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H Nordmann

Publications and source records attributed to H Nordmann.

7 recordsLinked to original sources
PubMed1985

Grip strength test and infrared thermometry as non-invasive methods to complement acute toxicity data in mice.

Acute toxicity testing in-vivo seeks a new approach minimising the number of animals used and increasing the number of quantitative and qualitative observations. The measurement of grip strength of mice (forelimbs), a classical tool for the evaluation of muscular force and the emitted heat measurement, as a tool for evaluation of basic metabolism, have been used. The aim of acute toxicity was, up to now, to determine LD50 level or eventually a minimal lethal dose. These non-invasive tests give an idea of general health condition and allow the determination of the minimal toxic dose while in the search for the minimal lethal dose. A computer-assisted grip strength test and an infrared thermometry test have been developed and calibrated with Na+ pentobarbital, theophylline and diazepam given once orally or intraperitoneally to 10 male NMRI (MAI) mice/dose. The tests were performed within one hour after administration and daily until the values of the surviving animals went back to normal. Dose-response curves were obtained and plotted against control animals (n = 10). Oral and intraperitoneal administration in ascending doses of Na+-pentobarbital, theophylline and diazepam (i.p. only) up to the lethal level have a parallel influence on grip strength and heat emission; the correlation with mortality is clear for Na+-pentobarbital and diazepam but not for theophylline.

Animals↗
PubMed1985

Protective effects of O-(beta-hydroxyethyl)-rutosides (HR) against adriamycin-induced toxicity in rats.

Adriamycin (Adriablastine), administered weekly at the dose of 5 mg/kg i.p. for 3 weeks in rats, produced a general decrease of vitality associated with a decrease of body weight, hypothermia, decreases of stroke volume and cardiac output. Hematocrit was decreased. Renal blood flow decreased whereas pulmonary blood flow increased. Mean blood pressure and heart rate remained unaffected. Biochemical evaluations revealed a decrease of blood urea and serum creatinine, which might be related to decreased food intake and protein metabolism. Morphological changes in the heart tissue could not be appreciated. Venoruton (HR), administered at the dose of 300 mg/kg p.o. daily for 28 days (5 days before and 23 days after the first injection of adriamycin), improved adriamycin-induced clinical signs and symptoms (loss of body weight, hypothermia and decreased general vitality). It tended to increase cardiac output and stroke volume.

Animals↗
PubMed1984

Hemodynamic studies in acute venous stasis edema in rats.

An increase in venous pressure in the rat tail is known to result in acute edema. Acute venous stasis edema of the rat tail was induced by applying a force-controlled banding of standard tension (200 g) proximally for a period of 6-12 h. The hemodynamic changes of acute venous stasis edema were evaluated using non-invasive plethysmography, fluorescence angiography, computer thermography and invasive radioactive microsphere techniques. It is shown here that reduction of tail circulation to 40% of the control value is followed by prolonged vascular disorder characterized by genesis of reversible edema, increased total blood flow to the tail and decreased local cutaneous blood flow, without affecting the general hemodynamics. The cutaneous circulation (decreased blood flow) seems to be principally involved in the edemogenic response, whereas the deeper vessels (hyperemia) may or may not play a determinant role in acute experimental venous stasis edema in rats.

Animals↗
PubMed1984

Influence of 3-methoxy 5,7,3',4'-tetrahydroxyflavan (ME) on experimental periodontitis in the golden hamster.

Experimental periodontal disease was induced in golden hamsters by feeding the animals with a Keyes 2 000 diet. The aim of the present study was to investigate the effect of 3-methoxy 5,7,3',4'-tetrahydroxyflavan (ME), a flavanoid derivative, on periodontally induced changes by this diet which was fed ad libitum to half of the animals for 2 months prior to the start of drug therapy. The animals were then divided into 4 groups: A) control animals on normal diet; B) ME-treated (200 mg/kg 3 times a week i.p.) animals on normal diet; C) animals on Keyes 2 000 diet; D) ME-treated (200 mg/kg 3 times a week i.p.) animals on Keyes 2 000 diet. ME inhibited the diminution of bone volume as measured morphometrically. The growth of dental plaque as evaluated by a sensitive index (PII) appeared to be retarded by ME. The average PII in the ME-treated animals reached after 2 months of diet remained unchanged during the drug therapy period (4 months); whereas it was significantly increased in the group C hamsters. The biochemical data further suggest that the resorption process of the alveolar bone was decreased by ME.

Animals↗
PubMedDate not supplied

Mathematical modelling and quantitative methods.

The present review reports on the mathematical methods and statistical techniques presently available for hazard characterisation. The state of the art of mathematical modelling and quantitative methods used currently for regulatory decision-making in Europe and additional potential methods for risk assessment of chemicals in food and diet are described. Existing practices of JECFA, FDA, EPA, etc., are examined for their similarities and differences. A framework is established for the development of new and improved quantitative methodologies. Areas for refinement, improvement and increase of efficiency of each method are identified in a gap analysis. Based on this critical evaluation, needs for future research are defined. It is concluded from our work that mathematical modelling of the dose-response relationship would improve the risk assessment process. An adequate characterisation of the dose-response relationship by mathematical modelling clearly requires the use of a sufficient number of dose groups to achieve a range of different response levels. This need not necessarily lead to an increase in the total number of animals in the study if an appropriate design is used. Chemical-specific data relating to the mode or mechanism of action and/or the toxicokinetics of the chemical should be used for dose-response characterisation whenever possible. It is concluded that a single method of hazard characterisation would not be suitable for all kinds of risk assessments, and that a range of different approaches is necessary so that the method used is the most appropriate for the data available and for the risk characterisation issue. Future refinements to dose-response characterisation should incorporate more clearly the extent of uncertainty and variability in the resulting output.

Animals↗