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Biomedical subjects

H Kostron

Publications and source records attributed to H Kostron.

At least 55 records · Page 3Linked to original sources
PubMed1985

Nimodipine treatment of ischemic neurological deficits due to cerebral vasospasm after subarachnoid hemorrhage. Clinical results of a multicenter study.

Intravenous Nimodipine was administered to 109 patients (65 female and 44 male) with either pre- or post-operative progressive neurological deterioration from cerebral vasospasm following subarachnoid hemorrhage from a ruptured aneurysm. In 91 of the patients the efficacy of Nimodipine in relieving ischemic symptoms was assessed and in all of the 109 patients the tolerance was evaluated. The aneurysms were related to following arteries: anterior communicating artery (41%), middle cerebral artery (24%), internal carotid artery (10%), vertebro-basilar arteries (4%) and others (5.5%); 11% of the patients had multiple aneurysms. On 16 of the 91 patients no surgery was performed. On 16% of the remaining 75 patients surgery was performed within 72 hours after the hemorrhage, 57% were operated between day 4 and day 15 and 29% after day 16. The ischemic neurological deficits occurred preoperatively in 67% of the patients and post-operatively in 23%. At the beginning of treatment 84% of the patients were graded III-V according to the Hunt and Hess grading system. Most of the patients received doses of 24-48 mg Nimodipine daily as constant i.v. infusion for 7-10 days. The grade of neurological deficit at the end of the treatment was evaluated according to the Glasgow Outcome Scale. 59 (65%) of the patients showed complete recovery or marked improvement of the ischemic symptoms while 22% remained unchanged and 11% died due to severe vasospasm. Administration of Nimodipine seemed to be more efficient in cases where treatment was started within 24 hours. In the patient group which was treated pre-operatively, recurrent hemorrhage was recorded in 8% of the patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1984

[Clinical experiences with nimodipine (Bay e 9736)].

In 27 patients, who suffered from SAH from a ruptured cerebral aneurysm direct operation and treatment with Nimodipine (Bay e 9736) was performed. Nimodipine was given intravenously over ten days (30 micrograms/kg bodyweight/hour) and thereafter orally over four days in diminishing dosages. There were no noteworth side effects. In comparison with a group of nine similar patients who were not given Nimodipine the study shows that Nimodipine is not able to reduce angiographic spasm or brain oedema in CT-scan. In spite of that the general recovery with Nimodipine was better than in the control group. The worse the initial neurological symptoms are, the more effective Nimodipine seems to be. The study shows that treatment should begin between the first and sixth day after SAH, at least two days before operation and at the latest two days after the onset of secondary spasm.

Calcium Channel Blockers↗
PubMed1984

[Intracerebellar hematomas; diagnosis and therapy].

This article deals with the diagnosis, therapy and prognosis of intracerebellar haematomas. The characteristic symptoms and the value of computer tomography for an early diagnosis and the surgical therapy are discussed. Prognosis and complications are analysed in comparison with other works. Guiding rules for a rapid diagnosis and the choice of the respective therapy are given and an early surgical therapy is recommended.

Adult↗
PubMed1983

Regional, cellular, and subcellular distribution of [3H]dexamethasone in rat brain edema.

The regional, cellular, and subcellular distribution of [3H]dexamethasone in brain edema of rats was studied. Edema was induced either by occlusion of the right carotid artery or by a cold lesion of the right temporal lobe. [3H]dexamethasone (0.3 mCi) was injected intravenously. After 30 minutes (unless otherwise stated) the brains and other desired organs were removed. In the control animals, 51% of the total [3H]dexamethasone activity was found in the cerebral hemispheres (27% in the right, 24% in the left), 24% in the cerebellum, and 24% in the brainstem. Time-course studies revealed a rapid decline of [3H]dexamethasone content in all regions of the brain. After 48 hours of ligation of the right carotid artery, 80% of the [3H]dexamethasone could be found in the cerebral hemispheres (48% in the right, 32% in the left), 10% in the cerebellum, and 9% in the brainstem. In the series in which cold lesions were induced, 74% of the [3H]dexamethasone was recovered in the cerebral hemispheres (40% in the right (lesion), 34% in the left (control]. Before the trauma, 75% of the dexamethasone was found in astrocytes and 25% in neurons; after the trauma, 48% was bound to astrocytes and 42% to neurons. At the subcellular level, accumulation took place in the microsomal, lysosomal, and cytoplasmic fractions of the damaged cells. These data demonstrate an increased uptake of dexamethasone into ischemic damaged brain tissue and into neurons, microsomes, and lysosomes.

Animals↗
PubMed1983

[Tumors of the 3d ventricle, clinical aspects and treatment].

Our last 30 patients, who were operated upon 3rd-ventricle-tumors, are discussed on symptomatology, diagnosis and therapy. Depending on the localization we classify oral, basal and caudal tumors. The peak of these tumors is found in the first ten years of life. They are distributed as followed: spongioblastomas, ependymomas, pinealoma and other rare tumors. Mainsymptom is the sudden diffuse headache depending on this skull's position. The three groups show different symptomatic features, the oral one sepecially that headache described above. The symptoms of the caudal group are due to signs of raised intracranial pressure and content the typical syndrome of the lamina-quadrigemina. Basal tumors lead to diencephalic disturbances. The CT scan should be done as the first diagnostic step, eventually connected with ventriculography or ventriculotomography. In any case therapy should be started by implantation of an atrio-ventriculare shunt. If the disease is progressing an invasive procedure has to be done. Irradiation therapy is bound to a clear histologic diagnosis or to a clear inoperability. Our 5-years survival was 40% in average.

Adolescent↗
PubMed1982

[The lucid interval in epidural hematoma].

On the basis of 191 patients with epidural haematomas in an observation period of 15 years, an analysis of the patient group with non-classical symptoms was carried out. The opinions and theories regarding the generation of long-lasting lucid intervals found in the literature are mentioned and discussed on the basis of 3 typical examples. Owing to improved examination methods and early recognition, the mortality rate of the patients with epidural haematomas could be reduced from 54 per cent in the years 1961 to 1965 to about 10 per cent in the years 1975 to 1980.

Adolescent↗
PubMed1981

[Cerebral vasospasm: clinical and biochemical aspects and treatment (author's transl)].

Cerebral vasospasm is caused by many factors. Primarily it is caused by Noradrenalin (NA) localised in the vessel walls and by platelet aggregation, with raising of the concentration of 5-HT in the intima. Its prolongation is based on blood breakdown products and or biochemical disturbances of brain metabolism. The most potent vasoconstrictors are acting through the vessel's own receptors (Serotonin, NE, Histamin), so the most effective therapy is based on the contractile system of the vessel. By blocking the alpha-receptors by Phenoxybenzamine, blockade of the Phosphodiesterase by Papaverin, Euphyllin to raise the concentration of cAMP and stimulation of Adenyl-Cyclase-System by beta-stimulation, it is possible to get good results in the treatment of cerebral arterial vasospasm.

Humans↗
PubMed1978

A characterization of the nucleotide uptake of chromaffin granules of bovine adrenal medulla.

Chromaffin granules isolated from bovine adrenal gland were incubated with (3)H-labelled nucleotides and [(14)C]noradrenaline to study the uptake of these substances. [(3)H]ATP, [(3)H]ADP and [(3)H]AMP are taken up by these organelles by the same temperature-dependent mechanism. The apparent K(m) for ATP and ADP is 1.4mm, and for AMP it is 2.9mm. The uptake of ATP has a flat pH optimum, whereas the catecholamine uptake increases with more alkaline pH. Atractyloside and carboxyatractyloside are competitive and specific inhibitors of nucleotide uptake, whereas reserpine inhibits only that for catecholamines. Mg(2+) ions activate uptake of both catecholamine and nucleotides, whereas EDTA and N-ethylmaleimide inhibit these processes. Nucleotide and catecholamine uptakes are inhibited by uncouplers of oxidative phosphorylation and by two ATP analogues. NH(4) (+) ions and nigericin in the presence of KCl inhibit only catecholamine uptake. It is concluded that nucleotide uptake, as proposed previously for catecholamine uptake, depends on an electrochemical proton gradient produced by a proton-translocating adenosine triphosphatase localized in the membrane of chromaffin granules. Furthermore, as suggested by the effect of NH(4) (+) and nigericin, catecholamine uptake apparently depends on the chemical part of this gradient, whereas the results for nucleotide uptake are consistent with its dependence on the electrical component.

Adenosine Diphosphate↗