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Biomedical subjects

H D Fischer

Publications and source records attributed to H D Fischer.

At least 37 records · Page 2Linked to original sources
PubMed1989

Adaptive changes in the central noradrenergic system in monocular deprived rats.

Noradrenaline and dopamine content, K+-stimulated release of 3H-noradrenaline, 3H-noradrenaline high-affinity uptake, 3H-prazosin and 3H-rauwolscine binding to alpha 1- and alpha 2-adrenoreceptors, respectively, were studied in isolated visual structures (visual cortex, superior colliculus, lateral geniculate nucleus) of three-month-old rats monocularly deprived by unilateral eyelid closure at postnatal day 11. Monocular deprivation resulted in a number of changes in comparison with normal littermates, mainly in the lateral geniculate nucleus, both ipsilateral and contralateral to the closed eye. K+-stimulated release of noradrenaline and high-affinity noradrenaline uptake were significantly increased, 3H-rauwolscine binding to alpha 2-adrenergic receptor sites was decreased in the contralateral and ipsilateral lateral geniculate nucleus. 3H-Prazosin binding to alpha 1-adrenergic receptors as well as the levels or noradrenaline and dopamine in the lateral geniculate nucleus were unaffected by monocular deprivation. The data support the suggestion that the lateral geniculate nucleus plays a key role in modulating visual information processing and that the lack of an adequate visual input within the first weeks of life interferes mainly with the development of the noradrenergic system at the level of the lateral geniculate nucleus.

Animals↗
PubMed1989

The antihypoxic effect of ethymisole: a comparison with other nootropic drugs.

Ethymisole reveals a potent antihypoxic effect which is produced probably both by an acute free radical scavenging property and a persisting restitutive component of action. This is seen in its effect on posthypoxic inhibition of dopamine release from striatum slices of adult rats. Though ethymisole is considered a drug which increases brain adaptive potency, it does not modify the stimulus-response relation of potassium-evoked dopamine release in an adaptation-like manner, as it is seen after a long-lasting piracetam treatment.

Animals↗
PubMed1989

Influence of hypoxia on the age dependent stimulus-effect-relation of K+-induced dopamine release from rat brain structures.

There is a well defined correlation between stimulus intensity (potassium concentration) and the so-called fractional efflux rate of radio-labelled neurotransmitter from loaded brain structures. K+-induced dopamine release shows an age-dependent parallel shift of the stimulus-effect-relation which obviously reflects quantitative developmental changes during maturation (increasing release) and involution (restricted release) of neuronal structures and functions without modification of involved mechanisms in a qualitative manner. On the other side, mild hypoxia results in quite different, even opposite changes of the stimulus-effect-relation exhibiting the most diverse vulnerability and reactivity of neuronal stimulus-release-coupling at different age.

Aging↗
PubMed1989

Influence of hypoxia on the release of DA from striatal preparations of rats.

The effects of hypoxia in adult and newborn rats on the release rate of DA from slices and synaptosomes of striatum were studied. In adult animals hypoxia (10 kPa oxygen tension in the inspiratory air) induces a decrease of the FER of DA from slices up to 70% dependent on the duration of the hypoxia. An early postnatal hypoxia (10 kPa, 2nd -11th day of life) brings about a long-term increase of the FER of DA from slices by about 30% when the release is measured at the age of 2-3 month. Slices show a relatively low release rate compared to synaptosomes. The hypoxia effects found with slices, i.e. a decrease of the FER in adult animals and increase in those that had experienced an early postnatal hypoxia, could not be confirmed in synaptosomes. The much lower release rate from slices suggests the action of inhibitory factors controlling the release of DA. In that case hypoxia would exert an indirect influence.

Aging↗
PubMed1989

Effect of pyritinol on the dopaminergic system and behavioural outcome in an animal model of mild chronic postnatal hypoxia.

Rats after mild chronic postnatal hypoxia always show late sequelae of behaviour and long-term alterations of neurotransmitter release from striatal slices. It was to test preventive or therapeutic actions of drugs using the model of mild chronic postnatal hypoxia of the rat. Pyritinol prevented the learning deficit due to hypoxia and decreases the potassium stimulated DA release from striatal slices. The experiments underline the high plasticity of the CNS during the neonatal period and stress the necessity of early therapy of perinatal brain damage.

Animals↗
PubMed1989

New aspects in mechanisms of antihypoxic piracetam action.

A long-term piracetam treatment leads to an improved stimulus-effect-coupling of potassium stimulated dopamine release: The maximum effect of the potassium stimulus is already obtained in presence of much lower Ca++-concentrations (Ca++-economizing effect) than normally. In consequence of the improved stimulus-effect-coupling by piracetam treatment the dose-dependent inhibitory effect of the calcium antagonist flunarizine on the fractional efflux rate of dopamine is decreased. The volume of vesicular structures is not involved in the piracetam effect.

Animals↗
PubMed1989

Antihypoxic effects of AWD 23-15 in mice and rats.

AWD 23-15 (6-Methyl-1,2,3,4-tetrahydro-pyrimidin-2,4 dion) which is known to improve learning and memory processes in laboratory animals, was investigated in several hypoxia models. The following results were obtained: 1. Increase of survival rate, 2. change in hypoxia-induced decrease of cerebral post-mortem adenylic energy charge and in concentrations of metabolic products in the brain and 3. antagonism of the hypoxia-induced decrease of dopamine release. However in the general behavioral test the drug was ineffective. These results support the idea that AWD 23-15 is a potential nootropic drug.

Adenine Nucleotides↗
PubMed1988

[Peroxidative vulnerability of synaptosomal high affinity Ca++-ATPase and pharmacologic effects].

The high affinity Ca++-ATPase participates essentially in the regulation of intrasynaptosomal calcium homeostasis. Related to posthypoxically restricted transmitter release, we examined the influence of newly-generated free radicals (ascorbic acid-ferric salt mixture) or sodium dodecyl sulfate in vitro and of a mild hypobaric hypoxia in vivo on the activity of synaptosomal high affinity Ca++-ATPase. Moreover we tested the effectiveness of piracetam, meclofenoxate hydrochloride, pyritinol and verapamil on the changed enzyme activity subsequent to a hypoxic exposure. The activity of synaptosomal high affinity Ca++-ATPase (1.04 +/- 0.03 mumol Pi/mg.h) is reduced by not more than 40% depending on the concentration of the ascorbic acid-ferric salt mixture used but is nearly totally inhibited by sodium dodecyl sulfate (0.2 mg/ml). Hypobaric hypoxia (18 h, 8.7 kPa) decreases the enzyme activity to 0.79 +/- 0.03 mumol Pi/mg.h. Piracetam, meclofenoxate hydrochloride and pyritinol are protectively effective on the decrease of enzyme activity induced by hypoxia. The results emphasize the importance of intact protein-phospholipid interactions for the enzyme activity and support relations between synaptosomal high affinity Ca++-ATPase and transmitter release.

Animals↗
PubMed1987

The co-occurrence of Reiter's syndrome and acquired immunodeficiency.

Thirteen patients who had the co-occurrence of severe Reiter's syndrome and the acquired immunodeficiency syndrome (AIDS) or its syndromes were studied. The arthritis was reactive in three patients and without defined cause in the others. Nine patients had HLA-B27. The two syndromes appeared simultaneously in four patients, suggesting a common biologic process, and in the others the immunodeficiency either preceded or followed the arthritis. Reiter's syndrome occurring in the setting of this profound immunodeficiency suggests that helper T cells were not involved in the pathogenesis of the rheumatic disease. Difficulties were encountered in the diagnosis of either syndrome in the presence of the other. Two patients with Reiter's syndrome developed Kaposi's sarcoma and fulminant AIDS after receiving methotrexate, which emphasizes the need for caution in the use of immunosuppressive therapy in Reiter's syndrome. An additional patient with undifferentiated spondylarthropathy subsequently developed psoriasis in conjunction with the onset of AIDS.

AIDS-Related Complex↗
PubMed1987

Respiratory function of rat brain mitochondria after hypobaric hypoxia and piracetam treatment.

After an acute hypobaric hypoxia the mitochondrial respiratory control index is reduced in consequence of a decreased active-state respiration. The finding is paralleled by decreased uncoupled respiration and a not significantly changed resting-state respiration. Long term hypoxic exposures show adaptive traits of this criterion of mitochondrial energy metabolism. The antihypoxic effect of piracetam may be reflected in a delayed normothermic in vitro aging of mitochondrial suspension.

Animals↗
PubMed1987

The influence of social isolation, hypoxia and immobilization on potassium-stimulated dopamine release from telencephalon slices of mice.

Dopamine release from mice telencephalon slices was investigated following immobilization or hypobaric hypoxia exposure during periods of social isolation of different length which itself affects dopamine release in a characteristic manner. Isolation initially results in a decreasing release, which is compensated at the end by adaptive processes. The decrease of dopamine release induced by immobilization is highly dependent on the foregoing isolation. On the other hand, a hypoxia-induced decrease of release always dominates the results. Adaptive processes in consequence of social isolation are supposed to be important in relation to immobilization effects but not to hypoxia-induced changes.

Adaptation, Physiological↗
PubMed1987

[ATP-metabolizing enzymes in suspensions of isolated coupled rat brain mitochondria].

An improved method for the isolation of rat brain mitochondria is described. The preparation exhibits a respiratory control index (RCI) of 6 or 7.3 in the presence of pyruvate and malate or glutamate and malate, respectively. RCI decreases to 2.5 in the presence of Mg++. When the phosphorylation of extramitochondrially added or formed ADP is suppressed by carboxyatractyloside (CAT) inhibition of the adenine nucleotide translocator, the remaining respiration amounts to 6 nmol O2/min X mg mitochondrial protein. These results and the ratio of 16 to 19 from the quotient of phosphorylating active-state respiration to CAT inhibited respiration refer to a high degree of mitochondrial coupling of respiration. Therefore the remaining respiration in the presence of Mg++ is due to a phosphokinase activity located outside the inner membrane of intact mitochondria or at nonphosphorylating mitochondrial fragments. The following activities were observed: Oligomycin sensitive ATPase, 47 mU/mg protein; hexokinase, 272 mU/mg protein; creatinphosphokinase, 116 mU/mg protein; and a surprisingly low activity of adenylatekinase, 57 mU/mg protein.

Adenosine Monophosphate↗
PubMed1987

Inhibition of stimulated dopamine release from striatum slices after hemorrhagic shock in the rat. Protective effect of piracetam.

The antihypoxic effect of piracetam was studied using a hemorrhagic shock model in the rat. Different shock severity was achieved by bleeding of 35% or 50% of estimated blood volume (EBV). Hemorrhagic shock caused an inhibition of K+ induced dopamine release from striatum slices in proportion to the magnitude of hemorrhage, reflecting the degree of membrane damage in dopaminergic transmission structures. Piracetam was effective in preventing the post-hemorrhagic changes in moderate shock and accelerated restitution of post-hemorrhagic release inhibition in severe shock.

Animals↗
PubMed1986

Postnatal administration of L-dopa normalizes hypoxia-induced long-term changes in dopamine release from striatum slices and in avoidance learning.

Newborn rats exposed to a mild chronic postnatal hypoxia always displayed at the age of 2-3 months an increased fractional efflux rate of dopamine (DA) from striatum slices combined with a decreased capacity for learning and retention. The protective effect of the administration of L-DOPA on these long-term changes was tested by the injection of L-DOPA 5-30 min prior to the beginning of daily exposure to hypoxia. L-DOPA administration during postnatal hypoxia prevents in a dose dependent manner the long-term effects of postnatal hypoxia as described. This finding supports the hypothesis that long-term changes in DA release and in behaviour due to early postnatal hypoxia may be brought about by changes in the DA-metabolism during a critical period of development.

Animals↗
PubMed1986

Protective and restitutive effects of antihypoxic drugs on posthypoxic dopamine release inhibition.

Exposure of rats to hypoxia results in a substantial decrease of dopamine release from striatum slices for several days. Nootropic drugs (piracetam, meclofenoxate hydrochloride, methylglucamine orotate, nicergoline) accelerate the restitution of posthypoxic release inhibition. In contrast, amphetamine is ineffective in this respect. The antihypoxic action of sedatives (diazepam, phenobarbital) prevents the decrease of dopamine release. Comparable results with free radical scavengers (cysteamine hydrochloride, sodium formiate, ouabain), ascorbic acid, natrii calcii edetas, selenium methionine and acetylsalicylic acid which protect dopamine release from hypoxically produced changes agree with and support the hypothesis of hypoxia induced free radical generation followed by phospholipid peroxidation altering particularly neuronal membrane function. On that account, dopamine release from rat striatum slices reflects not only the vulnerability of neuronal membrane function by hypoxia but also the preventive, protective and restitutive effects of antihypoxic drugs of different type and is able to contribute to discriminating drug investigation.

Amphetamine↗
PubMed1986

The vulnerable period of perinatal hypoxia with regard to dopamine release and behaviour in adult rats.

The relations between a perinatal exposure schedule and the outcome of dopamine (DA) release from striatum slices on the one hand and behaviour on the other, were studied in order to identify the vulnerable period. A mild chronic postnatal hypoxia (2nd-10th day of life) induces long-term effects on the DA release rate (FER) from striatum slices. A 10 h daily exposure to hypoxia for 5 days (2nd-6th day of life) induces the same long-term effects. Adult rats exposed to hypoxia (pO2 8.6 kPa) for 16 h respond with a drastic decrease of FER of DA. Exposure to early postnatal hypoxia prevented this drastic decrease of FER of DA when adult rats were again exposed to hypoxia. 3 ten h periods of hypoxia within the first 10 days of life were enough to the long lasting effects. Prenatal hypoxia as well as hypoxia during the adolescent period did not show any long-term effects on the dopaminergic system. Alterations in behaviour (decreased learning capacity as well as decreased reaction to stimuli after prolonged stress in adulthood) were found after 3-9 days of hypoxia between the 2nd and 10th day of life.

Aging↗
PubMed1986

Effects of nootropic drugs on some behavioural and biochemical changes after early postnatal hypoxia in the rat.

Piracetam (PIR) and dimethylaminoethanol (DMAE) were tested with respect to their ability to prevent changes of the locomotor behaviour and of the dopamine release from striatum slices after an intermittent postnatal hypoxia in the rat (2nd-10th day of postnatal life). The drugs given to pregnant rats (from 12th day of gestation) and continued after delivery to the newborns (till 10th day of postnatal life) displayed antihypoxic effects. Perinatal DMAE- but not PIR-treatment diminishes the consequences of postnatal oxygen deprivation regarding the motor activity as well as the dopamine release of adult animals. Hypoxia-caused open field hyperactivity of developing rats was found to be reduced to control values in PIR-treated rats. Only minor effects were seen after DMAE-treatment, but a marked depressant own effect on the explorative activity was detectable.

Animals↗