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Biomedical subjects

W Kromer

Publications and source records attributed to W Kromer.

8 recordsLinked to original sources

[Endorphins--endogenous peptides with morphine-like effects. 2. Biological importance, clinical apsects].

Since 1974 peptides with opiate-like action both in vivo and in vitro have been isolated from the nervous system of various vertebrates and man. The localization of these peptides (endorphins) within the central and peripheral nervous system reflects the possible biological functions in which they may participate: the response of the CNS to painful stimuli (dorsal horn of the spinal cord, central grey matter, thalamus); the control of emotions (limbic system); the regulation of vegetative functions (medulla oblongata); the response of the body to stress the control of endocrine function (hypothalamus, infundibulum, hypophysis); the control of extrapyramidal motor activity (brain stem) or the control of intestinal motility (intramural nervous plexus). Up-to-date knowledge suggests that the endorphins may function as neurotransmitters, neuromodulators or hormones and that such functions vary according to the special sites of synthesis, storage and action of these various peptides within the body.

Behavior

Porcine pituitary peptides with opiate-like activity: partial purification and effects in the rat after intraventricular injection.

A peptide material with opiate-like activity in the guinea-pig ileum was extracted from porcine pituitaries using a hot glacial acetic acid extraction method and was partially purified by gel filtration. When injected intraventricularly in rats, these purified peptides induced strong analgesia, catelepsy, respiratory depression and other opiate-like effects, which lasted for several hours.

Analgesia

[Continuing registration of muscle temperature during electromyography].

Measurements of muscle temperature were performed during and after contractions of human skeletal muscle using an electromyography-needle-electrode, which contains a thermo-element. The investigations aimed at explaining a drop in temperature during contraction, earlier described, and getting some aspects of possible employment of temperature measurements carried out simultaneously with electromyography. 1. The course of temperature during contraction (increase or decrease) depends on the heat of contraction, blood flow through muscle, penetration depth of the thermoelement, gradient of temperature and efficacy of a compression of blood vessels. It results from a superimposition of the single effects. 2. A decrease in temperature in various extremity muscles during contraction is explained by a compression of blood vessles caused by the shortening of muscle, as described earlier by other authors. 3. The interpretation of temperature curves, especially the quantitative interpretation, becomes very uncertain because of various sources of error. A differentiation between muscle heat and influence of blood flow is not sufficiently possible. 4. Nevertheless measurements carried out under conditions of disturbed blood supply, myopathies and polyneuropathies consistent with experiments performed during cooling and warming muscle in a water-bath, causing a reactive hyperemia or a defective circulation by using a blood pressure instrument show that changes in blood circulation are expressed by changes in temperature curves. Measurements carried out simultaneously on agonists and antagonists show satisfactorily the contrary changes in blood circulation known from the literature.

Adult

[In vitro inhibition of oxidative N-demethylation with carbon disulfide].

Earlier findings have shown that in experimental animals (rat) and in man inhaled carbon disulphide (CS2) reversibly inhibits the non-specific oxidative drug metabolism caused by hepatic microsomal enzymes. Very little is known concerning the underlying mechanism. The present investigations were undertaken to throw light on this question. After addition of an NADPH-regenerating system to liver microsomes isolated from adult female Wistar rats, the oxidative N-demethylation of aminopyrine was measured under simultaneous exposure to CS2 by quantitatively determining the formaldehyde obtained; the resulting data were evaluated using enzyme-kinetic parameters according to Lineweaver-Burk: 1. Following acute exposure to low and medium-grade CS2 concentrations (20-400 ppm/8 h), the pattern of inhibition in rat liver microsomes is identical to that obtained in normal liver microsomes to which CS2 had been added. This finding seems to suggest that the inhibitory process under in vivo and in vitro conditions is based on one and the same molecular mechanism. 2. Upon addition of CS2 the in vitro pattern of inhibition corresponds to a strong mixed-type inhibition. 3. It is concluded from the enzyme-kinetic behaviour that CS2 attacks at two different sites of the enzyme molecule: Binding to the first site is followed by inhibition, as evidenced by the rise of Km; after saturation of this site, a second site is occupied resulting in a reactivation and, beyond this, an activation of enzyme output, as shown by the decrease of Km. CS2 exhibits a high affinity for the first site, and a low affinity for the second site. Binding at the first site is reversible. The possibility that the active centre in the enzyme molecule is the site where binding of the inhibitor occurs is ruled out. 4. A continuous decrease of Vmax at increasing inhibitor concentration is causally related with the formation of an enzyme/substrate inhibitor complex. 5. The CS2 added to the microsomes can be eliminated by helium gas; this is followed by the return of the original enzyme activity. It is concluded from this behaviour that under in vitro conditions CS2 itself (rather than its metabolites) acts as the inhibitor. 6. Oxygen treatment of the microsome-containing reaction mixture enhances the inhibition. In substrate-free control mixtures, addition of CS2 was followed by the dose-dependent formation of formaldehyde; a causal explanation is not readily available at this time.

Air Pollutants