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H D Wehner

Publications and source records attributed to H D Wehner.

16 recordsLinked to original sources
PubMed1993

[Rate of ethanol clearance after oral and parenteral ethanol administration].

A crossover investigation of the ethanol concentration decline after oral and parenteral administration of ethanol respectively was performed with direct intra- and interindividual comparison. No significant differences in relation to the kind of administration were noted. An influence of the circadian rhythm on the rate of decline could be excluded. The low beta 60 values derived (average: 0.111 g/kg/h) can be explained by the long period over which the probands were denied food.

Adult↗
PubMed1993

[Methanol level and methanol elimination in alcoholic patients].

A total of 54 male alcoholics aged between 26 and 57 years who had been admitted in an intoxicated state to a psychiatric hospital for acute care and subsequent detoxification were included in the study. The blood ethanol concentration (BEC) and serum methanol concentration (SMC) at the time of admission (n = 49) and the methanol elimination curve during ethanol elimination (n = 19) and after the ethanol concentration had fallen to zero (n = 4) were investigated. On admission, the BEC ranged from 0.21 g/kg to 3.26 g/kg and the SMC ranged from 5 mg/kg to 44 mg/kg. The gamma-alcoholics (n = 28) exhibited higher ethanol concentrations than the delta-alcoholics (n = 11) but no difference was found in the methanol concentrations. The methanol level was found to be related to the ethanol level in gamma-alcoholics (r = 0.671; p < 0.001), but not in d-alcoholics (r = 0.215; p > 0.05). The methanol content of the most recently consumed and generally preferred type of alcoholic beverage was found to influence the SMC in all the alcoholics. The SMC did not fall during ethanol oxidation (BEC > 0.2g/kg). After the ethanol concentration had fallen to zero, methanol elimination was found to follow first order kinetics; the elimination constants ranged from 0.592 h-1 to 0.209 h-1, corresponding to elimination half-life values of 1.2 h to 3.3 h. No differences were found between these values and those of non-alcoholic subjects.

Adult↗
PubMed1992

The elimination kinetics of methanol and the influence of ethanol.

Four male subjects aged between 20 and 29 years were given intravenous injections of methanol at a dosage of 10 mg per kg body weight, once without prior administration of ethanol, and once after oral ingestion of 0.3 g ethanol per kg body weight. The serum methanol concentration was monitored over the next 5 h (after methanol administration alone) and 6-7 h (after methanol administration following ethanol ingestion). The elimination of methanol administered alone was found to follow first-order kinetics with a rate constant for the elimination phase of 0.475-0.259 h-1, corresponding to an elimination half-life of 1.8-3.0 h. When ethanol was also administered methanol oxidation was found to be completely blocked until the blood ethanol concentration had fallen to 0.2 g/kg. When the ethanol concentration had dropped to zero, methanol elimination followed exactly the same course as that observed in the experiment without prior administration of ethanol (k: 0.378-0.231 h-1; t1/2: 1.5-2.7 h).

Adult↗
PubMed1989

[Reference values of n-propanol elimination].

Injections of increasing doses of n-propanol provoke blood concentration curves of exponential decays with dose dependent rate constants. The n-propanol-specific clearance is approximately 10 ml/min. It is determined by a Michaelis-Menten-metabolism (max. velocity of metabolizing: approximately 2.5 mg/l min; Michaelis-Menten-constant: approximately 10 mg/l) and is inhibited in the presence of ethanol.

1-Propanol↗
PubMed1989

[Elimination properties of the congener n-propanol].

Intravenous injections of n-propanol (25 mg, 50 mg, 100 mg, 200 mg, 300 mg) provoke blood concentration curves having exponential shapes of dose dependent rate constants after a sufficiently long time (2 min). They have to be seen therefore as a result of a non-linear elimination process controlled by a Michaelis-Menten-kinetic. Using the Lineweaver-Burk-method the characteristic data of metabolism are determined, namely the maximal velocity of metabolizing beta PrOHmax as 2.5 mg/l min and the Michaelis-Menten-constant as 10 mg/l. An increase of the ethanol exposition causes a prolongation of the mean residence time of n-propanol in the body. This phenomenon is to be interpreted as the result of an inhibition of the n-propanol metabolism by ethanol. The inhibition constant KPrOHEtOH concerned with this process is determined experimentally and has a value of 0.1%.

1-Propanol↗
PubMed1984

[Acute polyneuritis in non-A, non-B hepatitis].

Neurologic involvement may occur in the course of acute viral hepatitis; acute polyneuritis is an extremely infrequent manifestation. Hepatic failure, leading to death on the 10th day of disease, became manifest in a 26-year-old man on the 6th day of postinfectious polyneuritis Guillain-Barré-Strohl requiring ventilation. Clinical aspects, additional diagnostic assessment and post mortem findings supported diagnosis of nonA-non-B hepatitis. A causal connection between both disease entities appears likely.

Acidosis↗
PubMed1982

[Ethanol clearance in the integrated tissue space].

Interchange of ethanol between the compartments of the body results from transport in a linked convection-diffusion system. This system can be described mathematically by dividing up the cardiac output in a shunt flow and a flow immediately mixed into the integrated solvent volume of the body. Experimental measurement shows that the ratio of shunt flow and mixing flow is nearly 1:1. Furthermore, this division allows a calculation of the arterial ethanol concentration from the venous one and an estimation of the quantity of ethanol diffused into the tissue volume.

Animals↗
PubMed1982

Compound action potentials in the peripheral nerve induced by shock-waves.

Projectiles hitting the human body cause shock waves spreading throughout the tissue. To verify a presumed interaction between these shockwaves and nervous tissue electrophysiological experiments have been performed showing the following results: 1. Compound action potentials (CAPs) are provoked in the peripheral nerves by the shockwaves. 2. The amplitude of the CAPs correspond to the magnitude of the shockwaves. 3. There is no electrical activity in the peripheral nerves below a certain threshold pressure. 4. "Saturation effect" is occurring beyond a certain pressure limit.

Action Potentials↗
PubMed1981

Shockwave-induced compound action potentials in the peripheral nerve.

To verify a presumed interaction between shockwaves arisen by impacts of high velocity projectiles and nervous tissue an electrophysiological experiment is performed with the following results: In peripheral nerves regular compound action potentials (CAPs) are provoked by shockwaves the amplitudes of which are increased corresponding to the pressure intensity of the shockwaves. The nerve shows no electrical activity below a certain pressure threshold (0.75 bar). Saturation of the CAP amplitude occurs beyond a pressure limit of 8 bar.

Animals↗
PubMed1981

The action of beta-adrenoceptor antagonist penbutolol on the pacemaker current of cardiac Purkinje fibres.

The action of beta-adrenoceptor antagonist penbutolol on the current underlying pacemaker activity in cardiac Purkinje fibres was analysed using the voltage clamp technique described by DECK et al. (1964). After the application of adrenalin, beta-blockers are able to counteract the well known shift of the s-kinetics of the pacemaker current. However, without any prior application of adrenalin the beta-blocker Penbutolol has no effect on these kinetics except for a small depression of the amplitude of the pacemaker current tails. The rectifier properties of the pacemaker current and the negative slope of the fully activated current voltage relationship of iK2 are unchanged. Penbutolol is able--even after a longer period of washout (about 60-90 min was necessary)--to protect the beta-adrenoceptors from the action of adrenalin (HASHIMOTO et al., 1979). These findings suggest that beta-blockers are competitive inhibitors of beta-stimulators and further support the notion that the pacemaker current in cardiac Purkinje fibres is controlled by beta-adrenoceptors.

Animals↗