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Biomedical subjects

V Sill

Publications and source records attributed to V Sill.

At least 19 recordsLinked to original sources
PubMed1993

[Modification of nonspecific bronchial hyperreactivity to cold air hyperventilation and carbachol by nedocromil and budesonide].

In a double blind crossover trial we compared the effect of a four week treatment with inhaled nedocromil (4 x 4 mg/d) or budesonide (2 x 400 micrograms/d by spacer) on non-specific bronchial hyperresponsiveness (BHR) to cold air hyperventilation (CHV) and carbachol. 15 persons with clinically mild asthma, who showed a more than 50% decrease in sG(aw) after CHV were randomly allocated to treatment groups. A double dummy technique was applied. Before and after both treatment periods, which were separated by an out wash period of four weeks, BHR to isocapnic cold air hyperventilation and carbachol was determined on two consecutive days. 13 persons completed the study. Maximum percentual drop of sG(aw-) and FEV1-values after CHV, the number of steps of carbachol-provocation carried out to reach a decrease in sGaw of at least 50% and the calculated cumulative breath units (CBU) of carbachol to cause a 50% (20%) decrease in sG(aw) (FEV1) were assessed. Peak-flow values were registered throughout the study. Data were compared by means of Wilcoxon's matched-pairs signed-ranks test. After budesonide most parameter showed a significant decrease of BHR (CHV: sG(aw) p < 0.1; FEV1 p < 0.05; Carbachol: provocation-steps: p < 0.05; CBU: PD50 sG(aw) p < 0.05; PD20 FEV1 p < 0.05). There was no evidence for an influence of nedocromil on BHR (p-values all > 0.2). Comparing both treatments there was a difference in favour of budesonide partly reaching significance at 5% level. Budesonide but not nedocromil treatment showed a significant increase in peak-flow values (morning p < 0.02, evening p < 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

[The lung in heart diseases].

The effects of "hypocirculation" and "hypercirculation" of the lungs are small. Hypocirculation has an influence of the ventilation/perfusion ratio, and can thus contribute to hypocapnia. In the early stages, hypercirculation--in particular via a left-to-right shung, leads to an increase in diffusion capacity; after a course of many years, a "counter-situation" occurs. Progressive pulmonary hypertension, as is exemplified for mitral stenosis, leads to measurable restrictive and obstructive impairment of function, and possible to unspecific hyper-reaction, as also, over the long-term, to a diminishement in membrane diffusion capacity. Chronic left heart failure is characterised by interstitial oedema at the level of the alveolar and bronchial capillary beds. The results are measurable restrictions in the static volumes, and in particular of the obstruction parameters and the closing volume that involve the small airways. In the individual case, no statement as to the extent of left heart failure is possible. In the passive pulmonary hypertension phase, diffusion capacity increases; in the further course of the disease, with development of interstitial and alveolar oedema, it decreases again. In acute left heart failure, the persistance and/or extent of pulmonary oedema is not determined solely by the magnitude of the pulmonary venous pressure. Permeability oedema--brought about by mediators--would appear to be significant on the basis of animal experiments. Not infrequently, left cardiac failure leads to small pleural effusions which occur in combination with substantial atelectasia, the aetiology of which is unclear. Interpretation difficulties are caused by the clinical findings and function-analytical data obtained in patients with a combination of chronic lung disease and reducted volume storage capacity of the pulmonary circulation and of the left heart failure, a common situation in the elderly patient. Diminished pulmonary function parameters that fail to adequate respond to bronchodilators may be an expression of left ventricular failure.

Heart Failure↗
PubMed1982

[Alveolitis after inhalation of leather-impregnation spray (author's transl)].

After inhalation of leather-impregnation sprays in a confined space five patients developed acute and severe symptoms of alveolitis, with disorders of ventilation and diffusion as well as marked radiological changes. In one case without any treatment pulmonary fibrosis developed. In the other four immediate administrations of steroids produced complete healing. Inhalation of small amounts of leather-impregnation spray produced no changes in pulmonary function tests in volunteers. There were no similarities with forms of alveolitis produced by other noxious inhalation agents.

Adolescent↗
PubMed1978

Cyclic nucleotide metabolism in experimental bronchial constriction in rabbits.

In anesthetized, spontaneously breathing rabbits, intratracheally administered isotonic saline, acetylcholine (Ach) and histamine (His) induced an increase of airway resistance up to 183, 571, and 312%, respectively, compared with untreated controls. This was accompanied by a decrease of the arterial pO2. Bilateral cervical vagotomy led to nearly complete inhibition of the saline- and Ach-induced bronchoconstriction, whereas the His effect was only reduced to 202%. Vagotomy did not improve the arterial pO2. While the bronchoconstrictive effects of isotonic saline and Ach revealed a significant linear correlation with the increased cGMP/cAMP ratio, His did not cause an alteration of the cGMP/cAMP ratio to a degree that corresponds to its bronchoconstrictive activity. These data indicate that (1) bronchoconstriction-inducing agents may act (a) by stimulation of the parasympathetic nerve or (b) by contracting smooth muscles directly; (2) alveolar ventilation is not regulated by the parasympathetic nerve, and (3) bronchoconstriction induced by parasympathetic stimulation is associated with or mediated by an increase of the cGMP/cAMP ratio.

Acetylcholine↗