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Biomedical subjects

B Wiggs

Publications and source records attributed to B Wiggs.

At least 19 recordsLinked to original sources
PubMed2000

Telelearning in a partnership between a university faculty and a regional health authority: benefits, challenges and strategies.

The University of Calgary's Faculty of Medicine and the Calgary Regional Health Authority understand that telehealth is an evolving field requiring both academic enquiry and operational readiness. Both parties are committed to quality educational programmes--the Faculty through its commitment to excellence and the Authority with its charge to maintain and enhance such programmes. There are shared applications, multi-learner user groups, shared strategies to overcome distances and shared infrastructure--technologies, communication pathways and resources. Having embarked on a joint telelearning venture, we have learned a number of lessons. Central to progress has been an appreciation and respect for unique mandates, a spirit of trust and flexibility, an agreement on a set of principles, ongoing communication between and participation from the users and, at times, redirection. Questions being answered include the following. How well is this collaborative model working? How functional is it at this time of health reform and restructuring? Can one meet complementary telelearning goals within a faculty-health authority relationship? These all have implications for future success.

Canada↗
PubMed1999

Effect of site and rate of contrast material injection on pulmonary vascular distention.

RATIONALE AND OBJECTIVES: The authors performed this study to determine if there were differences in vascular caliber measured on angiograms obtained with the injection protocol used for spiral computed tomography (CT) versus that used for pulmonary angiography. MATERIALS AND METHODS: The authors studied seven juvenile anesthetized pigs by using a prospective repeated measures experimental design. All pigs received injections of nonionic contrast material via catheters in the brachial vein, superior vena cava, main pulmonary artery, and left pulmonary artery. Weight-adjusted injection rates and volumes ranged from 0.05 mL/kg/sec (3.5 mL/sec, spiral CT protocol) to 0.56 mL/kg/sec (40 mL/sec, pulmonary angiography protocol). Heart rate and pulmonary artery and systemic artery pressures were recorded. During each injection, identically positioned pulmonary angiograms were obtained at full inspiration. Vessel diameters were measured at identical locations after each injection by two observers. The relationship between vessel diameter and hemodynamic parameters and injection site and rate was assessed with analysis of variance. RESULTS: At suspended full inspiration, no statistically significant difference (P > .05) in vessel diameter or hemodynamic parameters was found between the different injection sites or rates. There was no difference in vascular caliber between systole and diastole. CONCLUSION: The improved detection of subsegmental pulmonary emboli at pulmonary angiography compared with contrast material-enhanced spiral CT is not due to differences in vascular distention.

Angiography↗
PubMed1999

Comparison of the shear modulus of mature and immature rabbit lungs.

Maximal airway narrowing during bronchoconstriction is greater in immature than in mature rabbits. At a given transpulmonary pressure (PL), the lung parenchyma surrounding the airway resists local deformation and provides a load that opposes airway smooth muscle shortening. We hypothesized that the force required to produce lung parenchymal deformation, quantified by the shear modulus, is lower in immature rabbit lungs. The shear modulus and the bulk modulus were measured in isolated mature (n = 8; 6 mo) and immature (n = 9; 3 wk) rabbit lungs at PL of 2, 4, 6, 8, and 10 cmH(2)O. The bulk modulus increased with increasing PL for mature and immature lungs; however, there was no significant difference between the groups. The shear modulus was lower for the immature than the mature lungs (P < 0.025), progressively increasing with increasing PL (P < 0.001) for both groups, and there was no difference between the slopes for shear modulus vs. PL for the mature and the immature lungs. The mean value of the shear modulus for mature and immature rabbit lungs at PL = 6 cmH(2)O was 4.5 vs. 3.8 cmH(2)O. We conclude that the shear modulus is less in immature than mature rabbit lungs. This small maturational difference in the shear modulus probably does not account for the greater airway narrowing in the immature lung, unless its effect is coupled with a relatively thicker and more compliant airway wall in the immature animal.

Aging↗
PubMed1998

Recent trends in diagnosis and treatment of Clostridium difficile in a tertiary care facility.

BACKGROUND: With the prevalence of antibiotic use, the diagnosis and management of Clostridium difficile disease requires assessment. METHODS: In a retrospective review, patients with a positive culture, toxin, or both during 1 year were identified. Recent literature was reviewed. Results of culture and toxin, prior antibiotic use, antibiotic treatment history and cost were analyzed. RESULTS: Of 592 patients tested, 101 were positive; 96 of 101 were available for review. Of those positive tested for both, 45% were positive for toxin and culture. Sixty-two of 96 were treated with antibiotics; metronidazole was used in 90%. Ten of 62 antibiotic treatments were changed (mean 3 days). Ten days of metronidazole is 1/200th the cost of vancomycin. CONCLUSIONS: In 55% of the positive cases in which culture and toxin were obtained, one test was negative. As metronidazole's efficacy and cost compares favorably with vancomycin, metronidazole is the drug of choice. Any changes made to antibiotic regimens occurred prior to the 6 days recommended in the literature.

Adult↗
PubMed1998

Ultrastructure and tensile properties of human tracheal cartilage.

The cartilage of the walls of the trachea and bronchi acts to keep these airways open despite intrathoracic pressure differences during breathing that would otherwise collapse them and limit air flow. Changes in biomechanical properties and composition of airway cartilage may contribute to altered lung function in obstructive lung diseases. To investigate the relationship between collagen organization and equilibrium tensile modulus within the structure of airway cartilage, we used scanning electron microscopy (SEM), histochemistry and equilibrium tensile testing to analyze tracheal cartilage from 10 humans aged 17-81 yr. We show that the surfaces of tracheal cartilage matrix are collagen-rich and surround a proteoglycan-rich core. Collagen fibrils in the superficial zones are oriented in the plane of the cartilage surface. In deeper layers of the cartilage, collagen fibrils are oriented less regularly. Equilibrium tensile modulus of 100 microm thick strips of cartilage was measured and was found to decrease with depth; from 13.6 +/- 1.5 MPa for the ablumenal superficial zone to 4.6 +/- 1.7 MPa in the middle zone (means +/- S.D., n = 10, p < 0.001). Stress-strain curves were linear for strains up to 10% with minimal residual strain. This is consistent with a model in which collagen fibres in the outer layers of the cartilage resist tensile forces, and hydrated proteoglycans in the central zone resist compression forces as the cartilage crescent bends.

Adolescent↗
PubMed1997

Localization of leukaemia inhibitory factor to airway epithelium and its amplification of contractile responses to tachykinins.

1. In neural tissue, leukaemia inhibitory factor (LIF) is an important trophic cytokine. In this investigation, we determined if LIF was present in human and guinea-pig airways and examined the role of this cytokine in modulating airway responses to endogenous and exogenous tachykinins as well as muscarinic receptor and beta-adrenoceptor stimulation. 2. The presence of LIF in both human and guinea-pig airways was determined by immunohistochemistry. Guinea-pig tracheal explants were incubated in CRML-1066 media containing LIF (0.5, 5 or 50 ng ml-1) for periods of 3, 6, 24 and 48 h. Tracheal rings were then transferred to organ baths for measurement of isometric force in response to carbachol, capsaicin, the neurokinin1 (NK1) receptor agonist [Sar9,Met(O2)11]-substance P (SP), the NK2 receptor agonist neurokinin A (NKA) and isoprenaline. 3. LIF immunoreactivity was observed primarily in basally situated cells in the airway epithelium of both large and small airways. Less intense immunoreactivity was observed in vascular endothelium and glandular epithelium. 4. Treatment with LIF (0.5 ng ml-1) for 3 and 6 h significantly increased contractile responses to capsaicin by 42% and 43%, respectively, compared to time controls, whereas higher concentrations of LIF (5 and 50 ng ml-1) enhanced capsaicin-induced contractions only after 6 h. After 24 h, responses to capsaicin were not significantly different from 0 h control. Contractile responses to capsaicin following exposure to LIF at any concentration for 24 h were not significantly different from relative time control values. 5. Responses to [Sar9,Met(O2)11]-SP, carbachol and isoprenaline were not influenced by time in culture or by exposure to LIF for up to 48 h. Contractile responses induced by NKA were not influenced by 3 or 6 h exposure to LIF, but at 24 and 48 h the mean maximum contractile responses to NKA were significantly increased by 33% and 35%, respectively, compared to control. 6. These results demonstrate that LIF is present in guinea-pig and human airway epithelium, and modulates airway responses to tachykinins. In the acute setting LIF augments the capsaicin-induced release of endogenous tachykinins, whilst in the longer term (> 24 h), LIF increases airway smooth muscle responses to tachykinins via an NK2 receptor selective mechanism. We conclude that LIF may be an important effector molecule in the response of airways to injury or inflammation.

Animals↗
PubMed1997

Effects of anatomic variability on blood flow and pressure gradients in the pulmonary capillaries.

A theoretical model is developed to simulate the flow of blood through the capillary network in a single alveolar septum. The objective is to study the influence of random variability in capillary dimension and compliance on flow patterns and pressures within the network. The capillary bed is represented as an interconnected rectangular grid of capillary segments and junctions; blood flow is produced by applying a pressure gradient across the network. Preferred flow channels are shown to be a natural consequence of random anatomic variability, the effect of which is accentuated at low transcapillary pressures. The distribution of pressure drops across single capillary segments widens with increasing network variability and decreasing capillary transmural pressure. Blockage of one capillary segment causes the pressure drop across that segment to increase by 60%, but the increase falls to < 10% at a distance of three segments. The factors that cause nonuniform capillary blood flow through the capillary network are discussed.

Blood Pressure↗
PubMed1997

The effect of cigarette smoking on the bone marrow.

Chronic cigarette smoking produces a 20 to 25% increase in the number of peripheral blood leukocytes, and there is increasing evidence that these leukocytes are activated in the lung by the inhalation of cigarette smoke. The present study was designed to measure the effect of cigarette smoke inhalation on the rate of production and release of polymorphonuclear leukocytes (PMN) from the bone marrow into the peripheral blood. The thymidine analogue 5'-bromo-2'-deoxyuridine (BrdU) was used to pulse-label the dividing cells in the marrow of rabbits, measure their appearance in the peripheral blood, and calculate the time that PMN spend in the mitotic and postmitotic pools of the bone marrow. Comparison of animals exposed to 2 wk of cigarette smoke (n = 8) with sham-exposed controls (n = 9) showed that smoking decreased the mean transit time of PMNBrdU through the bone marrow from 97.3 +/- 3.0 h to 89.6 +/- 5.8 h (p < 0.001) by reducing the transit time of PMN in the postmitotic pool from 66.7 +/- 3.9 h to 53.7 +/- 0.7 h (p < 0.001). Both the mitotic (p < 0.05) and postmitotic (p < 0.05) pools of PMN increased in size following cigarette-smoke exposure. We conclude that chronic cigarette smoking stimulates the bone marrow, increases the size of the mitotic and postmitotic pools of PMN, and reduces the time PMN spend in the postmitotic pool in the marrow. These changes may contribute to the leukocytosis seen in cigarette smokers.

Animals↗
PubMed1997

Phagocytosis of small carbon particles (PM10) by alveolar macrophages stimulates the release of polymorphonuclear leukocytes from bone marrow.

Recent studies have shown that an increased concentration of ambient particulate matter (PM10) is related to decreased pulmonary function and respiratory and cardiovascular mortality. The mechanisms responsible for this excess mortality are unknown and the relationship between the level of PM10 and the circulating leukocyte counts has not been previously investigated. We postulated that the deposition of PM10 in the peripheral lung stimulates alveolar macrophages (AM), which results in polymorphonuclear leukocyte (PMN) release from bone marrow (BM). To test this hypothesis, either colloidal carbon (CC) (n = 3) or saline (n = 4) was instilled into the lungs of rabbits and PMN release from BM was evaluated by using 5'-bromo-2'-deoxyuridine (BrdU). CC instillation in the lung shortened the transit time of PMN through the BM to 71.0 +/- 6.9 h compared with the saline controls (85.5 +/- 2.8 h, p < 0.01). The role of AM in this response was further investigated by incubating isolated AM in tissue culture medium either with or without the presence of CC, and measuring the effect of the supernatants on the release of PMN from the BM. The supernatant of AM incubated with CC shortened the PMN transit time through the BM to 74.9 +/- 3.7 h (p < 0.05) compared with the supernatant from the unstimulated AM (98.6 +/- 1.9 h) and medium alone (94.3 +/- 3.7 h). We conclude that the phagocytosis of CC by AM releases mediators (cytokines) that stimulate the BM to release PMN. We speculate that these newly released PMN may play an important role in the decline in lung function and high mortality seen in populations exposed to high concentrations of atmospheric PM10.

Animals↗
PubMed1996

Polymorphonuclear leukocyte transit times in bone marrow during streptococcal pneumonia.

The release of polymorphonuclear leukocytes (PMN) from the bone marrow (BM) is a hallmark of acute inflammatory conditions. BM stimulation may increase the toxic potential of these newly released PMN and influence their behavior at inflammatory sites. The present study was designed to measure the transit time of PMN in the mitotic and postmitotic pools of the BM in rabbit using 5'-bromo-2'-deoxyuridine (BrdU). Blood samples were obtained at 2- to 24-h intervals from 24 to 192 h after a single BrdU injection, and BrdU-positive PMN (PMNBrdU) was detected as they appear in the circulating blood, using immunohistochemistry. The intensity of nuclear staining for BrdU was used to define a single generation of PMN and graded as either weakly (G1), moderately (G2), or highly (G3) stained. The mean +/- SE transit time of PMNBrdU through the BM was 95.6 +/- 3.6 h, with 51.1 +/- 5.9 h in the mitotic and 65.4 +/- 5.4 h in the postmitotic pool. Streptococcus pneumoniae instillation in the lung (n = 3) shortened the transit time of PMN through the BM to 54.0 +/- 2.6 h with a shorter time in both the mitotic (36.2 +/- 5.7 h) and the postmitotic pool 34.6 +/- 0.8 h). All these values were shorter than the control values (P < 0.05). We conclude that Streptococcus pneumoniae shortens the transit time of PMN in the mitotic and postmitotic pools in the marrow, which may result in the release of immature PMN with higher levels of lysosomal enzymes into the circulation.

Animals↗
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↗
PubMed1993

The predictive accuracy of home oximetry in patients with suspected obstructive sleep apnea.

To evaluate the predictive accuracy of home oximetry, we have performed a questionnaire, physical examination and home oximetry on 96 patients with suspected obstructive sleep apnea (OSA) within 2 weeks of laboratory polysomnography. We have developed a predictive equation that includes questionnaire, anthropometric and home oximetry data to diagnose OSA. We could confidently diagnose OSA in 20% of patients and exclude OSA in 5% of patients based on this prediction model and the population distribution.

Adult↗
PubMed1993

Comparison of neutrophil and capillary diameters and their relation to neutrophil sequestration in the lung.

Neutrophils [polymorphonuclear leukocytes (PMNs)] are sequestrated in the lung capillary bed because PMNs are delayed with respect to red blood cells (RBCs) as they pass through these microvessels. The present study examines circulating PMN size in relation to the distribution of capillary segment diameters in human, dog, and rabbit lungs and compares the shape of PMNs in suspension to that found within the pulmonary capillaries. The data show that 61, 67, and 38% of the capillary segments are narrower than the mean diameter of spherical PMNs in the rabbit, dog, and human, respectively. They also show that PMNs deform from a spherical to an ellipsoid shape in the pulmonary capillaries of all three species. These findings are consistent with previous studies showing that the pulmonary circulation restricts the passage of PMNs through the lungs and suggest that PMNs are delayed because they must deform to pass through restrictions encountered in the pulmonary capillary bed. We conclude that the discrepancy between PMN and pulmonary capillary size and the decreased deformability of PMNs with respect to RBCs are major determinants of the delay that PMNs experience with respect to RBCs in the pulmonary circulation.

Animals↗
PubMed1992

Neutrophil retention during a single transit through the pulmonary circulation.

Our laboratory has previously reported that 70-80% of polymorphonuclear cells (PMNs) are delayed with respect to erythrocytes (RBCs) in a single pass through the lungs of dogs, whereas only 5-15% of PMNs are delayed in a single pass through human lungs. Because these results were obtained using a direct blood sampling method in animals and an indirect gamma camera method in humans, the reported differences could be related to differences in measurement technique. The present study was designed to settle this question by comparing both techniques in a single species. The results show that the gamma camera technique previously used in humans underestimates the retention of PMNs with respect to RBCs during a single pass through the lung. They also show that this problem can be corrected by modifying the analysis of the data obtained using the gamma camera. We conclude that the pulmonary circulation retains PMNs with respect to RBCs to a comparable degree in animals and humans.

Animals↗
PubMed1991

Pulmonary hypertension induced by amosite asbestos: a physiological and morphologic study in the guinea pig.

Although there is increasing evidence that mineral dust exposure will produce obstructive lung disease, there is little information on the effects of mineral dust on the pulmonary vascular system. To examine whether exposure to amosite asbestos would affect the pulmonary vasculature and produce pulmonary hypertension, we instilled 5 mg amosite asbestor intratracheally into guinea pigs. After periods of 3 and 6 months, we examined their pulmonary and pulmonary vascular function, and compared these data to those obtained from groups of control animals. We found that, at both time periods, there was pulmonary arterial hypertension, with alteration of the vascular pressure-flow relationships. This was accompanied by abnormalities in the structure of the small pulmonary arterioles. The animals also showed airflow obstruction, with air trapping and an upward shift of the pressure-volume curve. There was evidence of emphysema, and the animals were moderately hypoxic. We found no consistent increase in inflammatory cells either in lavage or peripheral blood, and the histamine dose-response curves were similar in control and asbestos-exposed animals at 6 months. We conclude that intratracheal instillation of asbestos in the guinea pig produces pulmonary hypertension associated with modest hypoxia, emphysema, and airflow obstruction. Whether pulmonary hypertension reflects emphysema-induced hypoxia and loss of vascular bed, or is related to the brief but intense inflammatory infiltrate induced by asbestos, is unclear.

Animals↗
PubMed1991

Influence of weight on pulmonary function in the adult guinea pig.

We examined a group of 63 adult female Hartley strain guinea pigs with weight ranging from 625 to 1,200 g in order to ascertain whether pulmonary function tests including lung volumes, pressure-volume curves, and flow-volume curves were affected by the weight of the animal. We found that there was a weight effect on total lung capacity, vital capacity, residual volume, and the forced expiratory flow between 25 and 75% of total lung capacity, although there was no effect on other parameters of airflow. Flow-volume curves for each animal could be accurately fitted to a mathematical equation, and this equation did not vary with the animals' weight. Pressure-volume curves were affected by animal weight, but could be accurately fitted to a weight-corrected equation. We conclude that when pulmonary function tests are performed on adult guinea pigs, lung volumes may be altered in proportion to the weight of the animal. When pressure-volume or flow-volume curves are being considered, although weight can either be corrected for or has no bearing on the shape of the curve, there is a large between-animal variation, and it may be necessary to use large experimental groups when it is impossible to use the same animal as its own control.

Animals↗
PubMed1991

Oxygen consumption is independent of changes in oxygen delivery in severe adult respiratory distress syndrome.

We asked whether oxygen consumption is dependent on oxygen delivery in 17 patients who had severe adult respiratory distress syndrome (ARDS), 10 of whom had increased concentrations of plasma lactate. We determined oxygen consumption using analysis of respiratory gases while increasing oxygen delivery using blood transfusion. Oxygen consumption did not change after transfusion (from 227 +/- 83 to 225 +/- 82 ml/min, p less than or equal to 0.38). Oxygen delivery increased from 1,043 +/- 468 ml/min (24%, p less than or equal to 0.001). Even in the 10 patients who had increased concentration of plasma lactate and metabolic acidosis, oxygen consumption remained constant after increasing oxygen delivery (pretransfusion, 224 +/- 101 ml/min; post-transfusion, 225 +/- 99 ml/min; p less than or equal to 0.83). These data have more than 99% power of detecting a change in oxygen consumption of 20 ml/min after transfusion. Therefore, we conclude that directly measured oxygen consumption remains constant and independent of increases in oxygen delivery in our patients with severe ARDS. Because simultaneously determined oxygen consumption calculated from variables shared with the calculation of oxygen delivery yielded a dependent relationship, we speculate that finding dependence of calculated oxygen consumption on oxygen delivery may be the result of methodologic error.

Aged↗