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Biomedical subjects

C Sachs

Publications and source records attributed to C Sachs.

At least 109 records · Page 6Linked to original sources
PubMed1980

Autonomic control of cardiovascular reflexes in narcolepsy.

Six male patients with narcolepsy for several years, were studied without and with amphetamine in order to evaluate possible abnormalities in autonomic control of the cardiovascular system. Studies were made of (1) heart rate and blood flow in the resting forearm during contralateral isometric handgrip, (2) respiratory sinus arrhythmia and (3) heart rate response to the Valsalva manoeuvre. The patients had a slow heart rate, a reduced forearm blood flow increase on handgrip, and a subnormal sinus arrhythmia. Only two out of the six patients had an abnormal Valsalva ratio. Amphetamine did not alter the response to handgrip but increased the sinus arrhythmia in three patients and the Valsalva ratio in two. It is concluded that narcolepsy is accompanied by reduced vegetative reactivity in the cardiovascular system. Since this applies to functions mediated by both the sympathetic and parasympathetic systems, and since some parasympathetically-mediated functions are affected while others are not, the functional disturbance found probably is of central origin.

Adult↗
PubMed1980

[Effects of erythrocytes on electrometric pH measurements (author's transl)].

Erythrocyte interference in electrometric readings has been demonstrated and quantified in pH measurements. The presence of erythrocytes introduces a negative component into the final result of the electrometric reading, proportional to the hematocrit. There is indirect evidence that this does not correspond to a true proton concentration change, but to the presence of the erythrocytes per se. The authors suggest the use of a correcting factor (0.01 pH unit per tens of hematocrit units) to obtain the real pH from a pH value measured on whole blood: however the use of this correcting factor should be restricted to the type of equipment described.

Adult↗
PubMed1979

Micro determination of plasma renin activity in normal infants and children of capillary and venous blood.

Plasma renin activity (PRA) has been measured by microassay on capillary and venous blood sampled simultaneously in 21 subjects; there is no significant difference between these two groups of PRA values. PRA values in normal infants, children and adults have been measured with this microassay and the results are similar to those previously published by authors using different radioimmunological assays.

Adult↗
PubMed1979

Incidence of basal ganglia calcifications on computed tomography.

In a group of 3,800 computed tomography examinations, 14 patients (0.4%) were found to have high attenuating lesions suggesting calcifications within the basal ganglia. The lesions were bilateral in all patients. A majority of the patients had psychic symptoms and convulsions. Electroencephalographic changes were frequent and extrapyramidal symptoms occurred. Until now only three patients have been endocrinologically examined. One of them had hypoparathyroidism. Since parathyroid dysfunction frequently is associated with calcifications of the basal ganglia, these patients should be referred for endocrinological evaluation.

Adult↗
PubMed1978

Developmental plasticity of central serotonin neurons after 5,7-dihydroxytryptamine treatment.

Systemic administration of 5,7-HT to newborn rats produces an altered development of the 5-HT neurons in the central nervous system, with marked regional differences. 5,7-Hydroxytryptamine can enter the brain and elicit its neurotoxic actions after systemic administration in the neonatal stage due to an incompletely developed blood-brain barrier, which for 5,7-HT is elaborated between postnatal Days 5 and 7. Treatment with 5,7-HT at birth produces marked and permanent 5-HT denervation in the cerebral cortex and spinal cord, whereas hyperinnervation occurs in the 5-HT cell body-near regions (mesencephalon-pons-medulla). The latter effect is seen within the first week postnatally. Treatment with 5,7-HT also affects NA neurons in a similar manner, although the action is exerted preferentially on 5-HT neurons. A selective effect on 5-HT neurons can be achieved by DMI pretreatment, after which both NA and DA neurons develop normally. No signs of any interaction among growing 5-HT, NA, and DA neurons can be observed. Studies of the postsynaptic 5-HT receptor in vitro with [3H]-5-HT and [3H]LSD binding indicate that this receptor develops independently of presynaptic 5-HT nerve terminals. Neither 5-HT denervation nor 5-HT hyperinnervation was accompanied by any change in receptor-binding characteristics or receptor density. The results available are compatible with the view that the consequences for 5-HT neurons that occur after neonatal 5,7-HT administration are mainly due to a "pruning effect." The developing 5-HT neurons seem to be programmed to produce a certain quantity of nerve terminal arborizations, which they try to conserve after 5-HT-induced injury, leading to the observed rearrangement of 5-HT nerve terminals.

5,7-Dihydroxytryptamine↗
PubMed1978

Provoked visual impairment in multiple sclerosis studied by visual evoked responses.

Pattern-reversal VERs were studied during the visual impairment provoked by exercise in 2 patients with demyelinating optic neuritis. It was found that the transient reduction in visual acuity was correlated to a transient decrease in the amplitude of the major positive component of the VER, whereas no significant changes could be observed in the latency of the response. The normal VER was not influenced by exercise.

Adult↗
PubMed1977

[Electrometric determination of urinary ammonia using a continuous-flow automatic method].

A critical study has been designed to evaluate the application of an electrometric method to the assay of ammonia in urine. The use of NH3-gaz permeable membrane electrode with a continuous flow system seems to have solved most of the problems evoked by former studies. The results obtained show that the method is reliable for the use in clinical routine. The simplification of the ammonia measurement procedure thus achieved will allow an important increase in the number of renal function tests that a clinical routine laboratory can handle in a hospital.

Ammonia↗
PubMed1976

Regional changes in [3H]-noradrenaline uptake, catecholamines and catecholamine synthetic and catabolic enzymes in rat brain following neonatal 6-hydroxydopamine treatment.

6-Hydroxydopamine (6-OH-DA) treatment of rats at birth (with the analyses conducted in the adult stage) produced marked regional variations in changes in endogenous noradrenaline (NA) and [3H]NA uptake in the CNS. The most pronounced reductions were seen in the cerebral cortex, hippocampus and the spinal cord. Moderate changes or none at all were seen in the hypothalamus, septum and thalamus. Marked increases in endogenous NA and [3H]NA uptake were seen in the mesencephalon and the pons-medulla oblongata. There was in general a close correlation between the changes in endogenous NA and [3H]NA uptake. The results from the cerebellum varied, depending on the developmental stage at which the 6-OH-DA treatment was performed. 6-OH-DA treatment up to three days after birth generally led to a marked increase in both endogenous NA and [3H]NA uptake, while continuing the treatment caused a marked reduction of both parameters. The 6-OH-DA treatment caused no changes in endogenous dopamine (DA) in all regions analysed. Enzyme activity assays showed that DA-beta-hydroxylase (DBH) and tyrosine hydroxylase (TH) were greatly reduced in the cerebral cortex, while the activity of both enzymes was almost double in the pons-medulla. No changes in the activity of phenylethanol-amine N-methyltransferase (PNMT), DOPA decarboxylase, COMT and MAO were seen after 6-OH-DA at birth. Measurements of choline acetyltransferase activity displayed only minute changes. The present results strongly support the view that 6-OH-DA treatment in the neonate stage produces a very selective action on NA neurones belonging to the locus coeruleus system from a structural standpoint, leaving DA- and PNMT-containing neurones unaffected. [3H]NA uptake in whole CNS was almost unchanged, despite the marked regional variations. The results have been interpreted as being due to a 'pruning effect', where the permanent NA denervation in distant nerve terminal projections (e.g. cerebral cortex) leads to a compensatory sprouting and increased outgrowth of NA terminal projections in areas close to the perikarya (e.g. pons-medulla). Furthermore, the results support the view that the growing locus coeruleus neurones are strictly programmed to produce a certain quantity of nerve terminal volume and arborization during the postnatal development.

Age Factors↗
PubMed1975

Effects of 6-hydroxydopamine on central noradrenaline neurons during ontogeny.

The effects of the catecholamine neurotoxic compound, 6-hydroxydopamine (6-OHDA) have been investigated on central noradrenaline (NA) neurons after neonatal administration. In agreement with previous studies this treatment (1-3 X 100 mg/kg) led to a pronounced reduction of the in vitro uptake of [3H]NA and the endogenous NA in the cerebral cortex, while these parameters were markedly augmented in the pons and medulla oblongata, regions containing the NA perikarya. The 6-OHDA induced changes in the cerebral cortex and the pons-medulla could be completely prevented by the 'membrane pump' blocker desipramine, indicating that the effects are associated with a specific neurotoxic action of 6-OHDA on the NA neurons. Consistently, 6-OHDA acutely (within 2 h) produced a marked reduction of the [3H]NA uptake in both the cerebral cortex and pons-medulla. In the cerebral cortex the nadir (approximately 75% reduction) was reached within 6 h and remained so, while in the pons-medulla the [3H]NA uptake rapidly recovered, being maximally elevated after 14 days (50-80% increase) and remained so for at least 6 months. The [3H]NA uptake in the pons-medulla from 6-OHDA treated rats had the same kinetic and pharmacological properties as that of control. Thus the observed differences in [3H]NA uptake are most likely quantitatively related to actual changes in the number of NA nerve terminals. Treatment with lower 6-OHDA doses (10 or 50 mg/kg) resulted in less pronounced reduction of [3H]NA uptake initially, and there was a gradual recovery of tuptake with time in the cerebral cortex, which was more pronounced after the lower dose. These results are indications of regenerative growth, which may be possible when a critical part of the axon is spared from the neurotoxic effect of 6-OHDA. Administration of 6-OHDA on various days after birth disclosed that both the reduction of [3H]NA uptake in the cerebral cortex and the increase of [3H]NA uptake in the pons-medulla did not appear as permanent phenomena when 6-OHDA was given later than on the seventh postnatal day. This is most likely associated with the postnatal development of the blood-brain barrier. It may be concluded that the neonatal 6-OHDA treatment causes a marked NA denervation in the forebrain, e.g. the cerebral cortex, and an increased outgrowth of NA nerve terminals in the pons-medulla, which is preceded by a partial damage. This partial NA denervation is then followed by a regeneration (regenerative and/or collateral sprouting) and a stimulated outgrowth of NA nerve terminals.

Animals↗
PubMed1975

Control of the neurotoxicity of 6-hydroxydopamine by intraneuronal noradrenaline in rat iris.

In vitro studies with the neurotoxic compounds 6-hydroxydopamine (6-OH-DA) and 6-aminodopamine (6-A-DA) showed that noradrenaline (NA) markedly inhibited the autooxidation of 6-OH-DA, but not of 6-A-DA. In vivo studies of the adrenergic nerves in rat iris showed that the neurotoxic potency of 6-OH-DA, but not 6-A-DA, was increased after NA depletion by alpha-methyl-p-tyrosine methylester (H44/68). Neurotoxicity was evaluated by measuring the associated decrease in 3-H-NA uptake. Intraocular injection of NA counteracted the degenerative action of 6-OH-DA in both untreated and H44/68 pretreated rats. Intraocular NA did not interfere with the neurotoxicity of 6-A-DA. Additionally, octopamine did not affect the rate of autooxidation nor the neurotoxic potency of 6-OH-DA or 6-A-DA. Control experiments with 3-H-6-OH-DA showed that the intraneuronal NA levels did not significantly affect the intraneuronal accumulation of 6-OH-DA. The parallelism between the in vitro results on autooxidation and in vivo data on neurotoxicity makes it appear that the neurotoxic potency of 6-OH-DA and 6-A-DA is closely associated with their rates of autooxidation. The control of the degenerative action of 6-OH-DA by intraneuronal NA may be mediated via reaction of NA with radicals formed from oxygen during autooxidation of 6-OH-DA.

Animals↗
PubMed1975

5,7-Dihydroxytryptamine induced changes in the postnatal development of central 5-hydroxytryptamine neurons.

Systemic administration of the neurotoxic compound 5,7-dihydroxytryptamine (5,7-HT) to newborn rats led acutely (within 1--2 h) to a marked reduction of the in vitro uptake of [3H]5-hydroxytryptamine (5-HT) in homogenates from the cerebral cortex (75% decrease) and the pons-medulla (60% decrease). When 5,7-HT was administered postnatally we found that between days 5 an7 resistance developed in the cerebral cortex towards the 5,7-HT induced reduction in 3H-5-HT uptake. This was most likely the result of the postnatal development of the blood-brain barrier. These results show that 5,7-HT can pass the blood-brain barrier in the neonate stage and enter the brain to exert its well-known neurotoxic action on 5-HT neurons. The [3H]5-HT uptake in the cerebral cortex was reduced quantitatively to the same extent up to the 28th postnatal day, after which time a moderate recovery took place. Endogenous 5-HT was reduced by 40% in the cerebral cortex when measured in adult animals. In the pons-medulla there was a rapid recovery of the [3H]5-HT uptake during the first week after the 5,7-HT treatment and on the 14th postnatal day the increase was as much as 75% compared with the control. Endogenous 5-HT and [3H]5-HT uptake was increased by 40--50% when the analysis was performed 2 months after the 5,7-HT treatment. Studies of [3H]noradrenaline (NA) uptake after 5,7-HT administration at birth showed that this treatment similarly affected the NA neurons, though to a lesser extent. The effects on the NA neurons could be abolished by pretreatment with the "membrane pump" blocker desipramine, leaving the action of 5,7-HT on 5-HT neurons almost unaffected. Analysis of the [3H]5-HT uptake kinetics in the pons-medulla showed that the 5,7-HT treatment did not affect the Km while the Vmax was increased. It is concluded that neonatal 5,7-HT treatment produces a marked 5-HT denervation of the cerebral cortex, while there is a stimulated postnatal outgrowth of 5-HT nerve terminals in the pons-medulla, after an initial partial damage of the neurons.

Aging↗