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Biomedical subjects

N W Morrell

Publications and source records attributed to N W Morrell.

45 records · Page 3Linked to original sources
PubMed1994

Collateral ventilation and gas exchange in emphysema.

Resistance to collateral flow of gas is high in the normal human lung but may be lower in emphysema. However, the contribution of collateral ventilation to gas exchange in emphysema remains unclear. This study evaluates the role and magnitude of collateral ventilation between bronchopulmonary segments in six patients with clinical, functional, and computed tomographic evidence of emphysema, compared with our previous findings in 12 normal subjects. To assess collateral flow, a balloon-tipped catheter with a lumen that opened distal to the balloon was inflated in segmental bronchi during fiberoptic bronchoscopy. Respiratory gas tensions were sampled by mass spectrometer from beyond the occlusion via the catheter lumen. Subjects breathed air until occlusion was established and then switched to 79% helium/21% oxygen. The rate of rise of helium concentration was measured within occluded segments and used as an index of collateral ventilation. The mean (+/- SEM) rate of rise of helium concentration was ten times greater in emphysema patients (9.5 +/- 2.7%/min) compared with normal subjects (0.8 +/- 0.3%/min) (p = 0.009). The mean PO2 within occluded segments was similar in normal subjects and emphysema patients: 45.4 +/- 1.8 mm Hg and 44.8 +/- 3.6 mm Hg, respectively. Mean PCO2 within occluded segments was lower in patients (40.1 +/- 1.9 mm Hg) than in normal subjects (46.4 +/- 1.3 mm Hg), probably due to higher regional ventilation-perfusion ratios in emphysema patients rather than collateral ventilation. In emphysema patients there was a positive correlation between rate of rise of helium concentration and final PO2 within an occluded segment (r = 0.73; p = 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

The limitations of posterior view ventilation scanning in the diagnosis of pulmonary embolism.

In the diagnosis of pulmonary embolism some centres using 133Xe for comparison with multiple view 99Tcm perfusion images perform only single-breath posterior view ventilation scans. The purpose of this study was to test the reliability of the posterior view ventilation scan in the detection of lobar and segmental defects in ventilation. Occluding balloon catheters were placed in lobar and segmental bronchi during fibreoptic bronchoscopy to produce defects of known anatomical location and size in normal volunteers. Subjects breathed 81Krm/air during the occlusions and images were acquired in the posterior, posterior/oblique and lateral projections. The posterior view images were classified by three experienced nuclear medicine physicians as normal or abnormal. If abnormal, the observers were asked to state which lobe or segment was involved. Segmental defects were missed in 28% of scan readings. Segmental defects were detected but incorrectly sited in 50% of readings and correctly sited in only 22% of readings. The posterior view scan with a defect involving the entire lingula was judged to be normal by all observers. Defects involving the right and left lower lobes were underestimated. We conclude that ventilation scanning techniques that assess the distribution of ventilation in the posterior view alone are unreliable in the detection of segmental and lobar defects, and are likely to increase the false positive rate in the diagnosis of pulmonary embolism.

Administration, Inhalation↗
PubMed1993

Collateral ventilation and gas exchange during airway occlusion in the normal human lung.

The effectiveness of collateral ventilation in maintaining alveolar gas tensions in obstructed lung segments was investigated using fiberoptic bronchoscopy to place an occluding catheter-tip balloon in selected lobar and segmental bronchi in supine normal human subjects. Gas tensions from beyond the occlusion were measured with a respiratory mass spectrometer. Collateral ventilation is known to be minimal between lobes; therefore, values measured in obstructed lobes provide a control. No significant difference was found between the partial pressures of oxygen or carbon dioxide measured in obstructed lobes and in obstructed segments. In both cases respiratory gas tensions approached reported values for mixed venous levels. The time taken to attain a steady state of gas composition in the obstructed lung was rapid (approximately 50 s), and it was no different for lobes and segments. In addition, collateral ventilation was assessed by measuring the amount of helium reaching occluded lobes and segments when subjects breathed a mixture of 21% oxygen and 79% helium. The rate of rise in helium concentration was less than 1%/min in both lobes and segments, a figure that may be explained by delivery of helium in recirculated blood rather than by collateral ventilation. We conclude that intersegmental collateral ventilation has a negligible role in the maintenance of alveolar gas tensions in supine normal humans during tidal breathing.

Adult↗
PubMed1993

The underestimation of segmental defect size in radionuclide lung scanning.

Criteria used to place ventilation-perfusion lung scans into categories with different probabilities for pulmonary embolism depend largely on the size and anatomical distribution of defects recognized. These criteria assume that actual segmental defects appear segmental on the lung scan. This study examined the accuracy with which four experienced observers were able to estimate the size of defects of known anatomical location and size, using images of segmental defects in ventilation produced with a bronchoscopic technique and 81mKr. Of the 24 segmental defects produced in this study, 17% were interpreted as being < 25% of a segment; 23% were interpreted as being 25%-50% of a segment; 17% were interpreted as 50%-75% of a segment; 40% were interpreted as being 75%-100% of a segment and 4% were interpreted as being > 100% of a segment. Intra- and interobserver agreement as assessed by the Kappa statistic varied with the number of size categories used but was generally poor. Underestimation of defect size observed in this study may explain why many patients with pulmonary embolism do not have high probability scans. We conclude that the subjective impression of the size of a defect on a lung scan is an unreliable indication of a defect's true segmental or subsegmental nature and that scoring systems based on these criteria should be viewed with caution.

Bronchoscopy↗
PubMed1992

The anatomy of radioisotope lung scanning.

An appreciation of the appearances of segmental and lobar defects on a lung scan is important for the diagnosis of pulmonary embolism. The appearances of segmental and lobar ventilation defects of known anatomical location have been examined on 81mKr ventilation scans in normal human subjects, utilizing fibreoptic bronchoscopy to place temporary occlusions under direct vision at the orifices of lobar and segmental bronchi. Scans were obtained in the posterior, posterior-oblique and lateral projections. Anterior views were included if the defects could not be adequately visualized on the other views. The completeness of the occlusion and the site and size of each defect could be confirmed by ventilating the segment itself with 81mKr via the balloon catheter while the occlusion was maintained. Segmental defects located anterior to the hilum of the lung tended to be optimally visualized on the lateral view and defects located posterior to the hilum tended to be optimally visualized on the posterior-oblique view. The size of segmental defects could be underestimated on the lung scan, especially those involving the anterior and lateral basal segments of both lower lobes. Defects involving the medial basal segment of the right lower lobe were undetectable on any view. By implication, the same conclusions apply to 99mTc perfusion scans.

Adult↗
PubMedDate not supplied

Molecular and cellular basis of pulmonary vascular remodeling in pulmonary hypertension.

Clinical pulmonary hypertension is characterized by a sustained elevation in pulmonary arterial pressure. Pulmonary vascular remodeling involves structural changes in the normal architecture of the walls of pulmonary arteries. The process of vascular remodeling can occur as a primary response to injury, or stimulus such as hypoxia, within the resistance vessels of the lung. Alternatively, the changes seen in more proximal vessels may arise secondary to a sustained increase in intravascular pressure. To withstand the chronic increase in intraluminal pressure, the vessel wall becomes thickened and stronger. This "armouring" of the vessel wall with extra-smooth muscle and extracellular matrix leads to a decrease in lumen diameter and reduced capacity for vasodilatation. This maladaptive response results in increased pulmonary vascular resistance and consequently, sustained pulmonary hypertension. The process of pulmonary vascular remodeling involves all layers of the vessel wall and is complicated by the finding that cellular heterogeneity exists within the traditional compartments of the vascular wall: intima, media, and adventitia. In addition, the developmental stage of the organism greatly modifies the response of the pulmonary circulation to injury. This review focuses on the latest advances in our knowledge of these processes as they relate to specific forms of pulmonary hypertension and particularly in the light of recent genetic studies that have identified specific pathways involved in the pathogenesis of severe pulmonary hypertension.

Angiotensin II↗
PubMedDate not supplied

Genetic and molecular mechanisms of pulmonary hypertension.

Pulmonary arterial hypertension frequently occurs secondary to common cardiopulmonary diseases, and more rarely as a primary condition. Observations in animals and man have suggested genetic influences underlying the susceptibility to pulmonary hypertension. A gene underlying many cases of familial and apparently sporadic cases of primary pulmonary hypertension has now been identified, and a genetic approach to hypoxia-induced pulmonary hypertension promises to reveal new insights into the unique nature of the pulmonary circulation. The exploration of potential candidate genes influencing susceptibility and the identification of new genes promise new therapeutic approaches to the treatment of pulmonary hypertension.

Animals↗