[Surgical experience of idiopathic peripheral pulmonary arterial aneurysm; report of a case].

Peripheral pulmonary arterial aneurysm has rarely been reported, and although most cases show symptoms of hemoptysis. We experienced a case of idiopathic peripheral pulmonary arterial aneurysm in the asymptomatic period noted on medical examination. The patient was a 49-year-old man with coin lesion which was 15 mm in diameter in the right lower lung field on chest X-ray film at the 1st visit. It was strongly stained on enhanced computed tomography in the right S4 and continuity with the pulmonary arteries was suggested. The right middle lobectomy was performed under the diagnosis of peripheral pulmonary arterial aneurysm. Histological examination of the resected specimen revealed that the prominent thinning in the arterial wall, however, there was no evidence of specific chronic inflammation. The postoperative course was good. The patient has been well without new pulmonary arterial aneurysm for 2 years after the surgery.

[Squamous cell carcinoma of unknown origin affecting mediastinal lymph nodes].

A 65-year-old woman was admitted to the hospital because of an abnormal shadow on a chest X-ray film. Chest CT scans showed enlargement of the right mediastinal lymph nodes. However, no primary lesion was detected despite thorough examination. Mediastinoscopic biopsy revealed that the tumor was a lymph-node metastatic lesion of a squamous cell carcinoma of unknown origin. A thoracotomy was done and the mass was completely resected. Radiotherapy was given after the operation. We have followed the patient for 1 year since the operation, but no primary lesion has yet been detected. Metastasis of cancer of unknown origin to hilar or mediastinal lymph nodes is extremely rare, and only 6 cases have been reported previously in the Japanese medical literature.

[A case of bronchial neurinoma].

Neurinoma of the bronchial tree is extremely rare. We report a case of bronchial neurinoma involving a 21-year-old woman. The patient was admitted due to an abnormal shadow on chest X-ray, with cough and sputum production. Chest CT and MRI showed that the tumor arose from the left lower bronchus and bronchofiberscopic examination revealed complete obstruction of the lower bronchus by a polypoid tumor. A left lower lobectomy was performed based on the histological diagnosis of benign neurinoma and the postoperative course was uneventful. The tumor was 7.0 x 6.0 x 5.0 cm in size and had grown endobronchially without penetrating the bronchial wall. Pathological diagnosis was Antoni A type benign neurinoma. Since malignant or metastasized tumors have been reported in cases of tracheobronchial or intrapulmonary neurinoma, complete surgical resection of bronchial neurinomas should be performed.

Inhibition by a novel peptide leukotriene receptor antagonist ONO-1078 of airway wall thickening and airway hyperresponsiveness to histamine induced by leukotriene C4 or leukotriene D4 in guinea-pigs.

We studied the effect of intravenous administration of leukotriene (LT) C4 or LTD4 on airway responsiveness to histamine and airway wall thickening in guinea-pigs. Guinea-pigs were killed and the lungs were fixed in formalin. Slides from paraffin-embedded section of the lungs were stained and the airways that were cut in transverse section were measured by tracing enlarged images using a digitizer. Moreover, airway resistance (Raw) was determined by a pulmonary mechanics analyser and we calculated two indices, an index of airway wall thickening and the one of airway hyperresponsiveness to histamine, from changes of baseline-Raw and peak-Raw following intravenous administration of histamine before and after the intravenous administration of LTC4 or LTD4. The infusion of LTC4 or LTD4 induced an increase of the relative thickness of the airway wall in peripheral bronchi demonstrable by the histological examination. In analysis of airway function, intravenous administration of LTC4 or LTD4 induced airway hyperresponsiveness to histamine with airway wall thickening. The LTC4 and LTD4 receptor antagonist ONO-1078 inhibited these effects of LTC4 and LTD4, suggesting LTC4 and LTD4 may induce airway wall thickening and airway hyperresponsiveness through LTC4 and LTD4 receptors in the airways.

Inhibition by thromboxane antagonists of airway hyperresponsiveness to histamine induced by 13,14-dihydro-15-keto-PGF2 alpha in guinea-pigs.

We studied the effect of intravenous administration of 13,14-dihydro-15-keto-prostaglandin (PG) F2 alpha on airway responsiveness to histamine and airway wall thickening in guinea-pigs. Guinea-pigs were killed and the lungs were fixed in formalin. Slides from paraffin-embedded sections of the lungs were stained and the airways that were cut in transverse section were measured by tracing enlarged images using a digitizer. Moreover, airway resistance (Raw) was determined by a pulmonary mechanics analyser and we calculated two indices, an index of airway wall thickening and the one of airway hyperresponsiveness to histamine, from changes of baseline-Raw and peak-Raw following intravenous administration of histamine before and after the intravenous administration of 13,14-dihydro-15-keto-PGF2 alpha. Intravenous administration of 10 micrograms/kg 13,14-dihydro-15-keto-PGF2 alpha for 1 h did not induce an increase of the relative thickness of the airway wall by the histological examination. In analysis of airway function, intravenous administration of 10 micrograms/kg 13,14-dihydro-15-keto-PGF2 alpha for 1 h induced airway hyperresponsiveness to histamine without airway wall thickening. Thromboxane A2 (TXA2) receptor antagonists ONO-NT-126 and ONO-8809 inhibited the 13,14-dihydro-15-keto-PGF2 alpha-induced airway hyperresponsiveness to histamine, suggesting that the effect of 13,14-dihydro-15-keto-PGF2 alpha on bronchial hyperresponsiveness is likely to be mediated through TXA2.

[Bronchial hyperresponsiveness to histamine induced by intravenous administration of 13,14-dihydro-15-keto-prostaglandin F2 alpha in guinea pigs].

Prostaglandin F2 alpha (PGF2 alpha) has been suggested to play a role in the pathogenesis of bronchial asthma. In this study, the effects of intravenous administration of 13,14-dihydro-15-keto-PGF2 alpha, a stable metabolite of PGF2 alpha, on bronchial smooth muscle in guinea pigs were investigated by measuring dynamic respiratory resistance using a formula that excludes the effects of differences in airway wall thickness. With this formula, the ratio of bronchial smooth muscle constriction by histamine can be estimated as an index of bronchial hyperresponsiveness. Administration of 13,14-dihydro-15-keto-PGF2 alpha did not induce airway wall edema. The ratio of bronchial smooth muscle constriction by histamine was significantly enhanced by the administration of 13,14-dihydro-15-keto-PGF2 alpha. Moreover, TXA2 antagonists, ONO-NT-126 and ONO-8809, inhibited the effect of 13,14-dihydro-15-keto-PGF2 alpha administration. These results suggest that 13,14-dihydro-15-keto-PGF2 alpha can be important mediators affecting bronchial hyperresponsiveness, and TXA2 may play a part in the 13,14-dihydro-15-keto-PGF2 alpha-induced bronchial hyperresponsiveness.

Inhibition of bronchial hyperresponsiveness to histamine induced by intravenous administration of leukotriene C4 by novel thromboxane A2 receptor antagonists ONO-NT-126 and ONO-8809 in guinea-pigs.

We studied the effect of intravenous administration of leukotriene (LT) C4 on bronchial responsiveness to histamine and airway wall thickening in guinea-pigs. Guinea-pigs were killed and the lungs were fixed in formalin. Slides from paraffin-embedded sections of the lungs were stained and the airways that were cut in transverse sections were measured by tracing enlarged images using a digitizer. Moreover, airway resistance (Raw) was determined by a pulmonary mechanics analyser and we calculated two indices, an index of airway wall thickening and the one of airway hyperresponsiveness to histamine, from changes of baseline-Raw and peak-Raw following intravenous administration of histamine before and after the intravenous administration of LTC4. Intravenous administration of 3 microg/kg LTC4 for 1 hr induced an increase of the relative thickness of the airway wall in peripheral bronchi by the histological examination. In analysis of airway function, intravenous administration of 3 microg/kg LTC4 for 1 hr induced airway hyperresponsiveness to histamine with airway wall thickening. Thromboxane A2 receptor antagonists ONO-NT-126 and ONO-8809 inhibited the LTC4-induced airway hyperresponsiveness to histamine in a dose-dependent manner, but not the airway wall thickening induced by LTC4, suggesting that the effect of LTC4 on bronchial hyperresponsiveness is likely to be mediated through TXA2.

Inhibition of 9 alpha,11 beta-prostaglandin F2-induced bronchial hyperresponsiveness by thromboxane A2 receptor antagonists in guinea pigs.

We studied the effect of intravenous administration of 9 alpha,11 beta-prostaglandin F2 on bronchial responsiveness to histamine and airway wall thickening in guinea pigs. The infusion of 9 alpha,11 beta-prostaglandin F2 induced an increase of the relative thickness of the airway wall in peripheral bronchi demonstrable by histological examination. Analysis of airway function showed that the infusion of 9 alpha,11 beta-prostaglandin F2 induced airway hyperresponsiveness to histamine with airway wall thickening. The thromboxane A2 receptor antagonists, ONO-NT-126 (5(Z)-6-[(1R,2R,3R,4S)-3-(n-4-bromobenzenesulfonyl-aminomethyl) bicyclo[2.2.1]heptane-2-yl]hex-5-enoic acid) and ONO-8809 (n-decyl(Z)-6-[(1S,2S,3R,4R)-3-(4-bromobenzenesulfonylaminomethyl) bicyclo[2.2.1]hept-2-yl]-5-hexenoate), inhibited these effects of 9 alpha,11 beta-prostaglandin F2 in a dose-dependent manner.

[Effect of thromboxane A2 synthetase inhibitor (OKY-046) on leukotriene C4-induced airway hyperresponsiveness in guinea pigs].

In this study, we investigated the effects of peroral (p.o.) administration of a thromboxane A2 (TXA2) synthetase inhibitor, OKY-046, on the airway hyperresponsiveness (AHR) in guinea pigs induced by intravenous administration of leukotriene C4 (LTC4). A 3 micrograms/kg/hr LTC4 infusion induced airway wall thickening (AWT) and AHR to 1.8 and 3.6 micrograms/kg histamine bolus shot. OKY-046 100 mg/kg p.o. partially inhibited the AHR induced by LTC4 without inhibition of AWT. Previously, we have reported that LTC4-induced AHR was partially inhibited, to the same exert as by OKY-046, by TXA2 receptor antagonists, ONO-NT-126 and ONO-8809. These data suggest that intravenous administration of LTC4 generates TXA2, and TXA2 augments LTC4-induced AHR partially in guinea pigs.

[Effect of thromboxane A2 (TXA2) antagonists on bronchial hyperresponsiveness induced by intravenous administration of leukotriene C4 (LTC4) in guinea pigs].

Effects of TXA2 antagonists on bronchial hyperresponsiveness induced by intravenous administration of LTC4 in guinea pigs were investigated by measurement of dynamic compliance and dynamic respiratory resistance, using a formula to exclude the effects of changes in airway wall thickness. With the formula, the ratio of bronchial smooth muscle constriction by histamine can be estimated as an index of bronchial hyperresponsiveness to histamine. Administration of LTC4 induced airway wall edema. The ratio of bronchial smooth muscle constriction by histamine was enhanced by the administration of LTC4. TXA2 antagonists, ONO-NT-126 and ONO-8809, inhibited the increased ratio of bronchial smooth muscle constriction of LTC4. On the other hand, the antagonists showed no significant effects on airway wall edema by LTC4. These results suggest TXA2 may play a role in LTC4-induced bronchial hyperresponsiveness to histamine.

[Bronchial hyperresponsiveness to histamine induced by intravenous administration of 9 alpha,11 beta-prostaglandin F2 (9 alpha,11 beta-PGF2) in guinea pigs].

The effects of intravenous administration of 9 alpha,11 beta-PGF2, a stable metabolite of prostaglandin D2 (PGD2), on bronchial smooth muscle in guinea pigs were investigated by measurement of dynamic compliance and dynamic respiratory resistance using a formula to exclude the effects of differences in airway wall thickness. With this formula, the ratio of bronchial smooth muscle constriction by histamine can be estimated as an index of bronchial hyperresponsiveness to histamine. Administration of 9 alpha,11 beta-PGF2 induced airway wall edema. The ratio of bronchial smooth muscle constriction by histamine was significantly enhanced by the administration of 9 alpha,11 beta-PGF2a. TXA2 antagonists, ONO-NT-128 and ONO-8809, inhibited the effect of 9 alpha,11 beta-PGF2 administration. These results suggest that 9 alpha,11 beta-PGF2 act as important mediators affecting bronchial hyperresponsiveness, and TXA2 may play a role in 9 alpha,11 beta-PGF2-induced airway wall edema and bronchial hyperresponsiveness to histamine.

[Bronchial hyperresponsiveness to histamine induced by intravenous administration of leukotriene C4 (LTC4) and LTD4 in guinea pigs].

Leukotriene (LT) has been suggested to play an important role in the pathogenesis of bronchial asthma. In the present study, the effects of intravenous administration of LTC4 and LTD4 on bronchial smooth muscle in guinea pigs were investigated by measurement of dynamic compliance and dynamic respiratory resistance using a formula that excludes the effect of differences in airway wall thickness. With this formula, the ratio of bronchial smooth muscle constriction by histamine can be estimated as an index of bronchial hyperresponsiveness. Administration of LTC4 and LTD4 induced airway wall edema. The ratio of bronchial smooth muscle constriction by histamine was significantly enhanced by the administration of LTC4 and LTD4. Moreover, the LT antagonist ONO-1078 inhibited the effect of LTC4 and LTD4 administration. These results suggest that LTC4 and LTD4 can be important mediators affecting bronchial hyperresponsiveness.