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T Wichmann

Publications and source records attributed to T Wichmann.

At least 37 records · Page 2Linked to original sources
PubMed1990

Release of met-enkephalin and its modulation through acetylcholine receptors in the rabbit superior colliculus.

This report presents evidence for the depolarization-dependent release of met-enkephalin from the superior colliculus of the rabbit. Collicular tissue was placed in superfusion chambers and met-enkephalin accumulation in the superfusate was measured by radioimmunoassay. Exposure to high potassium concentrations (30 mM and 56 mM) increased met-enkephalin release. This is the fourth transmitter shown to be released from collicular tissue. Furthermore, we have obtained the first evidence that suggests that met-enkephalin release is susceptible to muscarinic modulation. While the depolarization-dependent release of met-enkephalin was depressed in the presence of atropine (1 microM), hexamethonium (100 microM) did not block the increase of met-enkephalin release induced by high potassium.

Animals↗
PubMed1990

Immunogold labelling of membrane receptors for scanning electron microscopical investigations of genetically determined disorders of lipid metabolism.

Receptors binding of low-density lipoprotein at surfaces of human lymphocytes was studied by immunochemical and scanning electron microscopical methods. Using colloidal gold sol binding ability of cells from several probands could be demonstrated by immunolabelling. We investigated cell material from normolipidaemic persons and from patients with heterozygote autosomal monogenic hypercholesterolaemia. We found a distinct decrease of labelled gold particles at the cell surface of patients with this disorder of lipid metabolism. The simple extraction possibility of lymphocytes from human venous blood and the demonstrated scanning electron microscopical results recommend the described procedure for genetic application.

Apolipoproteins↗
PubMed1989

Phentolamine blocks presynaptic serotonin autoreceptors in rabbit and rat brain cortex.

Possible antagonist effects of phentolamine at presynaptic serotonin autoreceptors were studied in slices of the occipito-parietal cortices of the rabbit and the rat. The slices were preincubated with 3H-serotonin and then superfused and stimulated electrically with single pulses or pulse trains. Nitroquipazine 1 mumol/l, a compound that inhibits the high affinity neuronal uptake of serotonin, was present in the superfusion medium in all one pulse-experiments as well as in experiments in which the effect of unlabelled serotonin was examined. In rabbit cortical slices, unlabelled serotonin reduced the single pulse-evoked overflow of tritium. Its concentration-response curve was not changed by the selective alpha 2-adrenoceptor antagonist idazoxan 1 mumol/l but was shifted to the right by phentolamine 1 and 10 mumol/l. Phentolamine 10 mumol/l also shifted to the right the concentration-inhibition curve of the selective 5-HT1-receptor agonist 5-carboxamidotryptamine. When the slices were stimulated by trains of 30 pulses at 3 Hz, phentolamine 1 and 10 mumol/l but not 0.1 mumol/l increased the evoked overflow of tritium, the maximal increase amounting to 178%; its effect was enhanced in the presence of nitroquipazine 1 mumol/l plus idazoxan 10 mumol/l (a drug combination that, when given alone, slightly increased the evoked overflow of tritium). The serotonin receptor antagonist metitepin at concentrations of 0.01-1 mumol/l also increased the overflow of tritium elicited by 30 pulses/3 Hz, the maximal increase amounting to 280%; its effect was potentiated in the presence of nitroquipazine 1 mumol/l plus idazoxan 10 mumol/l but was abolished or almost abolished in the presence of nitroquipazine 1 mumol/l plus phentolamine 10 mumol/l (a drug combination that, given alone, greatly increased the evoked overflow of tritium). When slices were stimulated by trains of 360 pulses at 3 Hz, there was no apparent antagonism of phentolamine 10 mumol/l against the inhibitory effect of unlabelled serotonin. In rat brain cortex slices, unlabelled serotonin reduced the overflow of tritium elicited by 4 pulses delivered at 100 Hz. Again, phentolamine 10 mumol/l shifted the concentration-response curve to the right. It is concluded that phentolamine blocks presynaptic serotonin autoreceptors in rabbit and rat brain cortex with pA2 values of 6.44 and 5.95, respectively. Previous failures to detect the antagonistic effect against exogenous agonists were probably due to stimulation conditions that led to marked endogenous autoinhibition of serotonin release.(ABSTRACT TRUNCATED AT 400 WORDS)

Adrenergic alpha-Antagonists↗
PubMed1989

Release and modulation of release of serotonin in rabbit superior colliculus.

The release of previously incorporated [3H]serotonin and its presynaptic modulation were studied in slices of rabbit superior colliculus. Electrical stimulation at frequencies of 0.017-3 Hz greatly increased the outflow of tritiated compounds; this response was almost abolished by tetrodotoxin and in a low calcium medium. Unlabelled serotonin, when added in the presence of nitroquipazine, an inhibitor of high-affinity neuronal serotonin uptake, reduced the electrically evoked overflow of tritium, an effect antagonized by metitepin. Given alone, metitepin caused an increase. The evoked overflow was also decreased by clonidine, and the effect of clonidine was counteracted by phentolamine. Phentolamine itself increased the overflow response. However, this was probably not due to antagonism against an inhibitory effect of endogenous noradrenaline because, first, the selective alpha 2-adrenoceptor antagonist idazoxan did not share with phentolamine the overflow-enhancing effect, second, phentolamine continued to increase the overflow after noradrenergic axons had been destroyed by 6-hydroxydopamine, and third, the facilitatory effects of metitepin and phentolamine were not additive. Phentolamine, like metitepin, antagonized the presynaptic inhibitory effect of serotonin, indicating that it may increase the evoked overflow of tritium by blocking serotonin receptors rather than alpha-adrenoceptors. Ethylketocyclazocine decrease the electrically evoked overflow, and its effect was prevented by naloxone: peptides selective for opioid mu- or delta-receptors caused no change. Nicotine increased the basal outflow of tritium (in the absence of electrical stimulation); the increase was attenuated by hexamethonium and low calcium medium. No or minimal changes in tritium outflow were obtained with beta-adrenoceptor, dopamine receptor, muscarine receptor and GABA receptor ligands or with substance P and glutamate. In conjunction with our previous studies, these results indicate that serotonin is a neurotransmitter in the superior colliculus. Its release is modulated through presynaptic autoreceptors (probably 5-HT1), alpha 2-adrenoceptors, opioid kappa-receptors and nicotine receptors, of which only the autoreceptors receive an endogenous input, at least under the experimental conditions chosen. Each of the three groups of collicular monoamine axons that we have studied recently (cholinergic, noradrenergic, serotoninergic) possesses a specific pattern of presynaptic, release-modulating receptors. A physiological role seems likely only for the alpha 2-autoreceptors at the noradrenergic and the 5-HT1-autoreceptors at the serotoninergic axons.

Animals↗
PubMed1988

[Scanning electron microscopy studies in the detection of apo-B,E receptor activity of the lymphocyte membrane for diagnostic verification of genetically determined disorders of lipid metabolism].

We present a scanning electron microscopic method for determining the quantity of the apo B,E-receptors at the surface of lymphocytes. We used human lymphocytes from venous blood. Gold particles, 50 nm in diameter, were conjugated to the receptors by indirect coupling. We visualized the gold particles by means of an electron microscope (JEM 100 S with scanning attachment ASID). The lymphocytes of control persons and of patients with primary hyperlipoproteinaemias were analysed. Scanning electron microscopic assay of labelled apo-B,E-receptors was shown to allow the rapid and accurate identification of patients with autosomal monogenic hypercholesterolaemia.

Cell Membrane↗
PubMed1988

Vascular sympathetic nerve function in congestive heart failure.

To determine if intrinsic abnormalities of sympathetic nerve function might contribute to enhanced vascular tone in congestive heart failure, chronic myocardial infarction (infarct) was produced in rats by coronary artery ligation 9 to 10 months previously for comparison with animals subjected to sham operation (sham). The excised pulmonary artery, preincubated with 3H-norepinephrine (NE) was superfused, and stimulated electrically at 2, 4, 8 and 16 Hz. The nonnormalized data at each frequency for electrically evoked 3H overflow in excess of basal outflow was similar in sham and infarct vessels (difference not significant); however, the shape of the frequency-response curves was different. The 3H overflow/pulse from sham vessels was constant between 2 and 16 Hz; however, for the infarct vessels there was a significant reduction (p less than 0.05) at the highest frequency (16 Hz). Because of an 18.4% lower peak 3H overflow at 16 Hz (difference not significant), the infarct frequency-response curve shifted significantly (4 and 8 Hz, p less than 0.025 and p less than 0.01) to the left when data were expressed as a percent of peak percent 3H overflow, suggesting an increased sensitivity of the system. These data suggest that an intrinsic vascular sympathetic nerve abnormality is not a major cause of the increased plasma NE in congestive heart failure; increased nerve activity or decreased clearance of NE may be more important.

Animals↗
PubMed1988

Release of acetylcholine and its dopaminergic control in slices from striatal grafts in the ibotenic acid-lesioned rat striatum.

Tritium accumulation during incubation with 3H-choline, and the efflux as well as the electrically evoked overflow of tritium during subsequent superfusion, were investigated in slices from unilateral striatal suspension grafts 16 to 20 weeks after implantation into the previously ibotenic acid-lesioned rat striatum. Slices from non-operated animals, from striata contralateral to grafts, and from animals with acute ibotenic acid lesions of the striatum were studied in parallel. The accumulation of tritium and the overflow of tritium in response to electrical stimulation (2 min, 3 Hz) were markedly impaired in acutely lesioned striata. In graft slices, tritium accumulation and the subsequent electrically evoked overflow were greater than in slices obtained after acute lesions, but were still smaller than in non-operated animals or in the contralateral striata. The dopamine D2-receptor agonist quinpirole inhibited the electrically evoked overflow of tritium in grafts, but only to a small extent. The D2-receptor antagonist sulpiride increased, whereas the dopamine uptake inhibitor nomifensine and the dopamine releasing drug amphetamine decreased the evoked overflow in slices from non-operated rats and from striata contralateral to grafts, but had no significant effect in grafts. As in graft slices, the release of acetylcholine in striata from animals in which the mesostriatal dopamine pathway had been lesioned by 6-hydroxy-dopamine was not changed by sulpiride and amphetamine, and was only minimally decreased by nomifensine. Our data show that striato-striatal grafts can partly restore the impaired choline accumulation and acetylcholine release in excitotoxin-lesioned striata. Functional D2-receptors are present on graft cholinergic cells, but are not activated by endogenous dopamine under the present in vitro conditions.

Acetylcholine↗
PubMed1988

Acetylcholine release in rat nucleus accumbens is regulated through dopamine D2-receptors.

Experiments in slices of rat nucleus accumbens were carried out in order to investigate whether the release of acetylcholine in this tissue is modulated through dopamine receptors. The slices were preincubated with 3H-choline and then superfused and stimulated electrically twice for 2 min each at a frequency of 3 Hz. The electrically evoked overflow of tritium averaged 2.9-3.9% of the tritium content of the tissue in the various groups. The D2-selective agonist quinpirole (0.01-1 mumol/l) reduced the evoked overflow of tritium by maximally 56%, an effect antagonized by the D2-selective antagonist (-)-sulpiride (1 mumol/l). The D1-selective agonist 2,3,4,5-tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine (SKF 38393) caused a slight decrease only at the high concentration of 10 mumol/l. (-)-Sulpiride (0.1-10 mumol/l) moderately increased the evoked overflow of tritium when given alone. The dopamine uptake inhibitor nomifensine (10 mumol/l) caused a decrease, and in its presence the increase produced by (-)-sulpiride became much more marked, amounting to maximally 149% (+)-Sulpiride (0.1-1 mumol/l) failed to change the evoked overflow of tritium in the presence of nomifensine. The dopamine-releasing agent (+/-)-amphetamine (1 mumol/l) also reduced the evoked overflow, an effect abolished by (-)-sulpiride. Finally, bretylium (1 mmol/l), which blocks the release of dopamine, increased the evoked overflow. (-)-Sulpiride (1 mumol/l) lost its facilitatory effect in slices treated with bretylium. We conclude that the release of acetylcholine in rat nucleus accumbens, like its release in the nucleus caudatusputamen, is modulated through dopamine D2-receptors.(ABSTRACT TRUNCATED AT 250 WORDS)

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1988

Uptake, release, and modulation of release of noradrenaline in rabbit superior colliculus.

The noradrenaline content, the uptake of [3H]noradrenaline, and the release of previously incorporated [3H]noradrenaline were studied in slices of rabbit superior colliculus. The concentration of endogenous noradrenaline was higher in superficial than in deep layers of the superior colliculus. Upon incubation with [3H]noradrenaline, tritium was accumulated by a mechanism that was strongly inhibited by oxaprotiline but little inhibited by 6-nitroquipazine. Electrical stimulation at 0.2 or 3 Hz increased the outflow of tritium from slices preincubated with [3H]noradrenaline; the increase was almost abolished by tetrodotoxin or a low calcium medium. Clonidine reduced the evoked overflow of tritium, whereas yohimbine increased it and antagonized clonidine. The evoked overflow was also reduced by the dopamine D2-receptor-selective agonists apomorphine and quinpirole, an effect antagonized by sulpiride. The preferential opioid kappa-receptor agonist ethylketocyclazocine produced an inhibition that was counteracted by naloxone. Nicotine accelerated the basal outflow of tritium; part of the acceleration was blocked by hexamethonium. The muscarinic agonist oxotremorine slightly diminished the electrically evoked overflow, and its effect was abolished by atropine. The oxaprotiline-sensitive uptake of [3H]noradrenaline as well as the tetrodotoxin-sensitive and calcium-dependent overflow of tritium upon electrical stimulation (presumably reflecting the release of [3H]noradrenaline) indicate that noradrenaline is a neurotransmitter in the superior colliculus. The release of [3H]noradrenaline is modulated through alpha 2-adrenoceptors as well as dopamine D2-receptors, opioid kappa-receptors and nicotine and muscarine receptors. No clear evidence was found for modulation through beta-adrenoceptors, D1-receptors, serotonin receptors, opioid mu- or delta-receptors or receptors for GABA or glutamate. Only the alpha 2-adrenoceptors receive an endogenous agonist input, at least under the conditions of these experiments. The pattern of presynaptic modulation resembles that found for noradrenaline release in other rabbit brain regions, suggesting that all noradrenergic axons arising in the locus coeruleus possess similar presynaptic receptor systems.

Animals↗
PubMed1987

Presynaptic opioid receptors in the portal vein of the rabbit.

The effects of opioids on sympathetic neuroeffector transmission were studied in superfused strips of the portal vein of the rabbit. In the first series of experiments, the tissue was stimulated electrically every 10 min with 10 pulses at 8 Hz and a current strength of 200 mA. The contractions evoked were concentration dependently inhibited by the slightly kappa-selective agonist ethylketocyclazocine and by the delta-selective agonists [D-Ala2,D-Leu5]enkephalin (DADLE) and [D-Pen2,D-Pen5]enkephalin (DPDPLE). The mu-selective agonist [D-Ala2,NMePhe4,Gly-ol5]enkephalin (DAGO) had no effect. The estimated EC50 values for ethylketocyclazocine and DADLE were 5.5 X 10(-8) and 2.9 X 10(-8) mol/l, respectively. Naloxone shifted the concentration-response curves of ethylketocyclazocine and DADLE to the right; the estimated Kb values were (1.7 +/- 0.4) X 10(-8) mol/l and (2.9 +/- 0.8) X 10(-8) mol/l, respectively. The delta-selective antagonist ICI 174864 antagonized only the inhibitory effect of DADLE but not that of ethylketocyclazocine. In the second series of experiments, the tissue was preincubated with [3H]noradrenaline then superfused and stimulated electrically three times for 3 min at 1 Hz and a current strength of 100 mA. Ethylketocyclazocine and DADLE inhibited the evoked overflow of tritium. The inhibition produced by ethylketocyclazocine was antagonized by naloxone. Our results show for the first time that opioid agonists inhibit noradrenaline release and hence, neurogenic vasoconstriction in a vein. As in other cardiovascular tissues of the rabbit, the presynaptic opioid receptors are of the kappa- and delta- but not the mu-type.

Animals↗
PubMed1987

Evidence for a neurotransmitter function of acetylcholine in rabbit superior colliculus.

Acetylcholinesterase staining and studies on the uptake of [3H]choline into the subsequent efflux of tritium from collicular slices were carried out in order to provide evidence for a neurotransmitter function of acetylcholine in rabbit superior colliculus. Acetylcholinesterase staining was dense and homogeneous in superficial layers whereas the staining was arranged in patches with slightly higher density caudally than rostrally in the intermediate layers. The accumulation of tritium in slices incubated with [3H]choline depended on time, temperature and concentration, and was inhibited by hemicholinium-3. Accumulation was slightly higher in caudal than in rostral slices. Electrical stimulation enhanced tritium outflow from slices preincubated with [3H]choline. Tetrodotoxin and a low calcium medium inhibited the evoked overflow whereas hemicholinium-3 caused an enhancement. Oxotremorine decreased the evoked overflow; atropine prevented this effect. The opioids [D-Ala2, MePhe4, Glycol5]enkephalin, [D-Ala2, D-Leu5]enkephalin and ethylketocyclazocine caused an inhibition. The effects of the latter two agonists were antagonized by naloxone. The GABAB-receptor-agonist (-)-baclofen decreased the evoked overflow at lower concentrations than GABA, whereas the GABAA-receptor-agonist muscimol was ineffective. Serotonin produced an inhibition which was prevented by metitepin, alpha- and beta-adrenoceptor as well as dopamine-receptor ligands caused no change. It is concluded that in the rabbit superior colliculus the pattern of acetylcholinesterase staining is comparable, but not identical to the distribution in other species. The accumulation of [3H]choline, as well as the tetrodotoxin-sensitive and calcium-dependent overflow of tritium upon electrical stimulation (reflecting presumably release of [3H]acetylcholine) indicate that acetylcholine has a neurotransmitter function in this tissue. The release of [3H]acetylcholine was modulated by various transmitter substances and related compounds. The pattern of modulation of release differed from the pattern in other cholinergically innervated tissues.

Acetylcholine↗
PubMed1985

[Behavior of HDL cholesterol and the apoproteins A1 A2 and B in the central circulation in patients with coronary disease and genetically determined hyperlipoproteinemias].

Seven lipid parameters, including apoproteins A1, A2 and B were determined in blood from different parts of the cardiovascular system in two groups of patients one with and the other without coronary heart disease. In addition, HDL cholesterol levels were compared in patients with coronary heart disease and primary monogenic combined hyperlipoproteinaemia. None of the seven parameters showed significant differences in samples from the pulmonary artery (mixed venous blood) and the hepatic vein of the control and patient groups. The expected significant concentration gradient between the two vascular regions was confirmed in the groups with and without coronary heart disease. HDL components showed a contrary behaviour: the hepatic vein and pulmonary artery exhibited significantly lower values of HDL cholesterol in patients with coronary heart disease than in the controls, but this was not true for HDL apoproteins A1 and A2. Patients with coronary heart disease and primary hyperlipoproteinaemia showed a significant concentration gradient between the two vascular regions for total and HDL cholesterol. These observations reveal the importance of genetic disturbances of lipid metabolism, particularly the implication of various lipid fractions in the pathogenesis of atherosclerosis.

Apoproteins↗
PubMed1985

Inhibition by diltiazem of norepinephrine release from sympathetic nerves in the rabbit pulmonary artery.

In order to determine if the calcium blocker diltiazem could alter excitation-secretion coupling in vascular sympathetic nerves, superfused rabbit pulmonary arterial strips were preincubated with 3H-norepinephrine and stimulated electrically (2-8 Hz) and by KCl (60 mM). Diltiazem significantly inhibited tension development with 4 Hz (1.5 X 10(-5) M) and 8 Hz (1.5 X 10(-6), 1.5 X 10(-5) M) stimuli, but only at 1.5 X 10(-5) M did diltiazem inhibit the 3H overflow evoked by an 8-Hz stimulus. No inhibition of 3H overflow was noted with the 2 and 4 Hz stimuli. With an 8-Hz stimulus the inhibition of tension development (45.4%) by diltiazem (1.5 X 10(-5) M) was significantly greater than the inhibition of 3H overflow (33.8%). A similar relationship was noted with 60 mM KCl stimulation. These data suggest that excitation-secretion coupling in vascular sympathetic nerves can be inhibited by diltiazem.

Animals↗
PubMed1984

Effects of verapamil, diltiazem and ryosidine on the release of dopamine and acetylcholine in rabbit caudate nucleus slices.

Slices of the rabbit caudate nucleus were preincubated with 3H-dopamine or 3H-choline and then superfused with label-free medium. Release of 3H-dopamine and 3H-acetylcholine was elicited by either electrical stimulation at 8 (in one series 2) Hz, or an increase in the K+ concentration by 50 mmol/l, or addition of L-glutamate 1 mmol/l. Verapamil 1 mumol/l, diltiazem 1 and 10 mumol/l, and ryosidine 1 mumol/l failed to the reduce the electrically-, K+- and glutamate-evoked overflow of tritium. Verapamil 1 mumol/l and diltiazem 10 mumol/l also failed to reduce the electrically-evoked overflow (2 Hz) when dopamine receptors, neuronal dopamine uptake, and neuronal choline uptake were blocked by domperidone, nomifensine and hemicholinium, respectively. Inhibition of the evoked overflow of tritium was only obtained when concentrations were increased to verapamil 10 mumol/l, diltiazem 100 mumol/l and ryosidine 10 mumol/l. The inhibition was generally small. It was more evident for slices preincubated with 3H-choline than for those preincubated with 3H-dopamine, because in the latter verapamil, diltiazem and (much less) ryosidine accelerated the basal efflux of tritium. The inhibition of the K+-evoked overflow of tritium was probably due to blockade of Ca2+ channels because this overflow was Ca2+-dependent but tetrodotoxin-resistant. In contrast, the inhibition of the electrically- and glutamate-evoked overflow possibly involved blockade of Na+ channels as well. The results indicate that three calcium antagonists from different chemical classes are very weak inhibitors of Ca2+ entry into, and hence transmitter release from, the terminal axons of central dopaminergic and cholinergic neurones. The function of the high affinity calcium antagonist binding sites that have been identified in brain remains unknown.

Acetylcholine↗
PubMed1983

[Behavior of important serum lipid fractions in chronic hemodialysis patients and following kidney transplantation].

In patients in the chronic programme of haemodialysis and 51 patients with transplanted kidney selected lipid-chemical parameters were investigated and compared. 1. Disturbances of the lipid metabolism more frequently occurred in patients with transplanted kidney than in chronically haemodialyzed patients. 2. Triglycerides, total cholesterol and LDL cholesterol were more frequently increased in patients with transplanted kidney than in chronically haemodialysed patients. 3. The HDL cholesterol of patients with transplanted kidney was only somewhat higher in comparison to patients in the chronic haemodialysis programme. 4. Sex-specific differences of the HDL cholesterol level were neither in chronically haemodialysed patients nor in patients with transplanted kidney. 5. Klimov-index and LDL/HDL cholesterol quotient referred to a permanently high risk of cardiovascular complications even after transplantation of a kidney.

Adolescent↗
PubMed1982

[Lipid chemical parameters and incidence of genetically determined hyperlipoproteinemias in patients between 20 and 45 years of age with coronary heart disease].

In 35 patients at the age between 20 and 45 years with a manifest coronary heart disease various lipid-chemical parameters were established and compared with a control group of the same age of laboratory-chemically and clinically inconspicuous test persons as well as with a group of patients with infarction older than 45 years. For HDL-cholesterol, LDL-cholesterol as well as LDL significant differences of the mean value were the result in the group of juvenile patients with a coronary heart disease and in the healthy control group as well as the group of older test persons with infarction, which confirm the accumulation of lipid-chemical risk constellations in "juvenile" patient with a coronary heart disease. Moreover, the proportion of primary hyperlipoproteinaemias is essentially greater in these patients than in older test persons with infarction. Apart from the recognition of primary hypercholesterolaemias the diagnostics of autosomally combined hyperlipoproteinaemias is of particular importance.

Adult↗
PubMed1981

[Lipid analytic investigations concerning the establishment of the forms of primary hypercholesterolaemia in patients with myocardial infarction].

The influence of genetic factors in the development of the coronary heart disease can be particularly impressively clarified at the instance of the primary hyperlipoproteinaemias. The exact diagnostics of the genetically determined disturbances of lipometabolism in patients with infarction is, however, still connected with difficulties. Determinations of serum cholesterol and triglycerides, lipid-electrophoretic recognitions as well as determinations of LDL- and HDL-cholesterol in the serum cannot always outline with utmost clearness the proportion of primary hyperlipoproteinaemias in the morbidity of infarctions. Before this background the practical value of the radiochemical screening test worked up at the model of lymphocytes is emphasized, which allows a clear diagnosis of primary forms of hypercholesterolaemia according to pathogenetic viewpoints and thus renders possible also family examinations within the primary prevention of the coronary heart disease.

Adolescent↗