or technique.

Adult↗
PubMed1988

Renal effects of fenoldopam in refractory hypertension.

Fenoldopam, a dopamine-1 (D1) agonist, was administered by a 6-h intravenous infusion to patients with refractory hypertension [diastolic blood pressure (DBP) greater than 115 mmHg while on triple therapy] in order to achieve a fall in DBP of 30 mmHg. The evolution of blood pressure, heart rate, glomerular filtration rate (GFR), renal plasma flow (RPF), urine volume, renal excretion of sodium, potassium, chloride, calcium, uric acid, phosphate, plasma renin activity (PRA), aldosterone and prolactin were evaluated. A significant fall in blood pressure (P less than 0.01) accompanied by an increase in heart rate (P less than 0.01) was attained after 30 min. GFR and RPF increased significantly (P less than 0.01) but the filtration fraction fell. Urine volume and urinary output of sodium, potassium, chloride, calcium, uric acid and phosphate increased markedly (P less than 0.01). Meanwhile, plasma potassium fell (P less than 0.01) and the hormonal parameters showed no significant change. We concluded that in refractory hypertension fenoldopam has potent renal and systemic vasodilatory properties through which blood pressure falls. The hypotensive effect of fenoldopam is also facilitated by its marked diuretic and natriuretic properties. The absence of variations of plasma prolactin confirm the D1 selectivity of fenoldopam and the lack of increase in PRA indicates that fenoldopam blocks the renin-angiotensin-aldosterone system.

Adult↗
PubMed1987

Alterations in regional energy metabolism in rat brain produced by small and by large doses of apomorphine: possible relations to autoreceptors.

Dose-dependent changes in behavioural patterns and in local cerebral glucose utilization (LCGU) following subcutaneous application of apomorphine were measured in conscious, unrestrained rats by means of a scoring system and of the autoradiographic [C14]2-deoxyglucose technique, respectively. The behavioural patterns of akinesia, ptosis, yawning and penile erections were scored. Akinesia and ptosis were most prominent after 0.02 and 0.07 mg/kg apomorphine but not after 0.18 mg/kg. Maximal scores for yawning and penile erections were obtained after 0.07 mg/kg. LCGU was not significantly changed after 0.07 mg/kg except for decreases in the cingulate cortex and hypothalamus. Apomorphine 0.5 mg/kg decreased LCGU in the cingulate, parietal and occipital cortex, anteromedial and lateral thalamus and lateral habenula but increased it in laminae IV and VI of the sensorimotor cortex, in the parafascicular nucleus of the thalamus, and in some parts of the basal ganglia and related nuclei. Similar changes in LCGU occurred after 2.0 mg/kg apomorphine, which also increased LCGU in the ventral tegmental area. The lower dose did not produce changes in LCGU opposite to those occurring after larger doses. The data obtained with LCGU do not support the idea that behavioural effects after low doses of apomorphine are elicited by activation of dopamine autoreceptors.

Animals↗
PubMed1987

Local cerebral glucose utilization and local cerebral blood flow in conscious rats after administration of flunarizine.

The effects of the calcium entry blocker flunarizine on physiologic variables, local cerebral blood flow (LCBF) and local cerebral glucose utilization (LCGU) were investigated. LCBF and LCGU were determined in 37 anatomically discrete brain regions in lightly restrained, conscious rats, using the quantitative, autoradiographic 14C-iodoantipyrine and 14C-2-deoxyglucose techniques. While 5 mg/kg flunarizine given i.v. did not change any of the measured physiologic variables, flunarizine increased LCBF in nearly all gray matter structures compared with saline-treated controls. LCGU was not changed compared to controls. In control as well as in flunarizine-treated rats coupling between LCGU and LCBF was tight. The ratio of LCBF/LCGU was increased after treatment with flunarizine. The data suggest that under normal physiological conditions the calcium entry blocker flunarizine does not change neuronal activity, but exerts primarily a cerebral vasodilating action.

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↗
PubMed1987

[Problem of pretherapeutic staging of cervical carcinoma. Studies of the diagnostic value of computerized tomography and magnetic resonance tomography in comparison with gynecologic palpation findings and pathologic-anatomic diagnosis].

In a prospective study of 20 cases, the importance of nuclear magnetic resonance as a diagnostic tool in cervix carcinoma was investigated. The results were compared with those of the Computer tomography as well as with those of the clinical examinations. The histology served as "Standard". In the evaluation of the local tumor invasion the gynecological examination appeared to be the most important. The involvement of regional lymph nodes was detected more accurately by the NMR as compared to CT. The exact clinical staging was not achieved by either method; thus these new diagnostic methods do not alter the planning and the technique of the operation.

Adult↗
PubMed1987

Cerebral circulation, metabolism, and blood-brain barrier of rats in hypocapnic hypoxia.

The effects of hypoxic hypoxia on physiological variables, cerebral circulation, cerebral metabolism, and blood-brain barrier were investigated in conscious, spontaneously breathing rats by exposing them to an atmosphere containing 7% O2. Hypoxia affected a marked hypotension, hypocapnia, and alkalosis. Cortical tissue high-energy phosphates and glucose content were not affected by hypoxia, glucose 6-phosphate, lactate, and pyruvate levels were significantly increased. Blood-brain barrier permeability, regional brain glucose content and lumped constant were not changed by hypoxia. Local cerebral glucose utilization (LCGU) rose by 40-70% of control values in gray matter and by 80-90% in white matter. Under hypoxia, columns of increased and decreased LCGU were detectable in cortical gray matter. Local cerebral blood flow (LCBF) increased by 50-90% in gray matter and by up to 180% in white matter. Coupling between LCGU and LCBF in hypoxia remained unchanged. The data suggest a stimulation of glycolysis, increased glucose transport into the cell, and increased hexokinase activity. The physiological response of gray and white matter to hypoxia obviously differs. Uncoupling of the relation between LCGU and LCBF does not occur.

Aminoisobutyric Acids↗
PubMed1986

Influence of an extract of Ginkgo biloba on cerebral blood flow and metabolism.

The purpose of the present investigation was to examine the effects of an extract of Ginkgo biloba (EGB) on blood glucose levels, on local cerebral blood flow as well as on cerebral glucose concentration and consumption. The local cerebral blood flow (LCBF) was measured in conscious rats by means of the 14C-iodoantipyrine technique and local cerebral glucose utilization (LCGU) by 14C-2-deoxy-glucose autoradiography. EGB increased the LCBF in 39 analyzed, anatomically defined brain structures by 50 to 100 per cent. No influence of EGB on LCGU was demonstrable. However, EGB enhanced the blood glucose level dose-dependently. Substrates and metabolites of energy metabolism were measured in the cortex of the isolated rat brain perfused at constant rate and with 7 mmol/l glucose added to the perfusion medium. In these experiments EGB decreased the cortical glucose concentration without other substrate levels being changed. These results suggest that glucose uptake may be inhibited by EGB. It is argued that the effects of EGB on brain glucose concentration and blood flow may contribute to its protection of brain tissue against ischemic or hypoxic damage.

Animals↗