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Biomedical subjects

L Verburgt

Publications and source records attributed to L Verburgt.

8 recordsLinked to original sources
PubMed2006

Short-term energy regulation of whitebellied sunbirds (Nectarinia talatala): effects of food concentration on feeding frequency and duration.

Avian nectarivores show compensatory feeding by adjusting their volumetric intake in response to variation in nectar concentration. This study used an infrared photo-detection system to investigate the short-term feeding patterns of whitebellied sunbirds (Nectarinia talatala) consuming three different sucrose concentrations (10, 20 and 30% w/w). Sunbirds increased their feeding frequency on the most dilute diet, but there was no change in feeding duration. Thus, the increase in total time spent feeding on the dilute diet was due to the increased feeding frequency. No difference in short-term feeding patterns was found between the 20% and 30% diets. Total time spent feeding was extremely short on all diets (96-144 s in every hour). Birds maintained the same steady increase in body mass over the course of the day on all three diets. Daily rhythms in feeding patterns were evident, with longer feeding duration and lower feeding frequency in the early morning and evening than during the rest of the day. Because ingestion rates on a particular diet may vary through the day, caution must be exercised in using feeding duration as a surrogate for meal size. Individual birds varied greatly in their feeding patterns irrespective of diet concentration.

Animals↗
PubMed1997

Bronchial vasodilatory response to ionic and nonionic contrast media.

It has recently been shown that bronchial arterial injection of conventional contrast medium causes a significant increase in bronchial blood flow (Qbr) and that this response is partially attenuated after infusion of N omega-nitro-L-arginine (L-NNA). However, the precise mechanism for this increase in Qbr is unknown. In this study we examined the effect of bronchial arterial injection of conventional ionic as well as nonionic contrast media. We measured Qbr in nine anesthetized, ventilated, open-chest sheep. Qbr was recorded before (baseline) and at the peak response to injection of 0.5 ml of either 0.9% saline (control; isosmolar with plasma), Omnipaque 300 (iohexol; nonionic), Conray 66 (sodium iothalamate; ionic), or 50% dextrose (viscous control). Measurements were made during a control period, after infusion of the alpha-agonist phenylephrine (5 x 10(-6) to 5 x 10(-7) M), and after bronchial arterial infusion of L-NNA (10(-2) M). The results were as follows: bronchial arterial injection of saline, Omnipaque, Conray, and dextrose caused an increase in Qbr (P < 0.05). During the control period, increases in peak Qbr on injection of saline, Omnipaque, Conray, and dextrose were 55 +/- 29, 112 +/- 62, 280 +/- 99, and 388 +/- 125% of baseline, respectively. Bronchial arterial infusion of L-NNA lowered baseline Qbr and partially attenuated the response to injection of saline, Omnipaque, and Conray (P < 0.05). Phenylephrine, in doses that decreased baseline Qbr to the same extent as did L-NNA, did not attenuate the bronchial vasodilation. There was a linear relationship between osmolality and the percentage increase in bronchial blood flow. We conclude that an osmolar stress is the trigger for the contrast-induced bronchial vasodilation and that the response is partially mediated by endothelial release of nitric oxide.

Animals↗
PubMed1996

Airway wall dimensions during carbachol-induced bronchoconstriction in rabbits.

Airway wall area is an important determinant of airway narrowing. We hypothesized that in cross-sectioned peripheral airways, the wall area internal to the outer smooth muscle border (inner wall area) would decrease and the airway wall area external to the outer smooth muscle layer (adventitial area) would increase during bronchoconstriction because of the relocation of blood and/or fluid between these compartments. To test this hypothesis, we used anesthetized open-chest rabbits and measured airway wall dimensions and smooth muscle shortening of membranous airways after carbachol-induced bronchoconstriction using morphometric techniques. Acute (3-min) and sustained (40-min) bronchoconstriction was induced by aerosol nebulization of carbachol and compared with saline treatment. After physiological measurements, the heart base was snared, and the lung and heart were excised en bloc and frozen by using liquid nitrogen while a transpulmonary pressure of 2 cmH2O was maintained. The lung was processed for light-microscopic examination by using a freeze substitution technique. Results show that adventitial area was significantly decreased after sustained but not acute bronchonconstriction. The mechanism of this change, which contradicts our hypothesis, is unclear. However, the decrease of adventitial area could increase rather than decrease the effect of lung parenchymal tethering and attenuate airway narrowing.

Administration, Inhalation↗
PubMed1996

Morphologic determinants of airway responsiveness in chronic smokers.

Nonspecific bronchial hyperresponsiveness (NSBH) occurs in asthmatics and in smokers who have airway obstruction. NSBH may be caused by different mechanisms in these conditions. We hypothesized that NSBH in smokers was a consequence of the structural changes that occur in chronic obstructive pulmonary disease (COPD) and lead to airway obstruction. We measured nonspecific bronchial responsiveness, assessed by PC20, in 77 smokers who had mild to moderate airflow obstruction prior to lung resection for a pulmonary nodule. We related airway responsiveness to baseline airway function (FEV1 % predicted), to functional (PLmax, PL90, and P-V curve shape) and morphometric (alveolar attachments) markers of lung elasticity as well as to thickening in small airways. Airway wall thickness, internal and external to the outer border of smooth muscle was quantified by plotting the square root of airway wall area versus a marker of airway size, airway internal perimeter (Pi). PC20 was significantly related to FEV1% predicted and PLmax. and when these functional parameters were controlled for, PC20 was also inversely related to airway wall thickness. There was also a trend for the most responsive patients to have fewer alveolar attachments per millimeter on the external perimeter of the airway walls. These data suggest that exaggerated nonspecific airway narrowing in COPD is secondary to structural changes caused by the disease.

Aged↗
PubMed1996

Human airway narrowing measured using high resolution computed tomography.

Exaggerated airway narrowing in response to bronchoconstricting stimuli is a characteristic feature of asthmatic subjects. It is unknown whether the site of airway narrowing differs in asthmatic subjects from that observed in normal subjects. Increased airway wall thickness has been suggested as a contributing cause for airway hyperresponsiveness in asthma, based on histologic measurements. We measured airway wall thickness and the site and magnitude of airway narrowing in response to inhaled methacholine in normal subjects and in patients with mild to moderate asthma using high resolution computed tomography (HRCT). After a comparable decrease in FEV1, there were no differences in the site or magnitude of airway narrowing for any category of airway size in asthmatic subjects and normals. However, the results show that the smaller airways of the asthmatic subjects are significantly thickened and that the airway wall area does not change after bronchoconstriction whereas it decreases in normal subjects. We conclude that airway wall thickening and the lack of a change in airway wall dimensions following bronchoconstricting stimuli could contribute to exaggerated airway narrowing in asthma.

Adult↗
PubMed1995

Endogenous nitric oxide influences acetylcholine-induced bronchovascular dilation in sheep.

To test whether endogenous endothelial nitric oxide (NO) influences baseline bronchial vascular tone and mediates acetylcholine (ACh)-induced bronchial vascular dilation and/or modulates bronchoconstriction in ovine airways, we studied anesthetized ventilated open-chest sheep and measured bronchial blood flow (Qbr) and pulmonary resistance (RL). In six sheep we measured the response of Qbr and RL to the dose of ACh required to produce 50% of the maximal increase in Qbr at baseline during infusion of the NO synthase inhibitor NG-nitro-L-arginine (L-NNA; 10(-2) M). Infusion of L-NNA decreased both the baseline Qbr (28 +/- 13 to 8 +/- 2 ml/min, P < 0.01) and the change in Qbr (delta Qbr) from the baseline value (84 +/- 42 to 33 +/- 18 ml/min, P < 0.05). There was no difference in baseline RL or in the response of RL to ACh at any time. In another six sheep, phenylephrine (5 x 10(-6) to 5 x 10(-7) M) decreased baseline Qbr (22 +/- 6 to 10 +/- 3 ml/min, P < 0.05) but not delta Qbr (62 +/- 13 to 66 +/- 21 ml/min, not significant). Infusion of L-NNA in these sheep decreased the baseline Qbr to a similar extent (11 +/- 5 ml/min) and also decreased delta Qbr (42 +/- 16 ml/min, P < 0.05). We conclude that endogenous endothelial NO influences baseline vascular tone and ACh-induced vasodilation of the ovine bronchial vasculature but has no effect on baseline RL or ACh-induced bronchoconstriction.

Acetylcholine↗
PubMed1995

Determinants of airway smooth muscle shortening in excised canine lobes.

There is marked heterogeneity of airway narrowing in intraparenchymal airways in response to bronchoconstricting stimuli. We hypothesized that this heterogeneity results from variations in the structure of the airway wall. Freshly excised dog lung lobes were inflated to transpulmonary pressures (PL) of between 5 and 15 cmH2O, and an aerosol containing a high concentration of carbachol was administered. The lobes were fixed and processed for light-microscopic examination and morphometric analysis of membranous airway dimensions. The relationships of smooth muscle shortening to PL and airway dimensions were analyzed using multiple linear regression. The results show that airway smooth muscle shortening was greater at lower PL and in airways with larger internal perimeter and a greater number of folds per internal perimeter and that it was less in airways with greater inner wall area. We conclude that the magnitude and variability of airway smooth muscle shortening and airway narrowing in response to maximal constricting stimuli are influenced by mechanical factors related to airway wall geometry.

Airway Resistance↗