Yasushi Hoshikawa

We report a case of tracheal bifurcation injury with destruction of carinal cartilage in association with blunt chest trauma. A 29-year-old male truck driver arrived at the emergency room of a local hospital with subcutaneous emphysema of the neck. His truck crashed into a larger truck from behind after he fell asleep at the wheel. He was unrestrained and hit his mid-chest hard on the wheel. He was diagnosed with a tracheal bifurcation injury and was brought to our university hospital. Chest roentogenogram and CT showed pneumomediastinum. Preoperative flexible bronchoscopy showed a laceration of ∅8 mm at the carinal cartilage of the tracheal bifurcation, through which air bubbles came in and out. This was repaired by complete carinal resection followed by montage-type carinoplasty, since we were afraid that simple repair of the laceration with debridement may have resulted in dehiscence of the suture line or airway stenosis by hypertrophic granulation. The patient was discharged on the 29th postoperative day without any anastomotic problems. There has been no report to our knowledge of carinal resection and reconstruction for a tracheal bifurcation injury. We propose that for a tracheal bifurcation trauma with a widespread destruction of carinal cartilage carinal resection and reconstruction should be selected over simple repair with debridement.

There were 2, 632 lung cancer patients who underwent pulmonary resection during the period from 1953 to 1995. In the patients, 578 (22%) underwent non-curative resection (relatively non-curative 221, absolutely non-curative 357). Of the 578 patients, we examined clinico-pathological features of 56 patients (9.7%) who survived for over 5 years after operation (Group A), and compared the patients with all the 578 patients who underwent non-curative resection (Group B).<BR>In the 56 patients (Group A), diagnostic criteria of 18 patients who underwent absolutely non-curative resection were residual carcinoma on bronchial stump in 9 patients, malignant pleural effusion in 5, pleural dissemination in 2 and residual carcinoma on surgical margin in 2 patients. Diagnostic criteria of 38 patients who underwent relatively non-curative resection were lobectomy and R1 dissection in 9 patients, partial resection·segmentectomy·lobectomy and RO dissection in 21, R2b dissection and metastasis to the 2b level lymph nodes in 8 patients. Combined resected organs were pericardium, chest wall, left atrium, or parietal pleura, and there was no case whose tumor invaded large vessels, diaphragm and esophagus. There were significantly lower ratio of T3·T4 disease, and significantly lower ratio of N2 disease in Group A compared with in Group B. Most of the long-term survivals in Group A were at relatively earlier stage in Group B. Some of patients who underwent relatively non-curative resection were cases whose tumor were resected completely by partial resection·segmentectomy or R0 ·RI dissection.

There were 2, 632 lung cancer patients who underwent pulmonary resection during the period from 1953 to 1995. In the patients, 578 (22%) underwent non-curative resection (relatively non-curative 221, absolutely non-curative 357). Of the 578 patients, we examined clinico-pathological features of 56 patients (9.7%) who survived for over 5 years after operation (Group A), and compared the patients with all the 578 patients who underwent non-curative resection (Group B).<BR>In the 56 patients (Group A), diagnostic criteria of 18 patients who underwent absolutely non-curative resection were residual carcinoma on bronchial stump in 9 patients, malignant pleural effusion in 5, pleural dissemination in 2 and residual carcinoma on surgical margin in 2 patients. Diagnostic criteria of 38 patients who underwent relatively non-curative resection were lobectomy and R1 dissection in 9 patients, partial resection·segmentectomy·lobectomy and RO dissection in 21, R2b dissection and metastasis to the 2b level lymph nodes in 8 patients. Combined resected organs were pericardium, chest wall, left atrium, or parietal pleura, and there was no case whose tumor invaded large vessels, diaphragm and esophagus. There were significantly lower ratio of T3·T4 disease, and significantly lower ratio of N2 disease in Group A compared with in Group B. Most of the long-term survivals in Group A were at relatively earlier stage in Group B. Some of patients who underwent relatively non-curative resection were cases whose tumor were resected completely by partial resection·segmentectomy or R0 ·RI dissection.

To study the effects of subacute hypoxia on alveolar epithelial ion transport, alveolar fluid clearance was measured in isolated fluid-filled rat lungs. After instillation of a solution containing about 5% bovine albumin, an increase in alveolar fluid clearance was measured over 2 hours. Alveolar fluid clearance was lower when rats were kept in hypoxic conditions (FiO₂=0.1) for 48 hours. Neither 10^-5M amiloride (a Na⁺-channel blocker) nor 10^-3 M ouabain (an inhibitor of Na⁺-K⁺-ATPase) inhibited fluid clearance in the hypoxia group, but they did in the normoxia group. These results indicate that subacute hypoxia may down-regulate both the Na⁺-channl and Na⁺-K⁺-ATPase, and thus decrease the absorption of excess alveolar fluid.

To study the effects of subacute hypoxia on alveolar epithelial ion transport, alveolar fluid clearance was measured in isolated fluid-filled rat lungs. After instillation of a solution containing about 5% bovine albumin, an increase in alveolar fluid clearance was measured over 2 hours. Alveolar fluid clearance was lower when rats were kept in hypoxic conditions (FiO₂=0.1) for 48 hours. Neither 10^-5M amiloride (a Na⁺-channel blocker) nor 10^-3 M ouabain (an inhibitor of Na⁺-K⁺-ATPase) inhibited fluid clearance in the hypoxia group, but they did in the normoxia group. These results indicate that subacute hypoxia may down-regulate both the Na⁺-channl and Na⁺-K⁺-ATPase, and thus decrease the absorption of excess alveolar fluid.

Prostaglandin E₁ (PGE₁) has been shown to be a potent pulmonary vasodilator in humans and in many animals. The effects of PGE₁ on the development of pulmonary hypertension and on pulmonary vascular remodeling were studied in a rat monocrotaline (MCT) model of human pulmonary hypertension. By 3 weeks after injection, MCT (80mg/kg S. C.) had resulted in high values of mean pulmonary arterial pressure and of the ratio of right ventricular weight to left ventricle+septum weight (RV/LV+S). PGE₁ inhibited the development of pulmonary hypertension (300μg/kg) and right ventricular hypertrophy (300 and 100μg/kg) induced by MCT. Three weeks after the injection, the media walls of pulmonary arteries in lungs from rats given MCT were significantly thicker than those from lungs of control rats. PGE₁ (300, 100, and 30μg/kg) resulted in significantly less of this morphologic change, in a dose-dependent manner. These results indicate that PGE₁ inhibits the development of pulmonary hypertension associated with lung vascular thickening induced by MCT. PGE₁ may be useful for the treatment of pulmonary hypertension in humans.

Prostaglandin E₁ (PGE₁) has been shown to be a potent pulmonary vasodilator in humans and in many animals. The effects of PGE₁ on the development of pulmonary hypertension and on pulmonary vascular remodeling were studied in a rat monocrotaline (MCT) model of human pulmonary hypertension. By 3 weeks after injection, MCT (80mg/kg S. C.) had resulted in high values of mean pulmonary arterial pressure and of the ratio of right ventricular weight to left ventricle+septum weight (RV/LV+S). PGE₁ inhibited the development of pulmonary hypertension (300μg/kg) and right ventricular hypertrophy (300 and 100μg/kg) induced by MCT. Three weeks after the injection, the media walls of pulmonary arteries in lungs from rats given MCT were significantly thicker than those from lungs of control rats. PGE₁ (300, 100, and 30μg/kg) resulted in significantly less of this morphologic change, in a dose-dependent manner. These results indicate that PGE₁ inhibits the development of pulmonary hypertension associated with lung vascular thickening induced by MCT. PGE₁ may be useful for the treatment of pulmonary hypertension in humans.

We performed unilateral pulmonary arterial occlusion test (UPAO) for the preoperative evaluation of lung function in patients undergoing lung resection. In this test, the main pulmonary artery of either side is occluded to simulate postoperative functional status. In order to evaluate the right ventricular hemodynamic function, we measured right ventricular ejection fraction (RVEF) and right ventricular end-diastolic volume index (RVEDVI) throughout UPAO by thermodilution method. We investigated the relationships between changes in right ventricular hemodynamic function and postoperative complications related to cardiac functions, namely arrhythmias or heart failure. Thirty-four patients without heart disease prior to lung resection were examined by UPAO, and RVEF and RVEDVI were measured. Analyses demonstrated that changes in RVEF were inversely correlated with changes in RVEDVI. In 6 cases, RVEDVI increased from control by over 20% during UPAO. All of these patients had postoperative cardiac complications. The hypothetical ventricular function curves showed a large increase in RVEDVI relative to right ventricular stroke work index (RVSWI), suggesting a decrease in right ventricular function. In conclusion, these results suggest that changes in RVEDVI during UPAO may predict postoperative cardiac complications in patients undergoing pulmonary resection.

We performed unilateral pulmonary arterial occlusion test (UPAO) for the preoperative evaluation of lung function in patients undergoing lung resection. In this test, the main pulmonary artery of either side is occluded to simulate postoperative functional status. In order to evaluate the right ventricular hemodynamic function, we measured right ventricular ejection fraction (RVEF) and right ventricular end-diastolic volume index (RVEDVI) throughout UPAO by thermodilution method. We investigated the relationships between changes in right ventricular hemodynamic function and postoperative complications related to cardiac functions, namely arrhythmias or heart failure. Thirty-four patients without heart disease prior to lung resection were examined by UPAO, and RVEF and RVEDVI were measured. Analyses demonstrated that changes in RVEF were inversely correlated with changes in RVEDVI. In 6 cases, RVEDVI increased from control by over 20% during UPAO. All of these patients had postoperative cardiac complications. The hypothetical ventricular function curves showed a large increase in RVEDVI relative to right ventricular stroke work index (RVSWI), suggesting a decrease in right ventricular function. In conclusion, these results suggest that changes in RVEDVI during UPAO may predict postoperative cardiac complications in patients undergoing pulmonary resection.