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Biomedical subjects

H R Wolf

Publications and source records attributed to H R Wolf.

At least 19 recordsLinked to original sources
PubMed1994

Efficacy and tolerability of etofibrate and gemfibrozil in combined hyperlipidaemia.

In a controlled clinical trial with a placebo prephase, the comparison of the two lipid-lowering drugs etofibrate and gemfibrozil showed no clinically relevant differences of lipoprotein profile modification in 50 patients with combined hyperlipidaemia. Under both treatments, there was a marked and significant reduction of triglycerides associated with a significant decrease of total cholesterol. In both treatment groups, the percent increase of high density lipoprotein HDL cholesterol was significantly correlated to the pretreatment levels of HDL cholesterol. Tolerance was better under etofibrate with no reported side effects compared to gemfibrozil with two reported cases of gastrointestinal side effects.

Cholesterol↗
PubMed1990

Expandable tubular stents for treatment of arterial occlusive diseases: experimental and clinical results. Work in progress.

The balloon-expandable vascular prosthesis consists of a flexible, knitted tantalum wire mesh tube. To demonstrate its pliability, this prosthesis was tested experimentally in 10 mongrel dogs by implanting it into the proximal femoral arteries. The maximum follow-up time was 1 year. On the basis of the experimental results, in which there was no relevant stenosis, occlusion, or migration of the vascular prosthesis, nine patients were treated: one with iliac artery occlusive disease and eight with superficial femoral artery (SFA) occlusive disease (four reocclusions after angioplasty and four unsatisfactory primary angioplasty results). One SFA lesion was treated with the crossover method from the contralateral side. All implants remained patent without hemodynamically significant stenoses, with the longest observation time being 6 months. Flexible, expandable vascular prostheses are promising adjuncts to angioplasty.

Aged↗
PubMed1990

Blood rheology and oxygen uptake.

Continuously measured oxygen uptake during constant work exercise (15' 50W) reveals increasing oxygen consumption in individuals with elevated blood viscosity parameters, indicating persistent contribution of anaerobic glycolysis during steady state exercise far below expected "anaerobic threshold". Improvement of viscosity parameters by prostaglandin E1--infusion (Prostavasin) 40 micrograms i.v., naftidrofurylhydrogenoxalat (Dusodril pi) 400 mg i.v. or hemodilution with 500 ml 6% hydroxyethylamylum MW 40000 (Onkohaes) in 5 patients results in significant reduction of this oxygen gradient in subsequent exercise test. Integrated VO2 during exercise above the mean value at rest or the quotient of VO2 during 15 min by VO2 during 30 min (including recovery time) are not differing significantly due to high variations inter- and intraindividually. Oxygen gradient during submaximal constant exercise permits direct clinical determination of microcirculatory performance in involved muscle tissue as a function of blood viscosity.

Adult↗
PubMed1988

[Percutaneously implantable balloon-inflatable vascular prostheses. Initial clinical results].

Restenosis and occlusion of atherosclerotic arteries are prevented by a newly developed arterial prosthesis consisting of a pliable and elastic wire mesh tube positioned to the balloon of an angioplasty catheter. As the balloon is inflated the prosthesis dilates and provides the arterial wall with a new mechanical support. This new device was successfully implanted in ten patients having an iliac artery stenosis and improved the therapeutic result of the preceding angioplasty. There were no complications.

Aged↗
PubMed1987

Serum alpha-tocopherol levels after high-dose enteral vitamin E administration in patients with acute respiratory failure.

Serum levels of tocopherols were measured in 5 healthy volunteers and in 14 patients with acute respiratory failure before and after onset of high-dose enteral vitamin E administration. The initial alpha-tocopherol levels did not differ between both groups (12.1 +/- 2.7 micrograms/ml in the volunteers and 11.3 +/- 3.5 micrograms/ml in the patients; mean +/- SD). After oral administration of 1 g d,l-alpha-tocopherylacetate per day the serum levels more than doubled within 1 day and reached a plateau between 22 and 30 micrograms/ml after 3 days in the volunteers. In contrast, application of even 3 g vitamin E/day by gastric tube in the patients with respiratory failure caused only a delayed increase of the serum levels with values nearly doubling after 5-10 days (6 patients), or there was no increase at all (8 patients). Serum alpha-tocopherol did not rise in patients without accompanying highmolecular weight formula diet and in patients with prolonged hemodynamic insufficiency and metabolic acidosis. The age of the patients, the fact of severe blood losses, hemodialysis and hemofiltration and the final outcome of death or survival appeared to be without influence on the response to enteral vitamin application. Neither in the volunteers nor in the patients with acute respiratory failure were there any detectable amounts of beta-, gamma- or delta-tocopherol or of alpha-tocopherolquinone or alpha-tocotrienol.

Acute Disease↗
PubMed1986

Generation of mediators by limited proteolysis during blood coagulation and fibrinolysis--its pathogenetic role in the adult respiratory distress syndrome (ARDS).

Products of blood coagulation and fibrinolysis, which are generated by limited proteolysis are able to effect the pulmonary circulation and gas exchange by biochemically mediated actions. Thrombin, fibrin and its degradation products provoke functional and morphological changes in the vessel wall. Fibrinopeptides, fibrin monomers and fibrin (ogen) degradation products induce vasoconstriction and vascular leakage. The vasoconstricting action of fibrin monomers is mediated by thromboxane A2 (TXA2) which is synthetized in the lung tissue itself. Thromboxane synthesis is stimulated by fibrin monomers only in the pulmonary circulation and not in the systemic circulation. Besides their vascular effects, fibrin monomers disturb the function of the surfactant components and increase the surface tension in surfactant monolayers. Proteinase inhibition as a general prophylactic and therapeutic concept with adult respiratory distress syndrome (ARDS) has to include the system of blood coagulation and fibrinolysis predominantly to prevent or stop the generation of products which are able to induce pulmonary vasoconstriction, vascular leakage and impairment of pulmonary gas exchange.

Animals↗
PubMed1985

Alteration of alveolar surfactant function after exposure to oxidative stress and to oxygenated and native arachidonic acid in vitro.

UNLABELLED: Alveolar surfactant is known to be impaired after inhalation of various oxidizing agents (NO2, ozone) as well as in inflammatory lung processes, in which leucocyte-derived active oxygen species or arachidonic acid oxygenation products may be involved. The effect of lipid peroxidation, oxygen-free radicals and oxygenated versus native arachidonic acid on the surface tension behaviour of natural surfactant was tested in vitro. The studies were performed on pooled surfactant material, obtained from bronchoalveolar lavage of rabbit lungs, in a Langmuir trough/Wilhelmy balance system. Initiation of lipid peroxidation with FeCl3/ascorbate or UV radiation and the generation of OH.(FeCl2/EDTA/H2O2), O2-. (xanthine/xanthine oxidase) and 1O2 (NaOCl/H2O2) provoked a common profile of changes: delayed reduction of surface tension during compression with an increase in minimal compressibility accelerated decrease of film pressure during expansion, reduction of hysteresis area and markedly augmented monolayer collapse rate. Addition of arachidonic acid resulted in decreased minimal compressibility, stability index and hysteresis area. Incubation with the arachidonic acid cyclooxygenase products, prostaglandin E2, I2, F2 alpha or thromboxane B2, with soybean lipoxygenase or with H2O2 and O2-exposure caused only moderate or no alteration of surfactant behaviour in vitro. CONCLUSION: oxidative stress, but not arachidonic acid oxygenation products, provoked altered surface tension behaviour of natural surfactant in vitro.

Arachidonic Acid↗
PubMed1985

Alteration of surfactant function due to protein leakage: special interaction with fibrin monomer.

In isolated rabbit lungs standardized amounts of edema were induced. Stimulation with the Ca ionophore A23187, leukotriene C4, Pseudomonas aeruginosa cytotoxin and human serum (activated complement) all resulted in protein leakage into the alveolar space with no change in the total phospholipid content. The pressure-volume characteristics of the lungs and the characteristics of the lavage surfactant (Wilhelmy balance) were markedly altered, correlating to the lavage protein content. The surfactant alterations were reproduced by addition of perfusion fluid protein to control surfactant in vitro. All changes were far less expressed or even missing in isolated lungs developing the same amount of edema due to omittance of proteins from the perfusion liquid. Different proteins added to control surfactant in the Wilhelmy balance showed a marked rank order of potency in interfering with surfactant function: immunoglobulins G and M and elastin less than albumin less than fibrinogen less than fibrin monomers. The fibrin monomer effect was reproduced by addition of thrombin to a surfactant fibrinogen mixture and was partly reversed by subsequent incubation with plasmin. In conclusion, high-permeability edema induced by different means results in alterations of lung mechanics and surface activity of lavaged surfactant, presumably due to protein surfactant interaction. Among different proteins, fibrin monomers are especially effective in interfering with surfactant function.

Animals↗
PubMed1983

Alteration of pressure-volume characteristics due to different types of edema induction in isolated rabbit lungs.

In a model of isolated, ventilated and perfused rabbit lungs the influence of a fixed amount of edema (standardized at 7 g weight gain/kg body weight) on the pressure-volume characteristics of the isolated lungs was investigated. Periodical stimulation with A 23187 or A 23187 plus indomethacin or A 23187 plus indomethacin plus glutathione evokes an increase in vascular permeability with subsequent severe alterations of the pressure-volume characteristics, reflecting a disturbance in the alveolar surfactant system, which is more extensive the more rapidly the edema develops. The alterations caused this way are markedly more severe than those caused by the same amount of weight gain due to mechanically increased capillary filtration pressure.

Animals↗
PubMed1982

Experimental and clinical results in shock lung treatment with vitamin E.

The adult respiratory distress syndrome (ARDS) is not confined only to late shock states but is a typical finding in intoxications with such oxidizing agents as O3, NO2, chlorate, or paraquat. Under experimental conditions, alpha-tocopherol in a high enteric dosage (2 x 50 mg/kg) was able to prevent alterations of pulmonary surface tension parameters (p less than 10(-5)) induced by microembolization of pulmonary vessels in awake rabbits. Parameters of gas exchange (PaO2' A-aDO2) were significantly less impaired (p less than 0.01) in the tocopherol group. Since there was no additional oxidative stress, the protective effect of tocopherol suggests an involvement of pathophysiologically occurring peroxidation mechanisms. Arachidonic acid (AA) metabolism is known to be a physiological oxygenation process yielding products with utmost biological efficacy. In a model of isolated, ventilated, and continuously perfused rabbit lungs, release or addition of AA resulted in an increase of pulmonary vascular resistance and permeability. The former could be ascribed to cyclooxygenase products, the latter to lipoxygenase products, of AA. The alpha-tocopherol effect in this model was a complex one: the antioxidative chromane structure (Trolox) as well as superoxide dismutase (SOD) decreased both pulmonary vascular resistance and permeability induced by AA metabolism dose dependently to a large degree, whereas the phytyl side chain augmented both effects. Pharmacological efficacy of high-dose alpha-tocopherol is not yet completely understood. Since 1977, we have applied all-rac-alpha-tocopheryl acetate (6-8 x 300-500 mg/day by gastric tube) to patients with manifest or threatening ARDS in addition to the required conventional complex therapy. Out of 176 patients being artificially ventilated for at least four days in the Internal Intensive Care Unit, Giessen University, 87 received tocopherol and 89 did not. There was no statistically valid stratification or randomization of the patients. In general, the tocopherol-treated patients were considered to have the worse prognosis, as is confirmed by higher maximum FIO2 and PEEP values. Thirty-four tocopherol patients (39%) and 15 nontocopherol patients (17%) survived. Surviving tocopherol patients were ventilated for a mean of 10.0 +/- 7.7 days (with maxima of 25, 28, and 41 days), whereas surviving nontocopherol patients were ventilated only for 5.5 +/- 1.1 days (none of these for more than 8 days). Absorption of alpha-tocopherol by these severely ill patients was shown by gas chromatography. A well-prepared clinical trial for tocopherol therapy of ARDS is suggested.

Animals↗