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Biomedical subjects

F Bergmann

Publications and source records attributed to F Bergmann.

At least 73 records · Page 4Linked to original sources
PubMed1989

Nonpsychotropic cannabinoid acts as a functional N-methyl-D-aspartate receptor blocker.

Binding studies using the enantiomers of the synthetic cannabinoid 7-hydroxy-delta 6-tetrahydrocannabinol 1,1-dimethylheptyl homolog in preparations of rat brain cortical membranes reveal that the (+)-(3S,4S) enantiomer HU-211 blocks N-methyl-D-aspartate (NMDA) receptors in a stereospecific manner and that the interaction occurs at binding sites distinct from those of other noncompetitive NMDA antagonists or of glutamate and glycine. Moreover, HU-211 induces stereotype and locomotor hyperactivity in mice and tachycardia in rat, effects typically caused by NMDA receptor antagonists. HU-211 is also a potent blocker of NMDA-induced tremor, seizures, and lethality in mice. This compound may therefore prove useful as a nonpsychoactive drug that protects against NMDA-receptor-mediated neurotoxicity.

Animals↗
PubMed1988

Interaction of thyrotropin-releasing hormone (TRH) and serotonin in cardiovascular control.

Intravenous injection of the synthetic TRH analog, MK-771, to anesthetised cats raised the blood pressure by a central mechanism, i.e. by activating the outflow of sympathetic stimuli from the CNS to the periphery and raising the plasma concentration of adrenaline and noradrenaline. In contrast, noradrenaline in the CSF was lowered by intravenously injected MK-771. The concentration of 5-HT in the CSF was increased and the pressor action of the peptide was correspondingly enhanced by 5-HT antagonists. These findings suggest that the release of 5-HT into the CSF lowers blood pressure and thus reduces the hypertensive effect of MK-771. Methysergide acts synergistically with MK-771 to combat the sudden fall in pressure induced by acute hemorrhage in the anesthetised cat. Combination of the two drugs enhanced and accelerated recovery from this hypotensive state.

Animals↗
PubMed1988

Further evidence of von Willebrand factor involvement in thrombotic thrombocytopenia purpura.

Fourteen patients diagnosed as having thrombotic thrombocytopenia purpura (TTP) were studied. Those who survived have been followed during a 1 to 7 year period. The clinical diagnosis was based on changing neurological findings, thrombocytopenia and evidence of microangiopathic hemolytic anemia. Laboratory tests included the determination of von Willebrand factor antigen (VWF:Ag), ristocetin cofactor (RiCof) and the electrophoretic mobility of von Willebrand factor (CIE VWF:Ag). The ratio of RiCof to VWF:Ag was then calculated. Control individuals included healthy subjects and patients with thrombocytopenia of several etiologies. Statistical differences between the values of RiCof, the ratio of RiCof:VWF:Ag and the CIE of VWF:Ag were found for samples comparing active disease and remission phase. The recovery from thrombocytopenia paralleled the correction of abnormal parameters. Similarly, significant differences were found when above parameters were compared between thrombocytopenia of TTP with other thrombocytopenic states. We suggest that these abnormal tests could be useful in distinguishing TTP from other disorders, and may have prognostic significance in patients already diagnosed as having TTP.

Adolescent↗
PubMed1988

Cerebral toxicity of the trichothecene toxin T-2, of the products of its hydrolysis and of some related toxins.

T-2 toxin and its metabolites (resulting from enzymatic hydrolysis by rat brain homogenate) were applied to the midbrain of albino rats, either in solid form or dissolved in dimethyl sulfoxide (DMSO). Solid implants of HT-2 toxin and of T-2 triol were lethal in the range of 10-20 micrograms per rat, i.e. similar to the effect of T-2 toxin itself. For four further trichothecenes, the following decreasing order of toxicities was found: T-2 tetraol = iso-T-2 toxin greater than T-2 tetraol tetraacetate greater than T-2 toxin acetate. Implants of the last compound were the least toxic in the present series of trichothecenes; its LD50 value was nearly ten times higher than that of T-2 toxin. A similar gradation of toxicity was observed upon intracerebral injection of the compounds dissolved in DMSO. Here the only exception was the markedly reduced toxicity of T-2 toxin itself. From these data, the role of free 3 alpha- and 4 beta-hydroxyl groups has been evaluated. For subcutaneous applications, the largest ratio of LD50 values was 5, i.e. for the pair T-2 triol-T-2 tetraol tetraacetate. Among the signs of central intoxication, convulsions, adipsia and aphagia were marked. Pathological changes in the brain tissue, mainly involving necrotic, hemorrhagic and inflammatory lesions at the sites of application, were similar for all trichothecenes tested in this study.

Animals↗
PubMed1987

T-2 toxin effect on rat aorta: cellular changes in vivo and growth of smooth muscle cells in vitro.

Rats were injected intraperitoneally with T-2 toxin and their aortas were studied by light and electron microscopy. The growth of smooth muscle cell explants taken from the tunica media of aortas of similarly treated animals was observed. A single large dose (2 mg/kg) or four injections of 0.3 mg/kg T-2 toxin caused damage and occasional necrosis of endothelial cells, accumulation of basement membrane-like material in the intima, and swelling and activation of smooth muscle cells in the tunica media. Three or more weeks after the last injection of 0.3 mg/kg T-2 toxin the endothelial cells were normal but an excess of fragmented intimal basement membrane-like material persisted and smooth muscle cells were still activated. Outgrowths from explants of aortic tunica media taken within 1 week of the last dose of T-2 toxin showed marked inhibition of smooth muscle cell growth. Three or more weeks after the toxin, the explants showed significantly increased outgrowths. These findings suggest that T-2 toxin causes early endothelial and smooth muscle cell injury accompanied by inhibition of smooth muscle cell growth in culture. This is followed by stimulation of the proliferative capacity of smooth muscle cells in vitro. If a similar mechanism is operative in vivo, it could explain the chronic vascular changes observed after limited exposure to T-2 toxin.

Animals↗
PubMed1987

Cutaneous injury by topical T-2 toxin: involvement of microvessels and mast cells.

Topical applications of various doses of T-2 toxin to rats led to delayed skin reactions. Following a dose-dependent latent period of 12-24 hr, there appeared vascular dilation, stasis, edema and mononuclear cell infiltration, with many degranulating mast cells. These signs were earliest and strongest in the subcutis. Epidermal necrosis occurred 1-2 days later and was probably caused secondarily by ischemia, due to microcirculatory failure. Ultrastructurally, endothelial cells of small vessels were the earliest sites of change. While intercellular junctions remained closed and pinocytosis decreased, the cytoplasm contained many ribosomes, vacuoles, and abnormal mitochondria. Another early effect of topical T-2 toxin was an increase in number and degranulation of mast cells, especially in the subcutis. The resemblance of the skin injury to that produced by irradiation is noted.

Animals↗
PubMed1985

The use of antiserotonergic agents for the treatment of acute hemorrhagic shock of cats.

In cats anesthetized with pentobarbitone sodium the effect of two types of antiserotonergic agents on cardiovascular recuperation after acute hemorrhage was examined. Methysergide, a competitive inhibitor for 5-HT receptors and p-chlorophenylalanine (PCPA), an inhibitor of tryptophan-5-hydroxylase, improved blood pressure recovery after bleeding. After extensive hemorrhage (40 ml/kg blood), treatment with methysergide improved survival. It is proposed that serotonin participates in the depressor response and survival of acute hypovolemic hypotension.

Animals↗
PubMed1985

Toxic and lethal effects of T-2 toxin upon intracerebral administration to rats.

T-2 toxin was given to rats in three ways: Subcutaneous or intracerebral injection of a solution in dimethyl sulfoxide (DMSO) and by implantation of toxin, adsorbed on talc, into various regions of diencephalon and brain stem. The latter method proved to be most effective. Within a few hours after administration of 10-20 micrograms toxin, the animals became restless, ataxic and dyspneic. These early symptoms were followed by depression and immobility. Prior to death, tachypnea and/or convulsions developed. The rats succumbed to implantation of toxin within 1 - 7 days; no fatalities occurred at later dates. Histologically, the toxin pellets caused necrosis a few days after implantation; at a later stage, the necrotic areas were surrounded by inflammatory infiltrates around small blood vessels. These morphological changes were limited to the application site and were insufficient to explain the lethal effect of intracerebral administration. After intracerebral injections of toxin solutions, the animals died within 24 h. No marked histological changes could be seen after such rapid fatalities.

Animals↗
PubMed1985

Influence of intake of sweet solutions on the analgesic effect of a low dose of morphine in randomly bred rats.

The time course for the development of morphine tolerance, following prolonged sweet intake, was examined in randomly bred Sabra rats. Exposure to 3% glucose in 6 mM saccharin solution increased drinking by about three times as compared to rats supplied only with water. Suppression of the analgesic effect of morphine was already detectable after 24 h of intake and became progressively more marked within the next 5 weeks. These results support an active interaction between sweet consumption and endogenous opioids in randomly bred rats.

Animals↗
PubMed1984

Simultaneous changes of catecholamines and of Leu-enkephalin-like immunoreactivity in plasma and cerebrospinal fluid of cats undergoing acute hemorrhage.

Cats, anesthetized with sodium pentobarbitone, underwent acute hemorrhagic shock by withdrawal of 15 ml blood/kg of body weight. The cerebral ventricular system was perfused with artificial cerebrospinal fluid (CSF). Blood and CSF samples were collected during 2 h, for the analysis of catecholamines (CA) and Leu-enkephalin-like immunoreactivity (LE-ir). The fall of blood pressure immediately after hemorrhage was accompanied by a rise of LE-ir in the CSF and by a decrease of norepinephrine and dopamine below their control values. About half an hour later, the LE-ir returned to its initial low level, while the CA were now markedly elevated. A similar opposite behavior of peptides and CA was observed during subsequent sampling periods, although blood pressure remained constant. These experiments demonstrate an inverse relationship of LE-ir and CA in the CSF, after acute hemorrhagic shock.

Animals↗
PubMed1984

Biphasic effects of chronic saccharin intake on pain responses of healthy and diabetic rats of two genetically selected strains.

Rats of the LC-2-HI strain, selected for high rates of self-stimulation, were supplied with a 3 mM saccharin solution. Within 1 week they developed markedly prolonged latencies to painful stimuli on a hot-plate. In contrast, a similar effect became manifest in LC-2-LO rats only after 3 weeks. Both strains of rats were made diabetic by injection of streptozotocin. LO rats showed more polydipsia and hyperglycemia than HI rats and, when drinking saccharin solution, developed cross-tolerance to morphine within about 2 weeks. It is assumed that saccharin consumption stimulates the release of endogenous opioid peptides, probably via stimulation of gustatory sweet receptors. The opioid peptides exert a biphasic effect: initially they raise the pain threshold, but at a later stage they cause chronic cross-tolerance to morphine.

Analgesia↗
PubMed1984

Effects of chronically elevated intake of different concentrations of saccharin on morphine tolerance in genetically selected rats.

Sixty-four LC2-Hi and LC2-Lo female rats were chronically supplied with either water or a solution of 1, 3 or 30 mM of sodium-saccharin. Pain sensitivity, as well as its reduction by a 2.5 mg/kg morphine injection, were measured in a hot-plate test. High saccharin consuming LC2-Hi rats did not exhibit significant morphine-induced analgesia (MIA) compared to baseline, after 38 days of drinking of saccharin, irrespective of concentration. MIA of those rats were maintained on water was significant. In contrast, the low consuming LC2-Lo animals maintained either on water or on 1 and 30 mM saccharin showed significant MIA compared to baseline, following the same exposure period. The findings demonstrate that chronically elevated saccharin intake, activates an endogenous opiate system leading ultimately to cross-tolerance to the analgetic effects of morphine.

Animals↗
PubMed1983

Dose effects of morphine on the spontaneous unit activity recorded from the thalamus, hypothalamus, septum, hippocampus, reticular formation, central gray, and caudate nucleus.

Spontaneous activity was recorded from 652 units in 8 subcortical structures of unanesthetized rats. Recordings were obtained in central gray, mesencephalic reticular formation, parafasciculus thalami, caudate nucleus, anterior and ventromedial hypothalamus, lateral septum, and dorsal hippocampus. Eighty recordings were obtained from untreated animals and 80 from saline-injected controls, none of which showed any significant changes of unit activity during the 4- 5-hr observation period. The effect of morphine, given in 5 incremental doses from 0.5 to 30.0 mg/kg ip, was followed in 492 units. Morphine enhanced or depressed spontaneous discharge rates, or caused biphasic effects, ie enhancement alternating with depression and vice versa. Naloxone induced increase in firing after either effect of morphine, or reduced spontaneous activity after morphine-induced increases. However, when morphine reduced neuronal discharges, naloxone never caused further depression. In 86 units, morphine at any dosage failed to alter neuronal activity, but in 54 of these units naloxone nevertheless induced alterations in firing rates. The pattern of responses to morphine differed between all 8 brain regions examined and was characteristic for each individual structure. This is the first systematic study describing the dose-response characteristics of morphine in 8 brain sites recorded simultaneously. Furthermore, it utilized freely behaving animals without the interference of anesthetics, which are themselves known to interact with opiates. The variety of response patterns seen supports the neuropharmacological evidence for multiple opiate receptors or multiple sites of opiate action.

Animals↗
PubMed1983

Improvement of skin flap survival by local injections of Regitine and propranolol. An experimental study in the rat.

An increase in the surviving area of skin flaps was achieved by local injections of alpha-adrenergic and beta-adrenergic blocking agents. Dorsal skin flaps of albino rats were injected postoperatively at their bases with Regitine (Ciba-Geigy, Switzerland), propranolol and a combination of these two drugs, two or three times daily for 6 days. All the pharmacologically treated animals showed a significantly better flap survival rate than did the control group (P less than 0.001). More frequent injections gave increasing flap survival areas. However, a combination of the above-mentioned drugs did not improve the results when compared with propranolol administered alone, and was less effective than Regitine administered alone.

Animals↗
PubMed1982

Stereotyped responses of rats to two 2-halogenoergolines: 2-bromo-alpha-ergocryptine and lergotrile.

Stereotyped responses to apomorphine, 2-bromo-alpha-ergocryptine (BEC) and lergotrile were compared in naive animals and after various pretreatments. Lergotrile was about half as effective as apomorphine in naive rats, while BEC produced intense stereotyped reactions only after pretreatment with p-chlorophenylalanine. Inhibitors of catecholamine biosynthesis (alpha-methyltyrosine and alpha-methyldopa) only impaired the response to BEC. Haloperidol, a dopamine antagonist, blocked the lergotrile-induced stereotypy within a few minutes, but had a rather slow effect on the response to BEC. It is concluded that lergotrile mainly activates dopamine receptors directly, similar to apomorphine. BEC, however, has a predominantly indirect effect, stimulating the formation and subsequent release of both dopamine and 5-hydroxytryptamine. The relationship of this difference in mechanism to the differences in structure is discussed.

Animals↗
PubMed1980

Growth disturbance following fracture of the tibia in children.

Orthoradiographs were produced from 13 to 36 months after tibial fractures in 85 children. Fifty-nine were complete i.e. tranverse or longitudinal, and 28 fractures were incomplete i.e. infractions or fissures. The difference in the length of the tibia from growth disturbance caused by the fracture was found to be related to the age of the child at the time of fracture and the sex. An overgrowth was found to occur in the age group from 3 to 10 years in girls and from 3 to 12 years in boys, whereas in the older children a growth retardation was demonstrated. No correlation with the type of fracture, or with the residual angulation after reduction, could be established. The growth disturbance appeared to last for 1 to 2 years. We conclude that a more concerned attitude towards residual shortening at the time of reduction should be adopted in girls from the age of 10 and boys from the age of 12 years in order to compensate for the growth retardation induced by the fracture.

Adolescent↗