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Tracheal obstruction can present insidiously or be acute and life threatening. This condition can occur acutely, as in cases of infection or foreign body aspiration, whereas posttraumatic tracheal stenosis or obstruction due to intraluminal tumor growth typically evolves more gradually. Tracheal stenosis secondary to intramural hematoma is exceedingly rare. We report a case of intramural tracheal hematoma causing obstruction following endobronchial ultrasound-guided transbronchial needle aspiration in a 69-year-old woman.
OBJECTIVE - The purpose of this article is to illustrate the usefulness and limitations of CT virtual endoscopy in the evaluation of large airway disease.
CONCLUSION - CT virtual endoscopy is a postprocessing tool that is easy to perform and that can aid in depicting disorders of the large airways without additional radiation or cost other than added time in postprocessing. The benefits of this technique include noninvasive diagnostic surveillance and preoperative planning.
Tracheal agenesis/atresia (TA) is a rare but fatal congenital disease in which the breathing tube fails to grow. The etiology of this serious condition remains largely unknown. We found that Bmp signaling is prominently present in the anterior foregut where the tracheal primordium originates and targeted ablation of Bmp4 (Bmp4(cko)) resulted in a loss-of-trachea phenotype that closely resembles the Floyd type II pathology, the most common form of TA in humans. In Bmp4(cko) embryos, tracheal specification was not affected; however, its outgrowth was severely impaired due to reduced epithelial and mesenchymal proliferation. In agreement, we also observed significant reduction in the expression of Cyclin D1, a key cell cycle regulator associated with cellular proliferation. However, the proliferative effect of Bmp signaling appears to be independent of Wnt signaling. Interestingly, we found significantly reduced expression of activated extracellular signal-regulated kinase (Erk) in the Bmp4(cko) ventral foregut, suggesting that Bmp signaling promotes Erk phosphorylation which has been associated with cellular proliferation. This study provides the first evidence linking Bmp signaling to tracheal formation by regulating the proliferative response of the anterior ventral foregut. Our finding sheds light on human tracheal malformations by providing a novel mouse model implicating Bmp signaling, non-canonical Erk activation and cellular proliferation.
BACKGROUND - Serum dipeptidyl peptidase IV (DPPIV) activity is decreased in some individuals with ACE inhibitor-associated angioedema. ACE and DPPIV degrade substance P, an edema-forming peptide. The contribution of impaired degradation of substance P by DPPIV to the pathogenesis of ACE inhibitor-associated angioedema is unknown.
OBJECTIVES - We sought to determine whether DPPIV deficiency results in increased edema formation during ACE inhibition. We also sought to develop an animal model using magnetic resonance imaging to quantify ACE inhibitor-induced edema.
METHODS - The effect of genetic DPPIV deficiency on peritracheal edema was assessed in F344 rats after treatment with saline, captopril (2.5 mg/kg), or captopril plus the neurokinin receptor antagonist spantide (100 mug/kg) by using serial T2-weighted magnetic resonance imaging.
RESULTS - Serum dipeptidyl peptidase activity was dramatically decreased in DPPIV-deficient rats (P < .001). The volume of peritracheal edema was significantly greater in captopril-treated DPPIV-deficient rats than in saline-treated DPPIV-deficient rats (P = .001), saline-treated rats of the normal substrain (P < .001), or captopril-treated rats of the normal substrain (P = .001). Cotreatment with spantide attenuated peritracheal edema in captopril-treated DPPIV-deficient rats (P = .005 vs captopril-treated DPPIV-deficient rats and P = .57 vs saline-treated DPPIV-deficient rats).
CONCLUSIONS - DPPIV deficiency predisposes to peritracheal edema formation when ACE is inhibited through a neurokinin receptor-dependent mechanism. Magnetic resonance imaging is useful for modeling ACE inhibitor-associated angioedema in rats.
CLINICAL IMPLICATIONS - Genetic or environmental factors that decrease DPPIV activity might increase the risk of ACE inhibitor-associated angioedema.
BACKGROUND - Though it is well known that cardiogenic and noncardiogenic pulmonary edema can cause changes in lung mechanics, actual alterations in tracheal diameter have not been described.
OBJECTIVE - To evaluate the effects of pulmonary edema induced by increased left atrial pressure (cardiogenic) and Perilla ketone (PK; noncardiogenic) on tracheal diameter in chronically instrumented awake sheep.
METHODS - We investigated the effects of two mechanistically distinct types of pulmonary edema on tracheal diameter in chronically instrumented awake sheep. Cardiogenic pulmonary edema (analogous to congestive heart failure in humans) was induced by increasing left atrial pressure ( upward arrowP(LA)) by inflating the balloon on a Foley catheter positioned in the mitral valve annulus to cause partial obstruction to flow across the valve (n = 18). Noncardiogenic pulmonary edema (increased pulmonary microvascular permeability pulmonary edema analogous to the acute respiratory distress syndrome in humans) was produced by the intravenous administration of PK (n = 11). Lateral chest radiographs (CXRs) were scored by a standardized 5-point scoring system for the severity of pulmonary edema, and tracheal diameter was measured at a fixed location in the carina. Three radiologists, blinded to sheep identification number and experimental protocol, evaluated the radiographs independently at different points in time for edema severity and tracheal diameter. The sheep were sacrificed immediately after the final CXR, and wet/dry lung weight ratio (W/D ratio) was determined.
RESULTS - Both upward arrowP(LA) and PK were associated with statistically significant tracheal narrowing ( upward arrowP(LA): 20.3 +/- 0.6 to 15.1 +/- 0.9 mm; PK: 20.2 +/- 0.6 to 14.1 +/- 1.4 mm). Tracheal narrowing correlated with the severity of the pulmonary edema determined radiographically ( upward arrowP(LA): r = -0.69, p < 0.01; PK: r = -0.62, p < 0.01) and by W/D ratio ( upward arrowP(LA): r = -0.64, p < 0.05; PK: r = -0.54, p < 0. 05).
CONCLUSIONS - We conclude that tracheal narrowing occurs in sheep models of both cardiogenic and noncardiogenic pulmonary edema and that the degree of narrowing correlates with the severity of the edema.
Copyright 1999 S. Karger AG, Basel