Repair of a recurrent pseudoaneurysm of the ascending aorta in an atomic bomb survivor with myelodysplastic syndrome.

The occurrence of infective aortic pseudoaneurysms tends to be intractable and difficult to treat. We experienced a very rare case of a recurrent infective pseudoaneurysm in the ascending aorta that occurred after cardiac surgery in an atomic bomb survivor with myelodysplastic syndrome. The pseudoaneurysm was successfully repaired using a femoral artery autograft with an omentopexy and the patient recovered well without any recurrence.

Opposing effect of p38 MAP kinase and JNK inhibitors on the development of heart failure in the cardiomyopathic hamster.

OBJECTIVE: p38 MAP kinase (p38 MAPK) and c-Jun NH2-terminal kinase (JNK) have been implicated in the pathophysiology of heart failure. We investigated the effects of chronic treatment with p38 MAPK and JNK inhibitors on the development of heart failure in dilated cardiomyopathy (DCM) hamster heart. METHODS AND RESULTS: BIO14.6 hamster hearts showed markedly increased p38 MAPK and JNK activities at 6 weeks of age when there was no significant increase in the area of fibrosis, heart weight/body weight, left ventricular (LV) chamber dilation and LV dysfunction. p38 MAPK and JNK activities were attenuated at 26 weeks of age and abolished at 40 weeks of age in BIO14.6 hamster hearts. BIO14.6 hamsters and the control BIOF1B hamsters were chronically treated (i.p.) with the p38 MAPK inhibitors, SB203580 (1 mg/kg/day) and FR167653 (3 mg/kg/day), or the JNK inhibitor, SP600125 (1 mg/kg/day) or vehicle for 20 weeks starting from 6 weeks of age. Treatment of BIO14.6 hamster hearts with SB203580 and FR167653 reduced the number of TUNEL-positive myocytes, the area of fibrosis and heart weight/body weight associated with a significant decrease of LV dimension and an increase in LV ejection fraction and LV contractility compared to the vehicle-treated counterpart. In contrast, treatment with SP600125 increased the number of TUNEL-positive myocytes and the area of interstitial fibrosis associated with aggravation of LV chamber dilation and LV dysfunction. CONCLUSIONS: These results suggest that chronic treatment with p38 MAPK and JNK inhibitors produces opposing effects on the development of heart failure in the DCM hamster heart.

Dystrophin is a possible end-target of ischemic preconditioning against cardiomyocyte oncosis during the early phase of reperfusion.

OBJECTIVE: Dystrophin is a sarcolemmal membrane protein that prevents the myocyte from oncosis induced by physical stress. Because ischemic preconditioning (IPC) protects mitochondria and prevents oncosis during reperfusion, we hypothesized that dystrophin is an end-target of IPC distal to mitochondrial protection. METHODS AND RESULTS: Isolated rat hearts were subjected to 30 min ischemia followed by reperfusion. IPC was introduced by 3 cycles of 5 min ischemia and 5 min reperfusion. The loss of sarcolemmal dystrophin and myocardial ATP during ischemia was comparable between the control and the IPC heart. Similar changes in sarcolemmal dystrophin and myocardial ATP were observed when the heart was treated with 2,4-dinitrophenol (DNP), an uncoupler of mitochondrial respiration, or oligomycin, an inhibitor of mitochondrial F1F0-ATPase. However, the IPC heart increased sarcolemmal dystrophin during reperfusion associated with an increase in tetramethylrhodamine ethylester (TMRE) uptake, an indicator of mitochondrial membrane potential (DeltaPsim), and myocardial ATP and inhibited myocyte oncosis. The increase in myocardial ATP and relocalization of dystrophin to the sarcolemma mediated by IPC was inhibited by treatment with DNP or oligomycin during reperfusion. In vitro experiments demonstrated that mitochondria isolated from the ischemic IPC heart increased ATP generation and facilitated relocalization of dystrophin from the insoluble to the soluble fractions in a manner sensitive to DNP and oligomycin. CONCLUSIONS: These results suggest that enhanced relocalization of dystrophin to the sarcolemma during reperfusion may be a mechanistic link between IPC-mediated improvement of mitochondrial function and its protection against oncosis during the early phase of reperfusion.

Role of oxidative/nitrosative stress in the tolerance to ischemia/reperfusion injury in cardiomyopathic hamster heart.

We investigated the role of oxidative/nitrosative stress in the tolerance to ischemia/reperfusion (I/R) injury in BIO14.6 cardiomyopathy hamster hearts at 6 weeks of age. These hearts showed no significant morphologic change and left ventricular (LV) dysfunction. However, expression and activity of iNOS, nitrotyrosine (NT) formation, and protein kinase C (PKC)-epsilon activity were increased in these hearts. When the BIO14.6 hamster hearts were isolated and subjected to 40 min of global ischemia, they showed smaller myocardial necrosis and greater recovery of LV function during reperfusion compared with the control hamster heart. All of these effects were abrogated by prolonged treatment with the antioxidant, 2-mercaptopropionylglycine (MPG). Brief preischemic treatment with MPG or the iNOS inhibitor 1400W also abrogated NT formation and activation of PKC-epsilon and inhibited the tolerance to I/R injury in the BIO14.6 hamster heart. Brief preischemic treatment with the PKC inhibitor chelerythrine or the K(ATP) channel blockers, 5-hydroxydecanoate (5-HD) and glibenclamide, had no effect on iNOS activation and NT formation but inhibited the tolerance to I/R injury in the cardiomyopathic heart. These results suggest that oxidative/nitrosative stress plays a role in the tolerance to I/R injury in the cardiomyopathic heart through activation of PKC and the downstream effectors, K(ATP) channels.

Bronchial stump reinforcement with the intercostal muscle flap without adverse effects.

OBJECTIVE: Bronchopleural fistula is a serious complication of pulmonary resection. For anatomical reasons, lower lobectomy is thought to carry a higher risk for bronchopleural fistula. We investigated the efficacy of bronchial stump reinforcement with a pedicled intercostal muscle flap after lower lobectomy and compared the responses in patients treated with the flap, without the flap, and with other types of flap. We also investigated whether harvesting the intercostal muscle flap leads to an increase in blood loss during surgery and whether the type of flap influences chest-tube volume and pain after surgery. METHODS: One hundred and sixty-eight patients had lower or middle-lower lobectomy between January 1990 and December 2004. The bronchial stumps were treated in one of the three ways: covered with an intercostal muscle flap (116 patients, group A), not covered with a muscle flap (32 patients, group B), or covered with free fat or pleura (20 patients, group C). In a separate study, we compared the blood loss during surgery, and chest-tube volume and pain after surgery between patients treated with the intercostal muscle flap (23 patients) and non-intercostal muscle flap (32 patients). RESULTS: No patients in group A exhibited bronchopleural fistula, and two patients in group B and one patient in group C exhibited bronchopleural fistula. These differences were not significant. Blood loss, chest-tube volume, and pain score after surgery did not differ significantly between treatment groups. CONCLUSIONS: Bronchial stump reinforcement with the intercostal muscle flap after pulmonary resection is safe and effective when performed during lower and lower-middle lobectomy and does not increase the risk of complications.

Pneumothorax after pneumonectomy: surgery with successful double lobe ventilation.

Contralateral pneumothorax is potentially lethal in patients who have undergone pneumonectomy. There are few reports about the diagnosis and treatment of this situation. This is a report of our experience with selective lobar ventilation of the middle and lower lobes using a guidewire and a bronchial blocker in the right upper bronchus of a patient who had previously undergone left pneumonectomy.

New tubular bioabsorbable knitted airway stent: biocompatibility and mechanical strength.

OBJECTIVE: This study examines the biocompatibility and suitability of a new tubular bioabsorbable knitted stent made of poly-L -lactic acid in normal rabbit airways and examines the mechanical strength of this stent in vitro. METHODS: A tubular knitted airway stent (group B, n = 15) made of poly-L -lactic acid wire was implanted operatively in New Zealand White rabbits intratracheally; silicone stents served as controls (group A, n = 8). The cervical trachea was exposed, and the stent was implanted. Up to 40 weeks after stent implantation, the rabbits were killed, at which time bronchoscopy, histologic examination, and scanning electron microscopic study was done. We tested poly-L -lactic acid stents and silicone stents for their mechanical strength in vitro. We subjected stents to area loads and measured their mechanical strengths. RESULTS: In group A, which received silicone stents, 3 (37.5%) rabbits died within 4 weeks of stent implantation as a result of airway obstruction by secretions inside the stent lumen. In group B, poly-L -lactic acid stents, 1 (6.7%) rabbit died 3 weeks after implantation because of weakness caused by anorexia. In the remaining animals, except for 1 animal with stent trouble, the bronchial lumen was fully open until the 40th week after implantation. After 40 weeks of follow-up, the stents disappeared, except for nonabsorbable suture in the bronchial wall. None of the animals in group B died of airway complication. Histologic examination and scanning electron microscopic examination of the group A silicone stents showed marked regression of ciliated cells under the stent. In group B the ciliated epithelium was preserved, and there were numerous capillary blood vessels in the submucosa. In scanning electron microscopy of the group B poly-L -lactic acid stents, the ciliated cells were preserved between the mesh holes of the stent. For diameters between 4 and 6 mm, the mechanical strength of silicone stents was greater than that of poly-L -lactic acid stents. However, the mechanical strength of poly-L -lactic acid stents increased as a function of their diameter. CONCLUSION: A new tubular bioabsorbable stent made of poly-L -lactic acid is biocompatible in normal rabbit airways, indicating that poly-L -lactic acid is a promising material for airway stents for clinical use.

Integrated pharmacological preconditioning in combination with adenosine, a mitochondrial KATP channel opener and a nitric oxide donor.

BACKGROUND: Mitochondrial K(ATP) channel activation is an essential component of ischemic preconditioning. These channels are selectively opened by diazoxide and may be up-regulated by adenosine and nitric oxide. Therefore, pharmacological preconditioning with diazoxide in combination with adenosine and a nitric oxide donor (triple-combination pharmacological preconditioning) may enhance cardioprotection. METHODS AND RESULTS: Isolated and perfused rat hearts underwent ischemic preconditioning with 3 cycles of 5 minutes of ischemia and 5 minutes of reperfusion before 5 minutes of oxygenated potassium cardioplegia and 35 minutes of ischemia. Pharmacological preconditioning was performed by adding adenosine, diazoxide, and a nitric oxide donor S-nitroso-N-acetyl-penicillamine each alone or in combinations for 25 minutes followed by 10 minutes washout before cardioplegic arrest. Only triple-combination pharmacological preconditioning conferred significant cardioprotection as documented by highly improved left ventricular function and limited creatine kinase release during reperfusion that was comparable to that afforded by ischemic preconditioning. Mitochondrial K(ATP) channel activity assessed by flavoprotein oxidation was increased by diazoxide, but no further increase in flavoprotein oxidation was obtained by ischemic preconditioning and triple-combination pharmacological preconditioning. Significant activation of protein kinase C-epsilon was observed in only ischemic preconditioning and triple-combination pharmacological preconditioning. Pretreatment with the mitochondrial K(ATP) channel inhibitor 5-hydroxydecanoate or the protein kinase C inhibitor chelerythrine abrogated activation of protein kinase C-epsilon and cardioprotection afforded by ischemic preconditioning and triple-combination pharmacological preconditioning. CONCLUSIONS: Integrated pharmacological preconditioning is not simply mediated by enhanced mitochondrial K(ATP) channel activation, but is presumably mediated through amplified protein kinase C signaling promoted by coordinated interaction of adenosine, mitochondrial K(ATP) channel activation, and nitric oxide.

Prognostic significance of p53, Ki-67, VEGF and Glut-1 in resected stage I adenocarcinoma of the lung.

OBJECTIVES: The purpose of this study was to evaluate the prognostic significance of various biological factors in patients with resected stage I adenocarcinoma. METHODS: We immunohistochemically examined 47 specimens of surgically resected adenocarcinomas to evaluate the expression of the biological markers p53, Ki-67, vascular endothelial growth factor (VEGF) and glucose transporter-1 (Glut-1). Angiogenesis grade and tumor vessel invasion was also investigated. Actuarial survival was analyzed by the Kaplan-Meier method. Clinical variables and biological markers were analyzed using the Cox's proportional hazards model for multivariate analysis to identify independent prognostic factors. RESULTS: The overall survival rate for the whole series was 85.1% at 3 years and 71.9% at 5 years, with a median survival time of 73 months. Differentiation, Ki-67, Glut-1, VEGF, tumor vessel invasion and microvessel density (MVD) were significant prognostic factors by univariate analysis, with Glut-1 expression the most important prognostic factor for survival (P<0.0001). After multivariate analysis, only Glut-1 expression remained as a prognostic factor for survival. CONCLUSION: Glut-1 expression can be a predictor for prognosis in patients with resected stage I adenocarcinoma of the lung.

A new method for establishing an intrapulmonary tumor in the rabbit.

OBJECTIVES: Local treatments against malignant intrapulmonary tumors, such as radiotherapy, photodynamic therapy, and laser ablation therapy, are sometimes used in preference to surgery or chemotherapy. The efficacy of such treatments is dependent not only on the pathological type of the primary tumor, but also on loco-regional settings such as location of the lesion and relationship between the tumor and surrounding organs as well as tissues. Therefore, in order to evaluate the efficacy of a newly developed local treatment, it is essential to have a model in which a tumor can be established at an intended location. In this study, we developed a model for the establishment of an intrapulmonary tumor, using the rabbit. METHODS: After induction of general anaesthesia, a catheter was inserted via the airway into the lung of a Japanese white rabbit, under X-ray guidance. The lung was then inoculated with a collagen gel matrix containing a suspension of VX2 cells derived from rabbit skin squamous cell carcinoma. Subsequent tumor growth was evaluated with X-ray imaging and pathological examination. RESULTS: Growth of a solitary tumor at the target site was pathologically confirmed in 9 of 12 rabbits that were inoculated with 1 x 10(8) cells. In addition, tumor growth could be followed in 8 of 9 rabbits by chest X-ray examination. That is, a solitary intrapulmonary tumor could be established in 8 of 12 animals (67%). CONCLUSION: The rabbit model reported here enables establishment of a solitary intrapulmonary tumor and thus can provide a suitable experimental setting for evaluation of local treatments of intrapulmonary tumors.

Enhanced mesenchymal cell engraftment by IGF-1 improves left ventricular function in rats undergoing myocardial infarction.

BACKGROUND: We hypothesized that enhanced mesenchymal cell (MC) engraftment with insulin-like growth factor-1 (IGF-1) improves left ventricular (LV) function and survival. METHODS AND RESULTS: IGF-1 (10 microg/ml) increased adhesion and inhibited apoptosis under hypoxia in vitro through activation of phosphatidylinositol 3-kinase (PI3K) in bone marrow-derived MCs obtained from transgenic rats expressing green fluorescence protein. Myocardial infarction (MI) in rats was produced by ligature of the left coronary artery. One month after MI, rat hearts were injected with MCs in the presence or absence of 10 microg/ml IGF-1 with or without PI3K inhibitor, 5 microM LY294002. IGF-1 significantly increased engraftment of MCs between 6 h and 3 days after transplantation associated with the increase in stromal cell-derived factor-1alpha in the infracted LV. The transplanted MCs had disappeared 1 month after transplantation in all groups. MC transplantation with IGF-1 significantly increased neovascularization and inhibited cardiomyocyte apoptosis 3 days and 1 month after MC transplantation. This was associated with improved LV function 1 month after MC transplantation and eventually survival. LY294002 abrogated all of the beneficial effects of MC transplantation with IGF-1. IGF-1 alone had no effect on neovascularization and did not improve LV function and/or survival. CONCLUSIONS: These results suggest that IGF-1 improves engraftment of MCs at the time of transplantation via activation of PI3K and this improved engraftment of MCs may be attributed to an increased neovascularization and inhibition of cardiomyocyte death, leading to improvement of LV function and prolongation of survival despite the eventual loss of the transplanted MCs.

Ossification does not cause any complication when a bronchial stump is reinforced with an intercostal muscle flap.

OBJECTIVE: An intercostal muscle (ICM) flap is used to buttress the bronchial stump or bronchial anastomosis during thoracic surgery for airway reconstruction. Such flaps sometimes show ossification after surgery. Previous reports have suggested that such ossification requires a functional periosteum and good vascularization. We examined the background of ICM flap ossification and its relationship with complications and pain after surgery. METHODS: We surveyed the clinical records of 47 patients who underwent bronchial stump reinforcement with an ICM flap during thoracic surgery at Kansai Medical University Hospital between January 2003 and December 2005. We reviewed the post-surgical chest computed tomography (CT) scans of 42 patients, and examined the degree of ICM ossification. We classified patients into two groups: those with ossification of the ICM flap (O group) and those without (non-O group). We compared the two groups for age, gender, the site of ICM flap placement, disease, type of lymph node dissection, and pretreatment. We also compared the two groups for pain levels and complications after surgery. Eight (19%) of the 42 patients showed ossification of the ICM after surgery. There were statistically significant differences between the O and non-O groups in gender (p=0.029), lymph node dissection (p=0.024) and pain levels after surgery (p=0.034). There were no complications attributable to ICM ossification in this series. CONCLUSION: Ossification of an ICM flap may be related to gender, lymph node dissection and pain after surgery. Ossification does not cause any complication after surgery when an ICM is used to reinforce bronchial stumps.

Evaluation of chest computed tomography in patients after pneumonectomy to predict contralateral pneumothorax.

PURPOSE: Contralateral pneumothorax is a severe complication after pneumonectomy. We evaluated the mediastinal shift and the residual lung in patients who had undergone pneumonectomy to predict the incidence of contralateral pneumothorax. METHODS: We evaluated 21 cases of pneumonectomy performed from 1996 to 2006. For this study, we excluded patients with recurrent neoplasm, empyema, or hemothorax. We reviewed the computed tomography (CT) results of 13 patients who had undergone pneumonectomy to compare the bullae in the residual lungs, carina shifts, and herniation of the residual lungs before and after pneumonectomy. When evaluating the degree of herniation 4-6 cm below the carina, the anterior and posterior pulmonary hernias were classified as grade A, B, or C. We also investigated the preoperative respiratory function in all 13 patients. Results. Two patients suffered contralateral pneumothorax after left pneumonectomy. Both patients who suffered contralateral pneumothorax after pneumonectomy had bullae. The percentage forced expiratory volume in 1 s (FEV(1.0%)) was <70% in these two patients. Carina shifts and lung herniation were found to be greater after left pneumonectomy than after right pneumonectomy. CONCLUSION: The bullae in the lung and obstructive pulmonary disease are associated not only with spontaneous pneumothorax but also with contralateral pneumothorax after pneumonectomy. Lung herniation and mediastinal shift are greater after left pneumonectomy than after right pneumonectomy, which may be related to contralateral pneumothorax after pneumonectomy.

Angiotensin II type 1 receptor blocker preserves tolerance to ischemia-reperfusion injury in Dahl salt-sensitive rat heart.

Oxidative stress is involved in the tolerance to ischemia-reperfusion (I/R) injury. Because angiotensin II type 1 receptor blockers (ARBs) inhibit oxidative stress, there is concern that ARBs abolish the tolerance to I/R injury. Dahl salt-sensitive (DS) hypertensive and salt-resistant (DR) normotensive rats received an antioxidant, 2-mercaptopropionylglycine (MPG), or an ARB, losartan, for 7 days. Losartan and MPG significantly inhibited oxidative stress as determined by tissue malondialdehyde + 4-hydroxynoneal and increased expression of inducible nitric oxide synthase (iNOS) in the DS rat heart. However, losartan but not MPG activated endothelial nitric oxide synthase (eNOS) as assessed by phosphorylation of eNOS on Ser1177. Infarct size after 30-min left coronary artery occlusion followed by 2-h reperfusion was comparable between DS and DR rat hearts. Although MPG and losartan had no effect on infarct size in the DR rat heart, MPG but not losartan significantly increased infarct size in the DS rat heart. A selective iNOS inhibitor, 1400W, increased infarct size in the DS rat heart, but it had no effect on infarct size in the losartan-treated DS rat heart. However, a nonselective NOS inhibitor, Nomega-nitro-l-arginine methyl ester, increased infarct size in the losartan-treated DS rat heart. These results suggest that losartan preserves the tolerance to I/R injury by activating eNOS despite elimination of redox-sensitive upregulation of iNOS and iNOS-dependent cardioprotection in the DS rat heart.

Preoperative steroid therapy stabilizes postoperative respiratory conditions in myasthenia gravis.

OBJECTIVE: We reviewed our experience from 1990 to 2005 to examine whether control of myasthenia gravis (MG) with steroid therapy before surgery could stabilize postoperative respiratory conditions, compared with the nonsteroid treatment. METHODS: Records of 43 consecutive patients with MG who underwent extended thymectomy at Kansai Medical University Hospital were retrospectively reviewed. Two groups, a steroid group (n = 28) and a nonsteroid group (n = 15) were compared. RESULTS: In the steroid group, steroid doses ranged from 10 to 100 mg every other day, or 40-60 mg daily. The patients showed significantly less thymus hyperplasia in the pathological findings (P = 0.023). Whereas 3 of 28 (7%) in the steroid group suffered respiratory insufficiency within 3 days of surgery, 5 of 15 (33%) in the nonsteroid group exhibited the same problem (P = 0.030). Univariate analysis showed that steroid treatment was the only significant factor (P = 0.041) affecting respiratory insufficiency. Patients in the steroid group achieved palliation of MG more quickly after surgery than patients in the nonsteroid group (86% vs. 57% within 6 months, P = 0.059; 84% vs. 42% within 1 year, P = 0.042). CONCLUSION: The control of myasthenia gravis with steroid therapy before surgery seems to stabilize postoperative respiratory status without having adverse effects on surgical infection.

Granulocyte-colony stimulating factor increases donor mesenchymal stem cells in bone marrow and their mobilization into peripheral circulation but does not repair dystrophic heart after bone marrow transplantation.

BACKGROUND: Hereditary disordered cardiac muscle could be replaced with intact cardiomyocytes derived from genetically intact bone marrow (BM)-derived stem cells. METHODS AND RESULTS: Cardiomyopathic mice with targeted mutation of delta-sarcoglycan gene underwent intra-BM-BM transplantation (IBM-BMT) from transgenic mice expressing green fluorescence protein. The host BM and the peripheral blood were completely reconstituted by donor-derived hematopoietic cells by IBM-BMT. Treatment with granulocyte-colony stimulating factor (G-CSF) markedly increased donor-derived mesenchymal stem cells (MSC) in the BM and their mobilization into the peripheral blood after IBM-BMT. Treatment with isoproterenol (iso) for 7 days caused myocardial damage and left ventricular (LV) dysfunction in the cardiomyopathic mice. Co-treatment with iso and G-CSF increased donor BM cell recruitment to the heart and temporarily improved LV function in the cardiomyopathic mice with or without IBM-BMT. However, the cardiac muscle was not replaced with donor BM-derived cardiomyocytes in the cardiomyopathic mice with or without IBM-BMT, and this was associated with no improvement of LV function of mice aged 20 weeks. CONCLUSIONS: These results suggest that G-CSF enhances engraftment of donor MSC in the BM and their mobilization into the peripheral circulation after IBM-BMT but MSC recruited to the heart do not differentiate into cardiomyocytes and do not repair the dystrophic heart.

Bilaterally repeated spontaneous pneumothorax with ankylosing spondylitis.

Ankylosing spondylitis is a chronic inflammatory disease that primarily affects the joints of the axial skeleton. Pleuropulmonary involvement is an uncommon, late event in the course. A 53-year-old man who had a diagnosis of ankylosing spondylitis since he was 40 years old developed a bilaterally repeated and refractory spontaneous pneumothorax. He was treated successfully with surgery to the left pneumothorax that had been refractory to conservative chest tube drainage and chemical pleurodesis. During the second episode of right-side pneumothorax, he developed severe respiratory insufficiency because of his coexisting restrictive lung disease. He was successfully treated with chemical pleurodesis to the right pneumothorax. In our experience, prophylactic treatment such as surgery and pleurodesis should be considered for patients with ankylosing spondylitis during the first episode of pneumothorax.

Early postoperative mobilization with walking at 4 hours after lobectomy in lung cancer patients.

OBJECTIVES: The aim of this study was to determine whether walking at 4 h after surgery as a more aggressive way to proceed with early mobilization could be a safe approach compared with the patients who walked the day after surgery. METHODS: We encouraged patients who had lobectomy for non-small-cell lung cancer at Kansai Medical University Hospital to walk at 4 h after surgery and start pulmonary rehabilitation between January 2003 and June 2005. A group of 36 patients walked at 4 h after surgery. We retrospectively reviewed the postoperative courses of the patients and compared them with 50 patients who walked the next day during the same period. RESULTS: No patient had major trouble with chest drainage tube, and no patients fell when walking at 4 h. Amount of drainage, changing rates of the heart load during the walking, and pain scores after walking did not show significant differences in patients walking at 4 h and those walking the next day. Although four patients who walked the next day had an arterial oxygen partial pressure/inspired oxygen concentration ratio of <300 on day 3, none in the patients walking at 4 h had a ratio below this level. Among the patients walking at 4 h, 24 (67%) needed oxygenation for less than 2 days compared with 17 (34%) of the patients walking the next day. CONCLUSION: Walking at 4 h after lobectomy in patients with non-small-cell lung cancers is a safe approach to starting pulmonary rehabilitation after surgery.