Therapeutic implication of genetic variants of IL13 and STAT4 in airway remodelling with bronchial asthma.

BACKGROUND: Several gene variants identified in bronchial asthmatic patients are associated with a decrease in pulmonary function. The effects of this intervention on pulmonary function have not been fully researched. OBJECTIVE: We determined the effects of high-dose inhaled corticosteroids (ICSs) on decreased pulmonary function in asthmatic Japanese patients with variants of IL13 and STAT4 during long-term treatments with low to mild doses of ICS. METHODS: In this study, 411 patients with bronchial asthma who were receiving ICSs and living in Japan were recruited, were genotyped, and underwent pulmonary function tests and fibreoptic examinations. The effects of 2 years of high-dose ICSs administered to asthmatic patients who were homozygous for IL13 AA of rs20541 or STAT4 TT of rs925847 and who progressed to airway remodelling were investigated. RESULTS: High-dose ICS treatment increased the pulmonary function of patients homozygous for IL13 AA of rs20541 but not of patients homozygous for STAT4 TT of rs925847. The increased concentrations of the mediators IL23, IL11, GMCSF, hyaluronic acid, IL24, and CCL8 in bronchial lavage fluid (BLF) were diminished after high-dose ICS treatment in patients homozygous for IL13 AA of rs20541. CONCLUSION AND CLINICAL RELEVANCE: IL13 AA of rs20541 and STAT4 TT of rs925847 are potential genomic biomarkers for predicting lower pulmonary function. The administration of high-dose ICSs to asthmatic patients with genetic variants of IL13 AA may inhibit the advancement of airway remodelling. The genetic variants of STAT4 TT did not respond to high-dose ICSs. Therefore, using medications other than ICSs must be considered even during the initial treatment of bronchial asthma. These genetic variants may aid in the realization of personalized and phenotype-specific therapies for bronchial asthma.

Evidence of acute inflammatory response in reexpansion pulmonary edema.

We analyzed edema fluid in two cases of reexpansion pulmonary edema during thoracotomy. High value of the fluid to plasma protein concentration ratio indicates an increase in pulmonary microvascular permeability. There were marked increases in polymorphonuclear leukocyte (PMN) count and concentration of PMN-elastase in edema fluid. There were also increases in concentrations of thromboxane B2 and 6-keto-PGF1-alpha in both edema fluid and plasma. These findings strongly suggest that the mechanism of reexpansion pulmonary edema is an inflammatory response and that PMNs in the reexpanded lung may play a role in the increase in permeability.

Migration of neutrophils from the lung into the pleural space after lung resection in humans and rabbits.

The origin of neutrophils that are found in pleural effusions after pulmonary resection is unknown. We measured neutrophil counts in pleural effusion sequentially for 48 h in patients who had undergone partial resection or pneumonectomy. Additionally, we measured neutrophil counts in the pleural effusions separately from the visceral pleura and parietal pleura in rabbits. In humans, we found that the maximum neutrophil counts in pleural effusion occurred more often in the patients who underwent partial resection (11.7 +/- 6.0 x 10(4) cells/microL) than in the patients who underwent pneumonectomy (3.7 +/- 1.2 x 10(4) cells/microL). There was no difference between neutrophil counts in blood of pneumonectomy group and that of the partial resection group. In rabbits, neutrophil counts were 1.5 times greater in the pleural effusion derived from the lung than in that derived from the parietal pleura. We conclude that movement of neutrophils occurs primarily from the lung into the pleural space after lung resection in humans and rabbits.

Prognostic assessment of 1310 patients with non-small-cell lung cancer who underwent complete resection from 1980 to 1993.

OBJECTIVE: The TNM staging system of lung cancer is widely used as a guide for estimating prognosis and selecting treatment modality. In 1997, the International Union Against Cancer and the American Joint Committee on Cancer have adopted a revised stage grouping for lung cancer. However, the validity of the new stage grouping has not been fully established. We investigated the prognoses of patients who had resection of non-small-cell lung cancer to confirm the validity of the revised classification. METHODS: A total of 1310 patients with non-small-cell lung cancer underwent complete resection and pathologic staging of the disease in our hospitals from 1980 through 1993. A pulmonary resection was performed with a systematic nodal dissection. The survivals were calculated with the Kaplan-Meier method on the basis of overall deaths, and the survival curves were compared by log rank test. RESULTS: There were significant differences in survival between patients with T1 N0 M0 and T2 N0 M0 disease and between those with T1 N1 M0 and T2 N1 M0 disease. However, there was no significant difference between patients with T2 NO M0 disease and those with T1 N1 M0 disease. No significant difference in survival was observed among patients with T2 N1 M0, T3 NO M0, and T3 N1 M0 cancer. Patients with different invaded organs of T3 subdivision (pleura, chest wall, pericardium, or diaphragm) had a different prognosis. There was no significant difference between patients with T3 N2 M0 disease and those with stage IIIB disease. CONCLUSIONS: We supported most of the revision, such as dividing stage I, dividing stage II, and putting T3 N0 M0 to stage IIB. Furthermore, we found some candidates for a subsequent revision, such as putting T3 N1 M0 to stage IIB, putting T2 N0 M0 and T1 N1 M0 together, regarding diaphragm invasion as T4, and putting T3 N2 M0 to stage IIIB.

Diagnostic results before and after introduction of autofluorescence bronchoscopy in patients suspected of having lung cancer detected by sputum cytology in lung cancer mass screening.

For the purpose of early detection, we have conducted population-based mass screening for lung cancer by sputum cytology since 1982. Although detection of lung cancer in its early stage is important for a good prognosis, it is often difficult to localize lesions in roentgenographically occult cancer. To clarify the role of autofluorescence bronchoscopy in localizing tumors in patients with roentgenographically occult cancer, we analyzed our diagnostic results. Fifty patients who had been detected by sputum cytology were screened by the light-induced fluorescence endoscope (LIFE)-Lung System from November 1997 to April 1999. We compared the results according to the screening methods: conventional bronchoscopy alone versus LIFE with conventional white-light bronchoscopy (November 1997 to April 1999). Twenty-eight cancerous lesions and 39 borderline lesions were detected by LIFE. Of the 39 borderline lesions, nine were detected only by LIFE. Multicentric lesions including cancer or dysplasia were also detected in 21 of the 50 patients by LIFE. The sensitivity by white-light bronchoscopy alone was 85.3%, whereas that of the LIFE-Lung System with white-light bronchoscopy was 94.1% (P=0.078). There were no cancerous lesions in the area observed as normal by LIFE. We also compared the diagnostic results of two localization methods: brushing of all bronchi (September 1986 to December 1990) and the LIFE-Lung System (November 1997 to April 1999). Although this was a historical comparison, the number of detected borderline lesions increased, which led to a high detection rate in patients with suspected-positive sputum (P=0.0006) by the LIFE-Lung System. In conclusion, the LIFE-Lung System is a safe and non-invasive system for detecting small intraepithelial lesions of the tracheobronchial tree. Autofluorescence bronchoscopy is more efficacious for localizing intraepithelial lesions and places fewer burdens on the patient than brushing of all bronchi.

Indirect estimate of perimicrovascular pressure rise in edema in isolated zone 1 lung.

To determine how liquid accumulation affects extra-alveolar perimicrovascular interstitial pressure, we measured filtration rate under zone 1 conditions (25 cmH2O alveolar pressure, 20 or 10 cmH2O vascular pressure) in isolated dog lung lobes in which all vessels were filled with autologous plasma. In the base-line condition, starting with normal extra-alveolar water content, filtration rate decreased by about one-half over 1 h as edema liquid slowly accumulated. We repeated each experiment after inducing edema (up to 100% lung weight gain). The absolute values and time course of filtration in the edema condition did not differ from base-line, i.e., the edema did not affect the time course of filtration. To compute the maximal initial and maximal change in extra-alveolar perimicrovascular pressure that occurred over each 1-h filtration study, we first assumed that the reflection coefficient is 0 in the Starling equation, then calculated perimicrovascular pressure and filtration coefficient from two equations with two unknowns. The mean filtration coefficient in 10 lobes is 0.063 g/(min X cmH2O X 100 g wet wt), and the initial perimicrovascular pressure is 3.9 cmH2O, rising by 4-7 cmH2O at 1 h. Finally we tested low protein perfusates and found the filtration rate was higher. We calculated an overall reflection coefficient = 0.44, a decrease in the initial perimicrovascular pressure to 1.9 cmH2O and a slightly lower increase after 1 h of edema formation, 2.2-6.6 cmH2O.

Alveolar liquid and protein clearance from normal dog lungs.

To determine whether liquid and protein clearance from the air spaces and lungs of anesthetized and unanesthetized dogs is the same as in sheep, we quantified these variables at three different time periods (4, 8, and 12 h) by instilling heparinized plasma (3 ml/kg) labeled with 125I-albumin into one lower lobe. Protein clearance, measured from the residual 125I-albumin in the lung homogenate, was slow and monoexponential (approximately 1%/h), similar to our previous data for protein clearance from the lungs in sheep. Lung liquid clearance in dogs, however, was 50% less than in previous experiments in sheep. Residual lung liquid (as percent of instilled) was 88.7 +/- 7.0 at 4 h, 70.5 +/- 9.1 at 8 h, and 64.0 +/- 5.8 at 12 h. At each time period, alveolar protein concentration increased by 0.6 +/- 0.4 g/dl at 4 h, 1.3 +/- 1.2 g/dl at 8 h, and 2.1 +/- 0.8 g/dl at 12 h. This increase in alveolar protein concentration was proportional to the volume of liquid removed from the lungs. beta-Adrenergic agonist therapy with terbutaline (10(-5) M mixed with the instilled plasma) doubled the volume of liquid cleared from the lungs over 4 h, and the alveolar protein concentration increased proportionally. However, lung liquid clearance in dogs that were treated with beta-agonists was proportionally (50%) less than in sheep treated with beta-agonists. The slower liquid clearance in dogs compared with sheep cannot be explained by differences in hemodynamics, pulmonary blood flow, anesthesia, mode of ventilation, or alveolar surface area.(ABSTRACT TRUNCATED AT 250 WORDS)

No gravity-independent gradient of blood flow distribution in dog lung.

The existence of a major gravity-independent gradient of blood flow in lungs has recently been described based on single photon emission computed tomography after intravenous injection of radioactively labeled macroaggregates. We wanted to test this hypothesis of a major gravity-independent gradient in lung blood flow in experiments with direct measurement of macroaggregate distribution in the dog lung. In six anesthetized (4 prone spontaneously breathing, 2 mechanically ventilated) dogs we injected 111In-labeled albumin macroaggregates intravenously. We killed the dogs, removed, inflated, and froze the lower lobes. We sliced the lobes 1 cm thick and made gamma camera images of the slices. We then cut three or four slices in each lobe into two or three concentric layers and measured the radioactivity per gram of tissue in a well-type gamma counter. In three of the dogs we also labeled the red cells (99mTc) so that blood volume in each sample could be determined. The gamma camera images were acquired on a 64 X 64 matrix with 4 X 4 mm pixels. On the numeric printouts from the individual slices we made two or three concentric layers and calculated activity per pixel in each layer. Neither by the well counting nor by the pixel analysis of the gamma scans did we detect any gravity-independent distribution of blood flow. With the well counting the distribution was the same whether macroaggregate activity was expressed per gram of tissue or per gram of blood-free tissue. We conclude that by direct measurements no major gravity-independent gradient of pulmonary blood flow can be detected in dog lungs.

Effect of catheter size on pressures recorded in small pulmonary veins in dog lung.

Controversy continues about the contribution of the veins to pulmonary vascular resistance. From data obtained in studies using intravascular catheters, it appears that a major fraction (up to 44%) of the total pulmonary vascular pressure drop resides in larger (greater than 1.0 mm diam) veins, whereas micropuncture data and various models give much less pressure drop. Theoretically, artifactual pressure drops can be obtained if an intravascular catheter partly obstructs the vessel. We made measurements of pressure in the same lung vein with two different-sized catheters (1.2 and 0.6 mm OD, respectively). In paired experiments the larger catheter always measured a higher pressure than the smaller one, except close to the large lobar vein outlet. In some of the experiments we measured the diameter of the vessel containing the indwelling catheter by freezing the lung and then serial-sectioned the frozen lung. From these data we could infer that the range of vein diameter in the which the smaller catheter measured a lower pressure was 1.5-4 mm. We conclude that the larger catheter overestimated the pressure because of greater obstruction. The pressures obtained with the smaller catheter suggest that little (less than 10%) of the total pulmonary vascular resistance resides in veins larger than approximately 1 mm diam under zone 3 baseline conditions.

Generation of oxidative stress contributes to the development of pulmonary hypertension induced by hypoxia.

Chronic hypoxia causes pulmonary hypertension and right ventricular hypertrophy associated with pulmonary vascular remodeling. Because hypoxia might promote generation of oxidative stress in vivo, we hypothesized that oxidative stress may play a role in the hypoxia-induced cardiopulmonary changes and examined the effect of treatment with the antioxidant N-acetylcysteine (NAC) in rats. NAC reduced hypoxia-induced cardiopulmonary alterations at 3 wk of hypoxia. Lung phosphatidylcholine hydroperoxide (PCOOH) increased at days 1 and 7 of the hypoxic exposure, and NAC attenuated the increase in lung PCOOH. Lung xanthine oxidase (XO) activity was elevated from day 1 through day 21, especially during the initial 3 days of the hypoxic exposure. The XO inhibitor allopurinol significantly inhibited the hypoxia-induced increase in lung PCOOH and pulmonary hypertension, and allopurinol treatment only for the initial 3 days also reduced the hypoxia-induced right ventricular hypertrophy and pulmonary vascular thickening. These results suggest that oxidative stress produced by activated XO in the induction phase of hypoxic exposure contributes to the development of chronic hypoxic pulmonary hypertension.

Superoxide possibly produced in endothelial cells mediates the neutrophil-induced lung injury.

BACKGROUND: The mechanism by which stimulated neutrophils (polymorphonuclear leukocytes [PMNs]) damage pulmonary vascular endothelium was investigated. METHODS: The ability of unstimulated and mechanically stimulated PMNs to adhere to pulmonary endothelial cells and, thereby, alter pulmonary vascular permeability was tested. Each series was conducted on 6 rats. To stimulate PMNs, they were agitated gently in a glass vial for 10 seconds. RESULTS: Perfusing lungs with the stimulated PMNs elicited a fivefold increase in permeability compared with lungs perfused with the unstimulated cells. This increase in permeability was blocked completely by preincubation of stimulated PMNs with CD18 monoclonal antibody. This increase in permeability was also blocked completely by superoxide dismutase (SOD) or the xanthine oxidase (XO) inhibitor allopurinol. Pulmonary vascular hemodynamics were unaffected by any treatment protocol. The accumulation of stimulated PMNs within the lungs was not inhibited by SOD but was partially blocked by allopurinol. CONCLUSIONS: These findings suggest that stimulated PMN-induced increases in pulmonary vascular filtration resulted from endothelial cell injury caused by superoxide anion possibly generated by XO, exclusively present in the endothelial cells.

MDM2 expression is associated with progress of disease and WAF1 expression in resected lung cancer.

Although MDM2, p21/WAF1, and p53 are considered as regulating each other based on in vitro studies, the relation in human lung cancer is not fully understood. The expressions of these proteins were examined immunohistochemically in 112 resected non-small cell lung cancer specimens and the correlation between them were analyzed. MDM2 was expressed in 45% of all lung cancers. In advanced stage, MDM2-positive cases were observed more frequently than in early stage, showing significant difference. No significant difference was observed in the prognosis of the patients regardless of the expression of any protein. Although no correlation was observed between MDM2 expression and p53 expression, or between p21/WAF1 expression and p53 expression, MDM2 expression was strongly related with p21/WAF1 expression. Therefore, MDM2 expression may relate to the progress of the stage of lung cancer, and MDM2 expression and p21/WAF1 expression may be associated not through the p53-related pathway.

Expression of Bcl-2, Bax, and p53 proteins in carcinogenesis of squamous cell lung cancer.

BACKGROUND: Apoptosis is regulated by many genes, including bcl-2, p53, and bcl-2 family genes. The expression of Bcl-2, p53, and Bax in very early lung cancers or precancer lesions is not been fully understood. MATERIALS AND METHODS: The expression of these proteins was examined immunohistochemically in 11 normal bronchial epithelia, 23 dysplasias, and 40 roentgenographically occult squamous cell lung cancers (ROCs). RESULTS: The expression of the Bcl-2 and p53 protein increased along with the advance of the morphological atypia in bronchial epithelial cells, whereas no difference in the Bax expression. The patients with Bcl-2 positive ROCs had a better prognosis than those with Bcl-2 negative ROCs. CONCLUSIONS: Bcl-2 and p53 proteins play important roles in early steps of carcinogenesis in squamous cell lung cancer of central type. The Bcl-2 protein could be a prognostic marker in ROCs.

Immunohistochemical study on tumor angiogenic factors in non-small cell lung cancer.

BACKGROUND: In order to elucidate the roles of tumor angiogenesis in lung carcinogenesis, the expressions of several angiogenic factors in lung carcinoma tissues were examined. MATERIALS AND METHODS: Tissue specimens from 112 cases of resected non-small cell lung cancer (NSCLC) were studied. The expressions of platelet-derived endothelial cell growth factor (PD-ECGF) and vascular endothelial growth factor (VEGF) were examined immunohistochemically. Microvessel density (MVD) was also evaluated. RESULTS: VEGF-positive cases were observed more frequently in advanced stage lung cancers than in early cancers, and VEGF-positive tumors had higher MVD than VEGF-negative tumors, while such differences were not observed for PD-ECGF. In squamous cell carcinoma, the patients with high-MVD tumor had significantly worse survival than those with low-MVD tumor. CONCLUSIONS: Our results suggest that VEGF plays an important role in angiogenesis of lung cancers, while the contribution of PD-ECGF may be limited.

Relaxation of human isolated pulmonary arteries by amrinone.

Amrinone, a selective phosphodiesterase III inhibitor, has been developed as a nonglycoside, noncatecholamine agent with positive inotropic effect. In this study, we examined the effect of amrinone on human pulmonary arterial strips in vitro to understand its action on human pulmonary circulation. Amrinone (10(-5)-10(-3) g/ml) caused dose-dependent relaxation of human pulmonary arterial strips precontracted with 60 mM KCl. Preincubation with either meclofenamate (3.1 microM), a cyclooxygenase inhibitor, or L-N(G)-nitroarginine (100 microM), a competitive inhibitor of EDRF/NO, failed to inhibit amrinone-induced pulmonary vasodilation. The cyclic AMP (cAMP) levels in the supernatant of the lung vessel homogenates increased after incubation with amrinone (10(-3) g/ml). These findings indicate that amrinone causes vasodilation of human pulmonary artery in vitro, and suggest a possible role for cAMP in the mechanisms of amrinone-induced pulmonary vasodilation. Because it is suggested that amrinone has not only positive inotropic effect but also pulmonary vasodilative effect in human in this study, we speculate that amrinone could be an useful agent for the treatment of an increase in right heart afterload and consequent pulmonary hypertension and right heart failure after lung resection in human.

A randomized trial of postoperative CDDP-based chemotherapy/chemoradiotherapy vs short-term immunochemotherapy in lung cancer.

BACKGROUND: Although a few reports indicated some benefit to survival, the effect of adjuvant therapy for the patients with resected lung cancer was still controversial. The aim of our study was to evaluate survival advantage of CDDP-based adjuvant therapy compared with short-term immunochemotherapy. EXPERIMENTAL DESIGN: prospective randomized trial. PATIENTS: from 1990 through 1994, 94 patients were registered. Forty-seven patients were randomly assigned to each group, i.e., CDDP-based therapy group (CB Group, CDDP+VDS+tegafur+OK-432 or CDDP+OK-432+mediastinal irradiation) or immunochemotherapy group (IC Group, tegafur+OK-432). PATIENTS in both groups were followed at 4-month intervals with the routine follow-up program of our department. RESULTS: No significant difference was observed between the patients' characteristics of two groups. Compliance of the regimen in each group was 79% in CB Group and 85% in IC Group. No treatment-related death was observed. Five-year survival rates of CB Group and IC Group were 49% and 51%, and 5-year disease-free survival rates were 46% and 44%, respectively. There were no statistical differences between the two groups. Furthermore, no survival differences could be found between CB Group and IC Group in any subgroup of patients. CONCLUSIONS: Both of these regimens were feasible. However, we have not observed any survival benefit in the CB Group in any subgroup, so far. Induction therapy, new chemotherapeutic agents, or anti-angiogenetic a agents may improve the survival of surgically treated lung cancer patients.

Vocal fold injection of collagen for unilateral vocal fold paralysis caused by chest diseases.

BACKGROUND: Patients having malignant chest diseases sometimes suffer from vocal fold paralysis. Treatment for vocal fold paralysis is important for such patients, because vocal fold paralysis causes lack of the versatility of the human voice which is essential for our communication. METHODS: Seventeen patients suffering from unilateral vocal fold paralysis were treated with vocal fold injections of collagen. Three patients received twice, and 20 treatments were conducted. A flexible bronchofiberscope was used under local anesthesia in order to observe the whole procedure of vocal fold injection. Using an injector and a long needle, collagen was injected with transcutaneous technique mainly through the cricothyroid membrane. The amount of collagen was determined with bronchoscopic findings. RESULTS: During and after treatment, no complication was observed. Of 20 treatments, a marked improvement was observed in 8, and moderate improvement was observed in 9 treatments. CONCLUSIONS: Vocal fold injection of collagen is a very useful and safe treatment for unilateral vocal fold paralysis caused by chest diseases.

Experience with fatal interstitial pneumonia after operation for lung cancer.

BACKGROUND: The number of patients with lung cancer is increasing. This study was undertaken to realize the probability, fate and management of acute fatal postoperative complications. Since interstitial pneumonia was one of the most fatal postoperative complications, to know its incidence and fate is very important. METHODS: A total of 2667 patients who underwent thoracotomy caused by malignant tumors during the past 17 years were reviewed and studied. We performed investigations on medical records, chest X-rays, whole-body CT films, operative records and pathological specimens for all inpatients. RESULTS: Nineteen patients died in hospital 30 days after thoracotomy (operative death). Nine patients died in hospital more than 31 days after thoracotomy (hospital death). Eight cases out of 28 patients (operative and hospital deaths) developed and finally died by interstitial pneumonia. Each case was treated with steroids, neutrophil-elastase inhibitor, and/or immunosuppressive agents. These patients could not be selected by any preoperative laboratory examination, such as preoperative pulmonary function tests, serum biochemistry tests, and chest X-ray or CT films. Interstitial pneumonia as a complication of postoperative stage, was fatal and once developed, it was very difficult to save their lives. CONCLUSIONS: Since we reported the cases who died from acute postoperative complications, especially interstitial pneumonia, we could not present effective management. However, in this report, several therapeutic trials that may solve the problems of acute postoperative interstitial pneumonia were proposed.

Functional evaluations for pulmonary resection for lung cancer in octogenarians. Investigation from postoperative complications.

We have reviewed the records of our twenty-four patients aged 80 years or older who underwent lung resections for bronchogenic carcinoma between 1983 and 1997 in our department. Eighteen patients were male and six were female. Adenocarcinoma was the histology in more than half of the cases (13 patients), along with 8 squamous cell carcinoma, 2 large cell carcinoma, and one small cell lung carcinoma. More than single lobectomy was performed in each patient. Unilateral pulmonary occlusion tests were employed in patients with impairment in pulmonary functions. Every patient, who underwent the unilateral pulmonary occlusion test, was certified that the total pulmonary vascular resistance index during unilateral pulmonary arterial occlusion test was less than 700 dyne.sec.cm-5.m2. Postoperative cardiovascular complications, such as paroxysmal atrial tachycardia, premature atrial contraction, premature ventricular contraction or atrial fibrillation, were seen in 10 patients. Postoperative respiratory complications, namely, sputa retention, retained secretions or atelectasis, were seen in 7 patients. The extent of dissection of mediastinal lymph node was not correlated to the postoperative pulmonary complications. However, the incidence of arrhythmias in the patients who received R2 mediastinal lymphnode dissection was much higher than in those who received R1 or R0 dissection. Complete blood counts and serum biochemical analysis performed at about three weeks after operations revealed leukocytosis and increases in levels of serum transaminase. These phenomena in leukocytosis and increases in the levels of serum transaminase in these patients were similar to those in younger patients. There was no operative death. We conclude that some patients over 80 years are candidates for lung resection after careful preoperative cardiopulmonary evaluation.

[Preoperative endovascular ultrasonography in lung cancer patient for detecting aortic wall invasion: a case report].

A 69-year-old man was admitted to our hospital because of left primary lung cancer. As tumor invasion to the descending artery was suspected, preoperative endovascular ultrasonography was performed. Part of the wall lacked respiratory movement. However, the wall of the descending artery was visualized as three layers, i.e., hyper-, hypo- and hyperechoic layers by sonography, so tumor invasion to the descending artery was diagnosed as negative. Although inflammatory tumor adhesion to the descending artery was found, left upper lobectomy was safely performed. Endovascular ultrasonography was considered to be useful in marking an accurate diagnosis of tumor invasion to the descending artery.