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D Bee

Publications and source records attributed to D Bee.

43 records · Page 3Linked to original sources
PubMed1981

Serum concentrations of vitamin D-binding protein (group-specific component) in cystic fibrosis.

Vitamin D-binding protein (DBP) concentrations were determined in the sera of 90 cystic fibrosis homozygotes, 57 obligate heterozygotes, and 46 normal controls. Very significantly lower mean concentrations were found in the sera of CF homozygotes compared with both heterozygotes and controls (P less than 0.01, Wilcoxon Rank Sums Test). Subdivision of the samples by Gc phenotype showed that this relationship held true both in the Gc1 and Gc2-1 phenotypes. The small sample size of the Gc2 genotype makes the significance levels of limited usefulness, but the pattern of variation of DBP levels among CF homozygotes, heterozygotes, and controls was consistent with that observed for the Gc1 and Gc2-1 classes. Haptoglobin levels showed high coefficients of variation when compared among CF homozygotes, obligate heterozygotes, and controls, presumably because of nonspecific elevation in the acute-phase response. Alpha 2-macroglobulin levels were, if anything, slightly elevated in CF homozygotes compared with controls, while albumin levels showed no significant mean differences between these groups. Since the DBP concentration does not vary with age nor with levels of vitamin D and its metabolites, we interpret our results to mean that DBP levels are specifically decreased in cystic fibrosis, perhaps as the result of impaired glycosylation of the protein.

Adolescent↗
PubMed1981

Quantitative significance of hypoxic vasoconstriction in the ferret lung.

Stimulus-response curves for the pulmonary vascular bed to alveolar hypoxia have been measured in ferrets under conditions of perfusion either at constant pressure or a constant flow in vivo or in isolated lungs. In all circumstances the relationship between alveolar oxygen tension and the fall in blood flow or rise in pulmonary artery pressure was sigmoid although there were important differences between the in vivo and in vitro preparations. The significance of these observations in constant pressure and constant flow preparations in relation to pulmonary hypertension and ventilation/perfusion regulation is discussed.

Animals↗
PubMed1981

Mechanical properties and reactivity of vessels in isolated perfused lungs of chronically hypoxic rats.

1. Chronically hypoxic rats kept in 10% (v/v) O2 for 3--6 weeks, were compared with littermate control rats. Pulmonary vascular resistance, measured from the slope of the pressure-flow relationship in isolated lungs perfused with blood of normal packed cell volume was higher in chronically hypoxic than control rats even during normoxia. 2. Chronically hypoxic rats weighed less than control rats but their pulmonary vascular volume, measured with labelled albumin was similar to control rats. This, together with evidence that the number of precapillary vessels is not reduced, does not suggest a large reduction in the vascular bed in chronic hypoxia. 3. A greater vasodilator action of isoprenaline and adenosine in chronically hypoxic than control lungs suggested a higher normoxic vascular tone. This higher tone was not the sole cause of increased resistance in chronically hypoxic lungs, since maximal vasodilatation did not reduce resistance to control levels. The chief cause was probably encroachment of new muscle on the vascular lumen of small vessels. 4. Pulmonary arterial compliance was reduced in chronically hypoxic lungs. 5. Reactivity of vessels to ventilation hypoxia, over a wide range of oxygen tension, to angiotensin II (ANG II) and to adenosine 5'-triphosphate (ATP) was significantly greater in chronically hypoxic than control lungs, but thresholds to these stimuli were not reduced.

Animals↗
PubMed1980

The effects of vincristine on platelet aggregation studied by a filter loop technique in the rat.

1 A method for measuring aggregation of platelets of adenosine diphosphate (ADP) is described using a filter inserted into the flowing aortic blood in the rat. 2 Repeated infusions of ADP resulted in a fall in the calculated aggregation index without significant changes in the platelet count. 3 Vincristine (0.05 mg/kg) intravenously caused significant inhibition of ADP-induced platelet aggregation. 4 Infusion of ADP caused some peripheral vasodilatation though it is unlikely that this contributed to the effects seen to any great extent.

Adenosine Diphosphate↗
PubMedDate not supplied

Effect of almitrine bismesylate on breathing pattern during hypoxia/hypercapnia in rats and ferrets.

1. Ventilatory measurements and functional residual capacity (FRC) were recorded from anaesthetized rats and ferrets using a whole body plethysmograph. Simulation of aspects of human chronic obstructive airways disease (COAD) was attempted by making animals acutely hypoxic or hypoxic and hypercapnic by causing them to breath appropriate gas mixtures or by increasing the tracheal resistance or dead-space. Some chronically hypoxic rats, which have muscularized pulmonary arterioles similar to COAD patients, were also studied. 2. In 18 chronically hypoxic (CH) rats and 17 littermate control rats (C), breathing air, doses of almitrine bismesylate caused greater increases in ventilation (VE) in C than in CH rats. FRC, which was initially greater in CH rats, increased significantly in both groups after almitrine. 3. In C rats, breathing hypoxic or hypoxic/hypercapnic gas mixtures caused large increases in VE. Slow infusions of almitrine caused a further increase in VE usually via an increase in tidal volume (VT) but not frequency (f). 4. In two series of rats (n = 9; n = 6) severe and moderate degrees of tracheal obstruction caused a fall in PaO2 and a rise in PaCO2, a fall in VE due to both VT and f and large changes in oesophageal pressure (Poes), which often became positive on expiration. Almitrine infusions usually caused a rise in PaO2, a rise in VT and no change in f; with moderate obstruction, Poes also rose. The results were thought to depend on the balance between improved ventilation and increased O2 demand of the respiratory muscles. 5. Eleven ferrets were made hypoxic and hypercapnic by adding a large dead-space to the trachea. A slow infusion of almitrine caused a significant rise in PaO2 before any significant change in VE was detected; PaCO2 fell at some time during the infusion, but not significantly. The initial significant rise in PaO2, at 2.5 min, was not associated with significant changes in T1 (time of inspiration) and VT/TI. At 5 min VT/TI and PaO2 were all significantly altered. 6. Infusions of almitrine into hypoxic and hypercapnic animals caused improvements in the arterial oxygen tension which were associated with subtle changes in the breathing pattern; inspiratory time and inspiratory flow rate changed in the absence of an increase in total VE. Possible conclusions with respect to the action of almitrine in patients with COAD are discussed.

Airway Obstruction↗
PubMedDate not supplied

Action of almitrine on the pulmonary vasculature in ferrets and rats.

The action of almitrine on pulmonary vessels was studied under constant ventilation during normoxia and hypoxia. We used ferrets, in which one lobe of lung was perfused with venous blood at constant flow rate in vivo and isolated lungs perfused with blood at constant flow in both ferrets and normal and chronically hypoxic (three weeks in 10% O2) rats. Almitrine caused constriction of the relaxed vessels of normoxic lung. During hypoxic pulmonary vasoconstriction, when pulmonary artery pressure (Ppa) was raised, almitrine had a dual action; it caused further constriction followed by dilatation over a wide dose range (0.7-118 micrograms X kg-1 in ferrets). Similar effects were seen in normal and chronically hypoxic rats; the latter have narrowed muscularized arterioles like patients with chronic obstructive airways disease. Almitrine caused a larger rise in Ppa in normoxic than hypoxic rat lungs (7.9 instead of 1.7 mmHg; p less than 0.001) and dilatation followed constriction in the latter. Verapamil reduced both the constrictor action of almitrine and hypoxic vasoconstriction and there was a strong correlation between the effect of the two stimuli before and after verapamil (r = 0.9). Attempts to identify a substance which might cause the dilator action of almitrine were unsuccessful.

Almitrine↗