Search PubMed⌕ Search

Biomedical subjects

H Blume

Publications and source records attributed to H Blume.

At least 73 records · Page 4Linked to original sources
PubMed1983

Changes in cerebrospinal fluid and plasma vasopressin in the febrile sheep.

Plasma and cerebrospinal fluid (CSF) concentrations of vasopressin (AVP) were measured in conscious sheep during fever induced by iv endotoxin. Body temperature and blood pressure were also measured. AVP concentrations increased in both CSF and plasma although increases were not parallel. AVP concentrations in CSF were significantly correlated to increases in body temperature whereas plasma AVP concentrations were not. Neither CSF nor plasma AVP concentrations were correlated with changes in blood pressure. These data indicate that there may be independent regulation of AVP release into plasma and CSF compartments and supports the idea that AVP may have several physiological functions to perform during fever.

Animals↗
PubMed1982

Endotoxin-stimulated opioid peptide secretion: two secretory pools and feedback control in vivo.

Small doses of endotoxin evoked a dramatic biphasic response of opioid peptide secretion into blood in sheep. The first phase began within minutes and coincided with a brief hypertensive response to endotoxin well before the appearance of fever or hypotension. The ratio of beta-endorphin to beta-lipotropin fell abruptly at the onset of the second phase of release, suggesting early depletion of a pool rich in beta-endorphin and subsequent emergence of a pool rich in unprocessed precursor. The concentration of cerebrospinal fluid opioids increased tenfold during the second phase. Naloxone administration augmented endotoxin-induced opioid secretion in both early and late phases, suggesting a short-loop feedback regulation of stress-induced endorphin secretion.

Animals↗
PubMed1982

[On the biotransformation of xenobiotics by rat liver mitochondria].

Rat liver mitochondria, isolated in succrose (0.25 mol/l), were frozen and stored for several weeks at -18 degrees C. Enzymic tests and electronmicroscopy were used to estimate freezing damage to mitochondria. The activities of the mitochondrial enzymes were altered significantly by freezing and thawing. The outer membrane enzyme activities were decreased by both, freezing and storing. On the contrary the activities of some inner membrane enzymes were initially increased by freezing (latency) and then decreased by storing. Storage of not frozen mitochondria suspensions lowered equally the activities of inner membrane enzymes and outer membrane enzymes. The decrease of the enzyme activities was connected to structural alterations, the mitochondrial membranes were damaged completely by freezing/thawing and storage.

Animals↗
PubMed1981

[Metabolism of the local anaesthetic fomocaine by rat liver mitochondria (author's transl)].

Fomocaine (Erbocain) is metabolized by different routes in rat and beagle. By highly purified rat liver mitochondria it was metabolized to its N-oxide only. The N-oxide was reduced to fomocaine by a reductase localised in the matrix or in the inner membrane of the mitochondria. C-Hydroxylation with subsequent conjugation reactions as well as oxidative N- or O-dealkylation found in intact animals were not observed in mitochondria.

Animals↗
PubMed1981

[Biotransformation of amphetamine derivatives by rat liver mitochondria/2nd communication; Oxidative deamination of amphetamine and reduction of phenylacetone].

Amphetamine is deaminated oxidatively by highly purified rat liver mitochondria. This monoamineoxidase (MAO) is an enzyme of the mitochondrial outer membrane and its activity is about two times higher than that of the microsomal MAO. Anaerobic incubations with mitochondria reduce phenylacetone, an important metabolite of amphetamine, to phenylisopropanol. The ketoreductase is localized in the mitochondrial inner membrane or its matrix.

Acetone↗
PubMed1981

[Biotransformation of amphetamine derivatives by rat liver mitochondria / 1st communication: Oxidative dealkylation of N,N-dialkyl- and N-alkylamphetamines (author's transl)].

Highly purified rat liver mitochondria catalyze oxidative dealkylation of N,N-dimethylamphetamine (I) and Methamphetamine (II). The demethylase activity is bound to the mitochondrial inner membrane or its matrix. Demethylation of N,N-dimethylaniline (1.231 nmol/mg/min) follows about two times faster than dealkylation of I (0.929 nmol/mg/min) or II (0.878 nmol/mg/min). Nitrazepam and other N-alkylamides seem to be no substrates for this mitochondrial enzyme at all. Under aerobic incubation conditions the rate of mitochondiral I-metabolism was about 1/8 of the microsomal rate, provided that both preparations have the some protein concentrations. NADPH was a much better cofactor for this reaction than NADH. The role of cytochrome P-450 as a possible essential cofactor for mitochondrial dealkylation could not be elucidated.

Amphetamines↗
PubMed1980

Adrenocorticotropic hormone may be transported directly from the pituitary to the brain.

Experiments were designed to test the hypothesis that pituitary hormones may be delivered directly to the brain. Concentrations of adrenocorticotropic hormone (ACTH) in the plasma were determined in blood samles obtained simultaneously from the carotid artery, the sagittal sinus, and the jugular vein of three awake sheep. Seizures were induced electrically to stimulate ACTH secretion, and at precise intervals thereafter several simultaneous comparisons were made in each animal. In many of the post-seizure comparisons, the ACTH plasma concentrations within the sagital sinus exceeded those within the carotid artery as well as those within the jugular vein, indicating that this hormone was released from the pituitary and carried directly through capillary beds of brain to the venous blood within the sagittal sinus. The experiment was repeated in one hypophysectomized sheep and, in this animal, ACTH concentration in the plasma was reduced, but that in the sagittal sinus still was elevated after the seizure, an indication that some ACTH (or ACTH-like material) was released from the brain itself.

Adrenocorticotropic Hormone↗
PubMed1980

[Contribution to the analysis of the hypoglycaemic agent tolbutamide. Part 2 (author's transl)].

The chemical identification reaction for tolbutamide (USP 1975) involves its hydrolysis by sulphuric acid with the formation of n-butylamine. This amine then reacts with diazotised p-nitraniline to give 8 red or yellow coloured compounds. A radicalic and an ionic mechanism for their formation, which are partially interrelated, are discussed. Other oral sulphonamide-hypoglycaemic agents give a positive result with this identification reaction.

Chemical Phenomena↗
PubMed1980

[Reduction of nitrazepam by rat liver mitochondria (author's transl)].

Highly purified rat liver mitochondria are able to reduce nitro groups of organic compounds to primary amines. This reductase-activity is bound to mitochondrial inner membrane or its matrix. It has no plain substrate specificity whereas it will attack the various substrates at widely different rates [nitrazepam (Mogadan) 1.7 times faster than 4-nitrobenzoic acid]. The activity was markedly inhibited under aerobic conditions. The rate of nitrazepam reduction by rat liver mitochondria was about 1/3--1/4 the rate by microsomal fraction, provided that both preparations contained the same protein amounts. NADH was required as a cofactor, but the nitroreduction was also stimulated by some Krebs cycle intermediates, especially by alpha-ketoglutarate. The reaction was markedly inhibited by organic solvents, even by little volumes. DMSO and DMF are cancelling every activity.

Animals↗
PubMed1978

[On drug metabolisation by mitochondria of rat liver (author's transl)].

Highly purified rat liver mitochondria, in spite of the permeability barrier of the mitochondrial membrane, are able to oxidise tertiary amines to amine oxides, to reduce N-oxides of tertiary amines and to oxidise substituted primary alcohols to the corresponding acids via instable aldehydes. This new information on the role of mitochondria in the metabolism of drugs was obtained with the aid of previous results on the biotransformation of the local anaesthetic fomocaine.

Alcohols↗
PubMed1978

[Clinical and laboratory aspects of malignant hyperthermia in children with special reference to creatine kinase isoenzymes (author's transl)].

The clinical and laboratory findings in 4 children with signs of malignant hyperthermia are reported. In all cases an extraordinary elevation of creatine kinase activity in serum was observed. By investigation of the creatine kinase isoenzyme activities we tried to determine the origin of creatine kinase. In contrast to other reports, creatine kinase BB derived from brain was found to be absent in all cases, although creatine kinase MM and MB showed remarkable alterations. A certificate for all patients who have survived malignant hyperthermia is suggested.

Alanine Transaminase↗
PubMed1976

[A contribution to the identification of the oral antidiabetic agent tolbutamide. 1st communication].

An identification reaction for tolbutamide given in several pharmacopoeias involves the reaction of n-butylamine, formed by acid hydrolysis of tolbutamide, with diazotised p-nitroaniline to yield a characteristic red colour of unknown structure(s). It is demonstrated that, by using TLC methods, this red colour can be separated into 8 red or yellow coloured components. The structures of these isolated compounds were determined by spectroscopical methods and, in six cases, confirmed by unequivocal synthesis. These coloured components include one pentazdiene, five triazenes and two nitro compounds.

Aniline Compounds↗