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Biomedical subjects

T Wegener

Publications and source records attributed to T Wegener.

34 records · Page 2Linked to original sources
PubMed1992

Rapid onset of action of inhaled formoterol in asthmatic patients.

Twelve patients with stable asthma (mean age, 39 years; asthma duration, 11 years; mean forced expiratory volume in 1 s, 65 percent of predicted; and reversibility, 31 percent) were studied in a double-blind crossover trial. The patients were studied during three test days. Airway resistance and specific airway conductance (Raw and SGaw) were measured using a body plethysmograph and pulse rate, blood pressure, tremor, and subjective effects were recorded before and 1, 3, 5, 10, 15, 30, 60, and 120 min after the test doses. A baseline Raw variability of +/- 20 percent was allowed between the test days. Formoterol 12 micrograms, 24 micrograms, and terbutaline 500 micrograms were given in a spacer (Nebulator) in a randomized double-blind crossover manner as two puffs with a 30-s interval in between. The effect of formoterol 12 micrograms on Raw was significantly better than terbutaline after 3, 5, 10, 60, and 120 min. Formoterol 24 micrograms was significantly better than terbutaline as soon as 3 min after inhalation and at every point in time after that. Formoterol 24 micrograms tended to be better than formoterol 12 micrograms but the differences were not significant at any point in time. All three treatments were well-tolerated. No differences were observed for pulse rate, blood pressure, tremor, or palpitations. The overall onset of bronchodilatation after formoterol 12 and 24 micrograms was faster than after terbutaline 500 micrograms. The tolerability of formoterol was good.

Administration, Inhalation↗
PubMed1988

Lack of correlation between the grade of methacholine-induced bronchial hyperreactivity and ipratropium bronchodilation in asthmatics.

In 46 never-smoking randomly chosen patients with non-allergic asthma, 40 to 60 years old, a methacholine hyperreactivity test and lung function tests were performed after inhalation of different doses of ipratropium bromide (IB). The grade of hyperreactivity was measured as the cumulative dose of methacholine necessary to produce a decrease in the forced expiratory volume in one second of 20% of the lowest post-NaCl value (PD20). The following lung function tests were carried out: Lung volumes, ventilatory capacity including flow-volume curves, airway resistance and nitrogen single-breath wash-out test. The bronchodilator effect, measured as a change in the different lung function tests for different doses of IB given (0.08 mg, 0.15 mg and 0.25 mg), was correlated to the grade of hyperreactivity (PD20 dose). No or only a slight correlation was found between the grade of methacholine-induced hyperreactivity and the bronchodilator effects of the different doses of IB. These results indicate a lack of correlation between an anticholinergic bronchodilator effect and the grade of methacholine-induced bronchial hyperreactivity, or possibly an insensitivity of the above-mentioned methacholine test.

Adult↗
PubMed1988

N-acetylcysteine in paraquat toxicity: toxicological and histological evaluation in rats.

The therapeutic effect of N-acetylcysteine (NAC) in paraquat-treated rats was investigated. The animals were divided into four groups: A = control; B = NAC; C = paraquat; D = NAC + paraquat. In the appropriate groups, paraquat 20 mg/kg body weight was administered intraperitoneally and 1% NAC solution was provided as drinking water. All surviving rats were killed on the seventh day after paraquat exposure. The lungs were graded histologically on the basis of oedema and cellular infiltration. On histological examination, the lungs of poisoned rats that had received NAC displayed a tendency towards less oedema and cellular infiltration than those of poisoned rats not treated with NAC. It is concluded that NAC might afford some therapeutic effect against paraquat toxicity in rats.

Acetylcysteine↗
PubMed1987

Effect of ipratropium bromide aerosol on respiratory function in patients under ventilator treatment.

Twenty patients, 36-78 years old, with a history of chronic obstructive lung disease, and immediately after operation mostly for cardiac disease, were treated with ipratropium bromide (IB, 15 cases) or placebo (5 cases). A metered dose inhaler with a new adapter was used during postoperative ventilator treatment. In the IB group the heart rate did not change, but the inspiratory resistance decreased and the arterial oxygen tension increased. This is considered to indicate an effect not only on large but also on small airways, or an improvement of the ventilation/perfusion relationship. The investigation also demonstrated the practical usefulness of the new adapter.

Adult↗
PubMed1987

Effect of nebulized ipratropium bromide on lung function in nonallergic bronchial asthma.

The present investigation was performed on 64 randomly chosen never-smoking patients, 40-60 years old, with nonallergic bronchial asthma with an average FEV1 of 69-73% of predicted, a positive methacholine test, a normal serum IgE level, and a negative RAST or skin test to common allergens and not receiving oral steroid treatment. Sensitive spirometric tests were used to evaluate the dose-response effect of inhalation of 0.08, 0.15 or 0.25 mg of ipratropium bromide. The drug caused bronchodilatation with a nearly linear dose-response relationship for static lung volumes, while the total lung capacity was unchanged after this inhalation. Airway resistance decreased and specific airway conductance increased after all doses. Ventilation and flows were better after doses of 0.15 and 0.25 mg than after 0.08 mg. The intrapulmonary gas distribution improved only after inhalation of 0.25 and 0.15 mg. The currently recommended dose of 0.08 mg seems to be suboptimal for dilatation of both small and large airways.

Administration, Inhalation↗
PubMed1987

Effect of N-acetylcysteine on pulmonary damage due to microembolism in the rat.

The effect of N-acetylcysteine (NAC), a free radical scavenger, was investigated in a microembolism rat model of adult respiratory distress syndrome (ARDS). Microembolism was induced by an intravenous injection of bovine thrombin and an intraperitoneal injection of a fibrinolysis inhibitor, trans-4-aminomethyl-cyclohexane-carboxylic acid (AMCA). NAC counteracted the experimentally induced increase in lung weight, the development of alveolar oedema, and the amount of fibrin in precapillary vessels. There was also a tendency to a decrease of the experimentally induced interstitial oedema caused by the NAC treatment, although it was not statistically significant. Surprisingly, NAC reduced plasma viscosity in both experimental and control animals. It also seemed to increase PaO2 in animals with pulmonary damage, but had a lowering effect on PaO2 in control animals. The results indicate that NAC has a significant preventive effect in this microembolism rat model of ARDS, and that this effect may be achieved through decreased deposition of fibrin, thus counteracting pulmonary oedema, and a decrease in plasma viscosity.

Acetylcysteine↗
PubMed1986

Effect of N-acetylcysteine on fibrin deposition in the rat lung due to intravascular coagulation.

Intravascular coagulation was induced in rats by i.p. injection of a fibrinolysis inhibitor, tranexamic acid (AMCA, 200 mg/kg B.W.), and i.v. injection of bovine thrombin (500 NIH units/kg B.W.) and the fibrin deposition in the lungs was assessed with 125I-labelled fibrinogen. Treatment with N-acetylcysteine (NAC) partly prevented the deposition of fibrin in the lungs, and the disappearance of fibrinogen from the blood, but did not seem to influence the elimination of fibrin in the lungs. The results indicate that NAC may counteract pulmonary damage in this experimental model, by inhibiting intravascular fibrin formation.

Acetylcysteine↗
PubMed1985

Blood viscosity and finger systolic pressure in primary and traumatic vasospastic disease.

Vasospastic reactions to cold have been suggested to be related to altered blood rheology, as has been reported in both primary (PVD) and traumatic (TVD) vasospastic disease. Measurements of whole blood viscosity, plasma viscosity, erythrocyte deformability and finger systolic pressure (FSP) were performed in 18 patients with PVD (Raynaud's disease) and 15 patients with TVD. FSP at 10 degrees C was significantly lower in both patient groups than in a normal reference group. All rheologic variables at 37 and 10 degrees C were normal, apart from increased erythrocyte deformability at 37 degrees C in the PVD group.

Adult↗
PubMed1984

Blood viscosity, finger systolic pressure and effect of dazoxiben treatment in primary vasospastic disease.

Whole blood viscosity, plasma viscosity, erythrocyte deformability, and finger systolic pressure (FSP) were measured in ten patients with primary vasospastic (Raynaud's) disease before and after a controlled double-blind prospective trial involving dazoxiben (a thromboxane inhibitor, Pfizer). Five of the patients were assigned to dazoxiben and five to placebo. Before treatment, the FSP at 10 degrees C in the patient groups was significantly lower than that in a normal reference group, but all rheologic variables, measured at 37 and 10 degrees C, were normal. There was no significant correlation between FSP and rheology. Dazoxiben did not yield any subjective relief or give any objective effect.

Adult↗
PubMed1983

Serial pulmonary angiography in rats with pulmonary damage due to intravascular coagulation.

Serial pulmonary angiography was performed in 30 rats with pulmonary damage caused by injection of a fibrinolysis inhibitor, tranexamic acid (200 mg/kg body weight injected intraperitoneally) and bovine thrombin (500 NIH/kg body weight injected into the right atrium or ventricle). The degree of inhomogeneity of the capillary phase was graded and compared with that in a group of normal rats. Changes in the capillary phase were well correlated to other signs of lung trauma, namely increase in lung weight and microscopic occurrence of interstitial and alveolar oedema and of intravascular fibrin deposits. Increased lung weight similarly was found to be well correlated to increased interstitial oedema. It had also a distinct relationship to increased inhomogeneity of the capillary phase. The disturbance of the capillary phase may have been caused by mechanical blockage due to intravascular coagulation with microembolism, and interstitial oedema, vasospasm of precapillary arteries, or by arteriovenous shunting. Inhomogeneity of the capillary phase is consistent with a gross change in the ventilation/perfusion ratio, which could explain arterial hypoxaemia observed in other investigations.

Angiography↗
PubMed1979

Effect of nicotinic acid on the posttraumatic increase in free fatty acids and fibrinolysis inhibition activity in the rat.

Nicotinic acid effectively inhibited the posttraumatic increase in both free fatty acids (FFA) and fibrinolysis inhibition activity (FIA) in the blood in rats, indicating that FFA might be involved in the posttraumatic increase of FIA. The FIA in the liver was greater than that in other organs studied and was increased in the posttraumatic phase. The possible role of the liver in the posttraumatic increase of FIA is discussed.

Animals↗
PubMedDate not supplied

Etiology of human liver cancer: controlled prospective study in liver cirrhosis.

The incidence of primary liver cell carcinoma was investigated in a prospective study over 6 yr and 5 mo in 403 clinically unselected patients derived from a homogeneous population by means of serial determination of alpha 1-fetoprotein (AFP) by radioimmunoassay. The diagnosis of liver cirrhosis was proved in 90% by laparoscopy and/or histology and/or autopsy. The incidence of primary liver cell carcinoma in liver cirrhosis in the clinically studied patients was 4.47%, significantly lower than in the autopsy material (11.03%; p less than or equal to 0.025). In the follow-up study, all patients with increasing AFP concentrations exhibited a primary liver cell carcinoma. A transitory rise of AFP (higher than 50 ng/ml) was observed in 15.1% of patients with liver cirrhosis without primary liver cell cancer. In contrast to the results of animal experiments, this transitory rise of AFP was not followed by malignant transformation of the cirrhotic tissue. Posthepatitic liver cirrhosis was observed in 21.57%, postalcoholic liver cirrhosis in 42.93%, and cryptogenic liver cirrhosis in 27.30%. Liver cirrhosis of other etiology occurred in 8.19%. The incidences of primary liver cell cancer in these 4 groups were 4.94, 4.62, 5.45, and 0%, respectively. These differences are not statistically significant, although in absolute figures postalcoholic liver cirrhosis is the main cause of primary liver cell carcinoma in this sample from West Germany. HBs antigen-positive liver cirrhosis was more often associated with primary liver cell cancer than HBs antigen-negative liver cirrhosis (6.58 versus 3.96%); this difference also is not statistically significant. Observations of larger groups of patients may show a higher risk of developing primary liver cell carcinoma in those with a combination of alcohol abuse and HBs antigenemia and/or acute hepatitis in the history. Patients without these 2 risk factors had an incidence of primary liver cell carcinoma of 2.61%; those with 1 risk factor, 5.77%; and those with both risk factors, 10.71%.

Carcinoma, Hepatocellular↗
PubMedDate not supplied

Videodensitometry in rats with pulmonary damage due to microembolism.

Serial pulmonary angiography with videodensitometry was performed in 18 rats with pulmonary damage caused by administration of a fibrinolysis inhibitor, tranexamic acid (200 mg/kg body weight injected intraperitoneally) and bovine thrombin (500 NIH/kg body weight injected into the right femoral vein). The mean transit time (MTT) was calculated from videodensitometry, the observed area of interest consisting of approximately one-third of the right lung, including both central and peripheral parts. The impact of the pulmonary damage was analysed by morphologic methods and correlated to MTT. Although a pressure rise presumably occurred in the pulmonary circulation, no change in MTT was found after induction of pulmonary damage, indicating opening of actual and potential anastomoses between pulmonary arterioles and venules to serve as by-pass portions and as a safety-valve mechanism for the capillary bed and the right heart, respectively. Another explanation to unchanged MTT may be opening of resting capillary beds. Two rats with very severe pulmonary damage showed prolonged MTT. These rats may have suffered from cardiac failure.

Absorptiometry, Photon↗
PubMedDate not supplied

Computed chest tomography in rats with pulmonary damage due to microembolism.

Computed chest tomography was performed in 13 rats with pulmonary damage due to microembolism, caused by injection of thrombin (500 NIH/kg body weight) and tranexamic acid, a fibrinolytic inhibitor (200 mg/kg body weight), and in 9 control rats. The purpose of the investigation was to perform attenuation measurements at two levels of the right lung, each with three regions of interest (anterior, mid and posterior). Alterations in attenuation, compared with controls, were correlated with lung weight. Compared with controls, the attenuation was significantly increased in the anterior and posterior regions at both levels in animals with pulmonary damage, but not in the mid regions. There was a statistically significant correlation between increasing attenuation and increasing lung weight. A significant difference was found between damaged and control lungs regarding the microscopic grade of interstitial oedema, alveolar oedema and fibrin. Histograms of attenuation values in computed tomograms might be of value in detecting alveolar oedema. It is concluded that computed chest tomography is a good method for detecting pulmonary oedema at an early stage of experimental microembolism in the rat.

Animals↗