• Journal of Chest Surgery
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• v.39 no.9 s.266
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• pp.659-667
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• 2006

Background: Experimental studies of vascular remodeling in the pulmonary arteries have been performed actively. These models required a persistent vascular insult for intimal injury induced by chronic hypoxia, monocrotaline intoxication or chronic air embolism and characterized medial hypertrophy and neointimal formation by active synthesis of the extracellular matrix protein. The purpose of this study was to determine the pattern of pulmonary vascular remodeling after obstruction of the pulmonary vein. Material and Method: Obstruction of the right pulmonary vein with a metal clip was performed in Sprague-Dawley rats $(352{\pm}18g,\;n=10)$ to cause pulmonary vascular disease. Fifteen days later, experimental studies were done and finally the both lungs and hearts were extirpated for experimental measurement. Pulmonary arterial pressure, weight ratio of right ventricle (RV) to left ventricle (LV) and ventricular septum (S) (RV/LV +S weight ratio), and pulmonary artery morphology (percent wall thickness, %WT) were evaluated and compared with normal control groups. Result: Pulmonary hypertension $(38{\pm}12mmHg\;vs\;13{\pm}4mmHg;\;p<0.05)$ and right ventricular hypertrophy (right ventricular/left ventricular and septal weight ratio, $0.52{\pm}0.07\;vs\;0.35{\pm}0.04;\;p<0.05$) with hypertrophy of the muscular layer of the pulmonary arterial wall (percent wall thickness, $22.4{\pm}6.7%\;vs\;6.7{\pm}3.4%;\;p<0.05$) were developed by 15 days after obstruction of the pulmonary vein. Conclusion: Obstruction of the pulmonary vein developed elevation of pulmonary blood pressure and medial hypertrophy of the pulmonary artery. These results are a part of the characteristic vascular remodeling. Theses results demonstrate that obstruction of the pulmonary vein can develope not only high pulmoanry blood flow of contralateral lung but also intima injury inducing vascular remodeling.

• Journal of Chest Surgery
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• v.25 no.1
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• pp.32-41
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• 1992

From August 1982 to December 1991, 58 consecutive infants with tetralogy of Fallot underwent primary repair. Age ranged from 22 days to twelve months [n=58, 8.7$\pm$2.7 months] and body weight from 3.1 to 13 kilograms [n=58, 7.8$\pm$1.7 kilograms]. Qne infant had absence of the pulmonary valve; one had Ebstein`s anomaly and one had supramitral ring. Thirty-two patients [56%] experienced anoxic spell. Preoperative pulmonary artery indices were measured in 38 cases, ranging 126-552mm2/M2BSA[n=38, 251$\pm$79mm2/M2BSA]. All infants required a right ventricular outflow tract patch; in 41, the patch extended across the pulmonary valve annulus, in 13 of them, monocusps were constructed. All had patch closure of ventricular septal defect. Two infants had REV operation for avoiding injury to the canal branch of the right coronary artery which cross the right ventricular out flow tract. Post repair PRV/LV were measured at operating room in 40 cases, which revealed mean value of 0.49$\pm$0.12 [range: 0.25-0.74]. The hospital mortality was 10.3% [6 patients], and causes of deaths were right heart failure due to sustained right ventricular hypertension[4] and right ventricular outflow tract obstruction, intractablesuraventricular tachyarrhythmia[1], hypoxia[1] due to residual right to left shunt across the atrial septal defect in patient associated with Ebstein`s anomaly. All infants were doing well at follow-up from 1 to 101 months[20.6 months /patient, 1, 072 patient-month] Serial postoperative echocardiograms revealed no residual ventricular septal defects and estimated RVOT gradients between 0 and 40 mmHg except 3 cases [50, 50, 60 mmHg]. There were no late deaths and late ventricular arrhythmias or congestive heart failure. Redo operations were done in 2 cases because of residual right ventricular outflow tract obstruction. This experience with infants with tetralogy of Fallot suggests that, if mortality is tolerable, eletive repair of tetralogy of Fallot could be reasonably undertaken during the first year of life, and even better results could be anticipated along with improvement of methods of myocardial protection and postoperative care.

• Journal of the Korean Society of Laryngology, Phoniatrics and Logopedics
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• v.30 no.2
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• pp.139-141
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• 2019

The causes of vocal cord paralysis include iatrogenic injury during thyroid or cervical surgery, heart and chest surgery, and tumorous lesion such as laryngeal cancer and lung cancer. In addition to these common causes, rarely, cardiovascular disease can also cause vocal fold paralysis. A disease known as Cardiovocal syndrome, or Ortner's syndrome, causes left vocal fold paralysis when the left recurrent laryngeal nerve is compressed by the pulmonary artery and aorta, which is occurred by pulmonary hypertension from heart disease. We report for the first case in Korea the diagnosis of vocal fold paralysis caused by Ortner's syndrome.

• The Korean Journal of Physiology and Pharmacology
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• v.26 no.2
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• pp.87-94
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• 2022

Myocardial infarction promotes cardiac remodeling and myocardial fibrosis, thus leading to cardiac dysfunction or heart failure. Peiminine has been regarded as a traditional anti-fibrotic Chinese medicine in pulmonary fibrosis. However, the role of peiminine in myocardial infarction-induced myocardial injury and fibrosis remained elusive. Firstly, rat model of myocardial infarction was established using ligation of the left coronary artery, which were then intraperitoneally injected with 2 or 5 mg/kg peiminine once a day for 4 weeks. Echocardiography and haemodynamic evaluation results showed that peiminine treatment reduced left ventricular end-diastolic pressure, and enhanced maximum rate of increase/decrease of left ventricle pressure (± dP/dt max) and left ventricular systolic pressure, which ameliorate the cardiac function. Secondly, myocardial infarction-induced myocardial injury and infarct size were also attenuated by peiminine. Moreover, peiminine inhibited myocardial infarction-induced increase of interleukin (IL)-1β, IL-6 and tumor necrosis factor-α production, as well as the myocardial cell apoptosis, in the rats. Thirdly, peiminine also decreased the myocardial fibrosis related protein expression including collagen I and collagen III. Lastly, peiminine reduced the expression of p38 and phosphorylation of extracellular signal-regulated kinase 1/2 in rat model of myocardial infarction. In conclusion, peiminine has a cardioprotective effect against myocardial infarction-induced myocardial injury and fibrosis, which can be attributed to the inactivation of mitogen-activated protein kinase pathway.

• Journal of Chest Surgery
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• v.25 no.12
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• pp.1508-1515
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• 1992

Between 1975 and 1992, forty five patients with trachea stenosis received tracheoplasty for relief of obstruction. The causes of airway problem are brain contusion[19 cases, 40%], cerebrovascular disease[3 cases, 7%], drug intoxication[8 cases, 18%], psychotic problem[2 cases, 4%], trachea tumor[3 cases, 7%], adult respiratory distress syndrome[9 cases, 20%] and direct trauma[1 case, 2%]. Direct causes of trachea stenosis were complications of tracheostomy[36 cases, 80%], complications of nasotracheal intubation[5 cases, 11%], tumor[3 cases, 6%] and trauma[1 case, 2%]. Thirty one patients underwent the sleeve resection and end-to-end anastomosis. Five patients performed a wedge resection and end-to-end anastomosis. Forteen patients received the Montgomery T-tube for relief of airway obstruction. Four patients have done simple excision of granulation tissue. Two, subglottic stenosis patients were received Rethi procedure[anterior division of cricoid cartilage, wedge partial resection of lower thyroid cartilage and Montgomery T-tube molding] and the other subglottic stenosis patient underwent permanent trachea fenestration. Including cervical flexion in all patients postoperatively, additional surgical techniques for obtain tension-free anastomosis were hyoid bone release technique in two cases, and hilar mobilization, division of inferior pulmonary ligament and mobilization of pulmonary vessel at the pericardium were performed in one case. Cervical approach was used in 39 cases, cervicomediastinal in 12 cases and transthoracic in one case. Complications of tracheoplasty were formation of granulation tissue at the anastomosis site[3 cases], restenosis[9 cases], trachea-innominate artery fistula[2 cases], wound infection[2 cases], separation of anastomosis[2 cases], air leakage[3 cases], injury to a recurrent laryngeal nerve[temporary 8 cases, permanent 2 cases] and hypoxemia[1 case]. Surgical mortality for resection with primary reconstruction was 6.7%, with one death due to postoperative respiratory failure and two deaths due to tracheo-innominate artery fistula.

• Journal of Chest Surgery
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• v.51 no.5
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• pp.344-349
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• 2018

Background: We report our surgical technique for nonintubated uniportal video-assisted thoracoscopic surgery (VATS) pulmonary resection and early postoperative outcomes at a single center. Methods: Between January and July 2017, 40 consecutive patients underwent nonintubated uniportal VATS pulmonary resection. Multilevel intercostal nerve block was performed using local anesthesia in all patients, and an intrathoracic vagal blockade was performed in 35 patients (87.5%). Results: Twenty-nine procedures (72.5%) were performed in patients with lung cancer (21 lobectomies, 6 segmentectomies, and 2 wedge resections), and 11 (27.5%) in patients with pulmonary metastases, benign lung disease, or pleural disease. The mean anesthesia time was 166.8 minutes, and the mean operative duration was 125.9 minutes. The mean postoperative chest tube duration was 3.2 days, and the mean hospital stay was 5.8 days. There were 3 conversions (7.5%) to intubation due to intraoperative hypoxemia and 1 conversion (2.5%) to multiportal VATS due to injury of the segmental artery. There were 7 complications (17.5%), including 3 cases of prolonged air leak, 2 cases of chylothorax, 1 case of pleural effusion, and 1 case of pneumonia. There was no in-hospital mortality. Conclusion: Nonintubated uniportal VATS appears to be a feasible and valid surgical option, depending on the surgeon's experience, for appropriately selected patients.

• Tuberculosis and Respiratory Diseases
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• v.45 no.6
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• pp.1223-1235
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• 1998

Background and Objective : Although prone positioning has been reported to improve gas exchange, prone positioning alone does not seem to be sufficient to increase systemic oxygen transport in an acute lung injury. The objective of this study was to investigate whether the combined therapy of low dose nitric oxide (NO) inhalation and prone positioning has an additive effect on the oxygenation and hemodynamics in patients with severe ARDS. Patients and Methods : Twelve patients with ARDS were included. Prone positioning alone, later combined with nitric oxide inhalation (5~10 ppm) from the supine position (baseline) were performed with serial measurement of gas exchange, respiratory mechanics and hemodynamic at sequential time points. The patient was regarded as a responder to prone positioning if an increase in $PaO_2/FiO_2$ of more than 20 mm Hg at 30 min or 120 min intervals after prone positioning was observed compared to that of the baseline. The same criterion was applied during nitric oxide inhalation. Results : Eight patients (66.5%) responded to prone positioning and ten patients (83.3%) including the eight just mentioned responded to the addition of NO inhalation. The $AaDO_2$ level also decreased promptly with the combination of prone positioning and NO inhalation compared to that of prone positioning alone ($191{\pm}109$ mm Hg vs. $256{\pm}137$ mm Hg, P<0.05). Hemodynamic parameters and lung compliance did not change significantly during prone positioning only. Following the addition of NO inhalation to prone positioning, the mean pulmonary artery pressure and pulmonary artery occlusion pressure decreased and cardiac output, stroke volume and oxygen delivery increased (P < 0.05) compared to those of prone 120 min. Conclusion : These findings indicate that NO inhalation would provide additional improvement in oxygenation and oxygen transport to mechanically ventilated patients with ARDS who are in a prone position.

• Journal of Chest Surgery
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• v.40 no.4 s.273
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• pp.247-255
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• 2007

Background: Lung injury that follows bypass has been well described. It is manifested as reduced oxygenation and lung compliance and, most importantly, increased pulmonary vascular resistance reactivity; this is a known cause of morbidity and mortality after repair of congenital heart disease. Injury to the pulmonary vascular endothelium, and its associated alterations of endothelin-1, is considered to be a major factor of bypass-induced lung injury. Removing endothelin-1 after bypass may attenuate this response. This study measured the concentration of serum and peritoneal effluent endothelin-1 after performing bypass to determine if endothelin-1 can be removed via peritoneal dialysis. Material and Method: From March 2005 to March 2006, 18 patients were enrolled in this study Peritoneal catheters were placed at the end of surgery. Serum samples were obtained before and after bypass, and peritoneal effluents were obtained after bypass. Endothelin-1 was measured by enzyme linked immunosorbent assay (ELISA). Result: In the patients with a severe increase of the pulmonary artery pressure or flow, the mean preoperative plasma endothelin-1 concentration was significantly higher than that in the patients who were without an increase of their pulmonary artery pressure or flow (4.2 vs 1.8 pg/mL, respectively, p<0.001). The mean concentration of plasma endothelin-1 increased from a preoperative value of $3.61{\pm}2.17\;to\;5.33{\pm}3.72 pg/ml$ immediately after bypass. After peritoneal dialysis, the mean plasma endothelin-1 concentration started to decrease. Its concentration at 18 hours after bypass was significantly lower than the value obtained immediately after bypass (p=0.036). Conclusion: Our data showed that the plasma endothelin-1 concentration became persistently decreased after starting peritoneal dialysis, and this suggests that peritoneal dialysis can remove the circulating plasma endothelin-1.

• The Korean Journal of Medicine
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• v.93 no.6
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• pp.565-570
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• 2018

Postcardiac injury syndrome (PCIS) is an inflammatory process that usually occurs within 1 to 6 weeks after an injury to the pericardium, epicardium, or myocardium. As more interventions are performed for complicated coronary artery obstructive lesions, there have been some recent reports on PCIS following percutaneous coronary intervention (PCI). The medical management of PCIS depends on nonsteroidal anti-inflammatory drugs (NSAIDs), in addition to colchicine or steroids. An 80-year-old male patient underwent a PCI. Unfortunately, the guidewire piercing failed but he showed no immediate signs of complication. However, 5 hours after the procedure, he complained of chest discomfort. An electrocardiogram showed widespread ST elevation. Chest X-ray and computed tomography showed pulmonary congestion with pleural effusion, while thoracic echocardiography showed a moderate amount of pericardial effusion. NSAIDs were initiated, but there was no improvement of symptoms. We describe an unusual case of atypical earl onset PCIS after PCI, recovered rapidly by steroids.

• Journal of Chest Surgery
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• v.30 no.7
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• pp.733-738
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• 1997

Sequential bilateral lung transplantation may result in a variety of perioperative and postoperative complications, showing high perioperative morbidity and mortality rates. This research was performed to investigate the hemodynamic changes in adult mongrel dogs after bilateral reimplantation, two methods preferred for avoiding or minimizing graft rejection. The anterior portion of the pulmonary artery and the left atrium proximal to the superior and the inferior pulmonary veins were resected out and then re-anastomosed one hour later to prevent torsion or stenosis of the anastomotic site and the formation of a thrombosis in the left atrium. An everted suture technique was employed for the left atrium; An hour after the division, however, the main bronchus was tightly anastomose by interrupted sutures of No. 4-0 prolene in a telescope method. A modified I-C solution mixed with PGEI was infused into the cut portion of the pulmonary artery at the rate of 15 mllkglmin and at a pressure of 40 cmH20 for a total dosage of 70 mlfkg in order to preserve the transected lung. Topical cooling using wet gauzes soaked with cold I-C solution was performed for one hour to prevent ischemic lung injury. The above procedures are considered to be beneficial for achieving a satisfactory outcome for bilateral lung reimplantation.