Search PubMed⌕ Search

Biomedical subjects

R Kraemer

Publications and source records attributed to R Kraemer.

At least 91 records · Page 5Linked to original sources
PubMed1989

Osmolality changes in nebulizer solutions.

Paradoxical effects (bronchoconstriction instead of bronchodilatation) have been reported after inhalation of beta2-mimetics in asthmatic children, and it has been suggested that this was due to osmolality and pH changes of the nebulizer solution. We tested commercially available nebulizer solutions and found osmolality changes after 5, 10 and 15 min of nebulization. Osmolality was measured in the nebulizer chamber and the airsteam of two types of jet nebulizers. When normal saline was nebulized chamber, from 282 +/- 7 mmol.kg-1 to 432 +/- 18 mmol.kg-1 resulted. Salbutamol ready made solution, and terbutaline respules were isotonic, whereas fenoterol, disodium cromogylcate (DSCG), beclomethasone dipropionate (BDP) and salbutamol (respirator solution 0.5%) were hypotonic (60-100 mmol.kg-1). When a mixture of sodium chloride (NaCl) and the drug solution (salbutamol, terbutaline, fenoterol) was nebulized for 10-15 min, the osmolality in the nebulizer cup increased to 420-500 mmol.kg-1. However, mixtures of the same beta 2-agonists with DSCG or with BDP remained hypo-osmolar. The same osmolality changes were present in the airstream. This study shows that after 10-15 min of nebulization osmotic changes occur in the nebulizer cup and airstream and that these changes differ according to the drug mixtures and the amount of the solution in the nebulizer chamber.

Adrenergic beta-Agonists↗
PubMed1989

[Etiopathogenetic aspects of allergic pulmonary diseases in childhood].

Anamnestic findings and clinical signs of wheezing attacks, which respond to beta-2-agonists, are the most important criteria in deciding whether a wheezy bronchitis is already a part of bronchial asthma. In this scope advanced lung function testing permits to search for functional abnormalities already in early childhood. Clinically, a study, carried out in ten ambulatory practices on about 1000 schoolchildren has shown that three diagnostic elements have to be distinguished. An "obstructive element" is based on the presence of clinical signs like cough, wheezing and rales. The "chronic element" is defined by the duration of the wheezing attacks and the number of attacks. Finally a third element, the "pulmonary hyperinflation" must clinically be recognized. The critical goals in the long term management of children with asthma are freedom of symptoms and optimal lung function. In this approach stratification into different aetiopathogenetic groups based on anamnestic, clinical and immuno-allergic findings is helpful and the follow-up of subclinical functional sequelae must be considered by repeated lung function tests. Only by these measures can the ongoing immuno-allergic process of airway inflammation be handled.

Adolescent↗
PubMed1988

Short-time response characteristics of salbutamol in infants with broncho-pulmonary diseases.

The effects of salbutamol 0.225 mg/kg given systemically on lung function in infants have been measured by whole-body plethysmography in 60 children with broncho-pulmonary diseases (24 after respiratory distress syndrome, 21 with wheezy bronchitis and 15 with cystic fibrosis). A therapeutic action was demonstrated in 74% of the tests, taking into account changes in end-expiratory resting level (state of inflation) and associated changes in airway resistance. There was a significant decrease in thoracic gas volume as an estimate of pulmonary hyperinflation, which was due to improved alveolar ventilation and to a consequential decrease in end-expiratory resting level. The improvement in airway resistance, as an estimate of airway obstruction, reflects a substantial relaxation of bronchial smooth muscle increasing the diameter of the airways. The extent to which similar results may be achieved by topical administration of nebulised beta agonists remains to be determined.

Airway Resistance↗
PubMed1988

Activated neutrophils release mediators that may contribute to myocardial injury and dysfunction associated with ischemia and reperfusion.

Neutrophils accumulate in the ischemic myocardium and exacerbate postischemic cardiac dysfunction and injury. The formation of lipoxygenase metabolites of AA, derived either directly from the neutrophils or by interactions with other blood elements or cells, may promote neutrophil-mediated injury. Recognition of the roles played by neutrophils and AA metabolites in reperfusion injury may lead to the development of new therapies that can be used in conjunction with thrombolytic drugs to reduce the complications associated with restoring blood flow to the ischemic heart.

Arachidonic Acid↗
PubMed1988

Dose-response relationships and time course of the response to systemic beta adrenoreceptor agonists in infants with bronchopulmonary disease.

The lung function response to three doses of salbutamol 0.075 mg/kg given at 10 minute intervals by gastric tube was studied in 31 infants aged 2-22 months with bronchopulmonary disease (eight after the respiratory distress syndrome, 15 with wheezy bronchitis, and eight with cystic fibrosis). Lung function was measured by whole body plethysmography. Seven of 31 infants had normal lung function and 10 of the remaining 24 had an increase in thoracic gas volume (TGV), 10 an increase in airway resistance (Raw), and four an increase in both the TGV and Raw. The response of TGV and Raw to salbutamol was analysed by circular statistics, enabling analysis of coupled, directional data. Thirty minutes after administration of the first dose of salbutamol there was a reduction in TGV or Raw in 21 of the 24 infants, 11 showing a decrease in TGV ("volume responder") and 10 a fall in Raw ("flow responder"). These results indicate that in most infants with bronchopulmonary disease an improvement in lung function can be documented after systemic administration of beta agonists if both TGV and Raw are measured.

Airway Resistance↗
PubMed1987

Leukocyte-derived metabolites of arachidonic acid in ischemia-induced myocardial injury.

Within minutes of occlusion of a major coronary artery the polymorphonuclear leukocytes (PMNs) are activated whereby they adhere to the vascular endothelium and migrate through the endothelial layer. Interactions with the endothelium can promote increased vascular resistance, diminished collateral flow, capillary blockade, and predisposition to vasospasm, as well as enhanced vascular permeability. On subsequent reperfusion entrapped leukocytes contribute to the no-reflow phenomenon, while more leukocytes gain access to the previously ischemic region. The leukocytes infiltrate the myocardium where they exacerbate the process of tissue injury and the development of arrhythmias. The release of leukocyte-derived mediators including arachidonic acid (AA) metabolites and oxygen-derived free radicals probably underlies these activities of the leukocytes. PMNs contain active lipoxygenase enzymes capable of metabolizing AA to products that are not normally found in the myocardium, and can dominate the metabolic profile of that tissue, leading to changes in myocardial integrity and function. Inhibitors of the lipoxygenase enzymes suppress the accumulation of leukocytes into the ischemic myocardium and reduce infarct size. However, because the drugs prevent cell invasion it cannot be inferred that a lipoxygenase metabolite per se is deleterious to the ischemic heart, inasmuch as any leukocyte-dependent mechanism of injury will be attenuated whether it is mediated by eicosanoids or by any other leukocyte-derived product. Additional studies with specific inhibitors/antagonists are required to determine the biochemical mechanisms underlying the different aspects of leukocyte-mediated myocardial injury.

Arachidonic Acid↗
PubMed1987

Efficacy of inhaled amikacin as adjunct to intravenous combination therapy (ceftazidime and amikacin) in cystic fibrosis.

Eighty-seven patients with cystic fibrosis were admitted to hospital with an acute exacerbation of pulmonary symptoms associated with isolation of Pseudomonas aeruginosa from sputum. The patients were randomly allocated to receive intravenously administered ceftazidime (250 mg/kg/day) and amikacin (33 mg/kg/day) alone or with inhaled amikacin (100 mg twice a day). Other aspects of the 2-week treatment were constant. The two therapy groups were comparable in all aspects. At the completion of therapy, the addition of aerosolized amikacin produced temporary eradication of P. aeruginosa in 70% of the patients, compared with 41% in the intravenous therapy only group (P less than 0.02). Suppression of P. aeruginosa in sputum cultures was correlated with the amikacin sputum concentrations. However, both regimens resulted in similar improvements in clinical, radiologic, laboratory, and pulmonary function measurements, and within 4 to 6 weeks most patients were recolonized with P. aeruginosa. There was no serious toxicity or adverse effect. In patients with cystic fibrosis, the addition of aerosol aminoglycoside to systemic antipseudomonal combination therapy is not clinically beneficial.

Acute Disease↗
PubMed1987

Myocardial salvage induced by REV-5901: an inhibitor and antagonist of the leukotrienes.

Lipoxygenase metabolites of arachidonic acid have been implicated in myocardial injury induced by coronary artery occlusion and reperfusion, as dual inhibitors of the lipoxygenase and cyclooxygenase enzymes, but not selective cyclooxygenase inhibitors, reduce infarct size. However, interpretation of these studies has been clouded by the lack of specificity of the drugs previously used. A specific 5-lipoxygenase inhibitor, REV-5901, has recently been developed. This drug inhibits A23187-induced immunoreactive leukotriene B4 generation by canine neutrophils (IC50 approximately 2.5 microM), and when given intravenously, attenuates the formation of a leukotriene D4-like material in blood ex vivo. The release of bioassayable leukotriene-like material from rabbit hearts infarcted in vivo and subsequently perfused in vitro is prevented by REV-5901. Moreover, the inhibitor also acts as an end-organ antagonist to prevent the spasmogenic effects of the peptide-containing leukotrienes in vitro with an IC50 approximately 0.1 microM. REV-5901 (10 + 2 mg/kg i.v.) reduces infarct size produced by coronary artery occlusion and reperfusion in the anesthetized dog from 56.6 +/- 2 to 28.6 +/- 3.7% of the hypoperfused zone. Salvage of the ischemic myocardium occurs independently of any apparent hemodynamic effect of the drug, but is accompanied by a diminution in neutrophil accumulation in the ischemic heart. It is proposed that inhibition of leukotriene B4 formation by REV-5901 suppresses the accumulation of neutrophils, thereby attenuating neutrophil-mediated cardiac damage.

Animals↗
PubMed1987

Effects of regular inhalation of beclomethasone dipropionate and sodium cromoglycate on bronchial hyperreactivity in asthmatic children.

The efficacy of beclomethasone dipropionate (BDP) was compared with sodium cromoglycate (SCG) and placebo in a double-blind parallel group study of 30 asthmatic children over a two-month period. All the three treatment groups received salbutamol concomitantly. Lung volumes, airway mechanics and the nonspecific bronchial hyperreactivity to carbachol were measured at the beginning and the end of the study. Two patients were excluded because of unequal clinical conditions at the entry and the end of the study and three because of lack of co-operation. Three patients (1 on SCG, 2 on placebo) dropped out because of worsening clinical symptoms. The improvement in airway mechanics shown by the group treated with BDP (n = 7) was significantly greater (p less than 0.01) than in the group treated with SCG (n = 8). Nonspecific hyperreactivity to carbachol improved significantly in the BDP group (factor 5.9) compared to the SCG group (factor 1.9). Childhood asthma seems to be better controlled by a combination of BDP and salbutamol, than by SCG and salbutamol.

Administration, Inhalation↗
PubMed1987

[Helium wash-in time as a critical factor in the determination of functional residual capacity in children].

The wash-in time (twi), defined as time until gaseous equilibrium between lungs and spirometer is reached during helium dilution rebreathing, and cumulative inspired volume (CIV) ventilated during this time were measured in 64 healthy children (30 boys and 34 girls, aged 6.5-14.7 years). The interrelationship between twi, CIV, respiratory frequency, tidal volume and lung growth was studied. Functional residual capacity (FRC) was compared with the plethysmographically determined thoracic gas volume. CIV is linearly related to standing height, and the ratio CIV/FRC is an age-independent constant (5.05 +/- 0.75). twi was found to be multi-linearly dependent of standing height and minute ventilation. A close relationship was found between FRC and thoracic gas volume (r = 0.94). It is concluded that FRC determination in children with lung disease should be standardized with respect to the predicted age-dependent twi for helium.

Child↗
PubMed1987

[Not Available].

Explore the source record for details and available documents.

Germany↗
PubMed1987

A neutrophil-derived cytochrome P450-dependent metabolite of arachidonic acid modulates neutrophil behavior.

Recently, the metabolism of arachidonic acid to two unidentified products (Peak 1 and Peak 2) by a cytochrome P-450 dependent mixed function oxidase has been described in canine polymorphonuclear leukocytes (PMNs). This study assessed the biologic activity of one of these metabolites, Peak 2, on PMN function. Peak 2 was formed biologically following addition of exogenous arachidonic acid to canine PMNs pretreated with BW755c to inhibit lipoxygenase and cyclooxygenase enzymes, and purified by high performance liquid chromatography following separation by column chromatography. Peak 2 (20-200 ng/ml) inhibited calcium ionophore A23187-induced aggregation and the second phase of LTB4-induced aggregation. Additionally, Peak 2 inhibited A23187-induced PMN adhesion to columns of Sephadex G-25. BW755c (94 microM), which increased the formation of Peaks 1 and 2 by almost 300%, also inhibited A23187-induced PMN adhesion. In contrast, Peak 2 did not inhibit the release of superoxide anions or immunoreactive LTB4, after stimulation of the PMNs with A23187. Thus, Peak 2 may modulate some activities of canine PMNs. Because the biologic activity of Peak 2 is opposite to that of LTB4, which promotes PMN aggregation and adhesion, and because LTB4 may be metabolized by a cytochrome P-450-dependent mixed function oxidase to less active metabolites, this enzyme system may play a central role in the control of PMN function.

4,5-Dihydro-1-(3-(trifluoromethyl)phenyl)-1H-pyraz↗
PubMed1986

[Epidemiologic aspects of bronchial asthma in childhood].

Bronchial asthma was studied in 813 children subdivided into 5 etiopathogenetic groups by lung function tests performed in the symptomfree "interval phase" of the disease. The patients were followed up for a 5-year period (1980-1984). 56% had continuous perennial asthma, 24% seasonal asthma, 14% infection-induced asthma, 3% psychogenic asthma and 3% exclusively exercise-induced asthma. With regard to functional abnormalities, 32% of patients presented with values within the range of normal, 23% showed pulmonary hyperinflation (FRC greater than 130% predicted), 42% had bronchial obstruction (Raw greater than 130% pred.) and 3% showed restriction of static lung volumes (TLC less than 80% pred.). 91 patients with perennial continuing asthma have been followed up under regular anti-asthmatic treatment over 2 years, during which at least 3 lung function tests have been performed. The study shows that asthmatic children must be evaluated according to the kind and degree of functional abnormalities and within certain age groups. Best improvement after treatment, mainly by inhalation of beta-2-mimetrics and mastcell stabilisators, and partly also by topical steroids, was found in the age groups 8-10 years and 11-13 years respectively. In spite of treatment asthmatic children showed an increase in bronchial constriction in the 5-7 year age group and an increase in pulmonary hyperinflation in the 14-16 age group. These two age groups seem to represent vulnerable periods in the development of childhood asthma which are determinant for the later prognosis.

Adolescent↗