• Journal of Chest Surgery
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• v.9 no.1
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• pp.20-26
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• 1976

Author has performed experimental study on hemodynamic changes of lung following radical hilar stripping and contralateral pulmonary artery ligation. In view of hemodynamic changes in group 1 (right pulmonary artery ligation only) and group 2(left hilar stripping+right pulmonary artery ligation). group 2 showed remarkable decrease rate in oxygen uptake (P<0.001) and total pulmonary blood flow(P<0.001), and the more increase rate in mean pulmonary artery pressure(P<0.02) and total pulmonary vascular resistance (P<0.001). Meanwhile, the decrease percent of left lung vascular resistance was lower than group 1(P<0.001). The hemodynamic changes in group 1 returned to control range two weeks later. In the group 2, two dogs were expired as a result of atelectasis and pulmonary hypertension. Among allying 8 dogs, five months after operation, follow up studies performed in two dogs, which showed normal pulmonary hemodynamics similar to preoperative data. The altered blood gas values and decreased oxygen uptake are more remarkable in denervated lung, which may due to pulmonary hypertension and partly retained more secretion in bronchial trees than usual. Important factors of raising pulmonary vascular resistance and pulmonary artery pressure are considered as the increased blood flow to remaining left lung and dysfunction of pulmonary vascular bed to accept the increased blood flow after denervation. Loss of nerve innervation had a influence, to some extent, to the decrease of oxygen uptake and the increase of pulmonary vascular resistance and pulmonary artery pressure. There can be little question that denervation does impair the pulmonary hemodynamics, however, intact pulmonary nerve innervation is not absolutely essential for survival of the animal.

• Tuberculosis and Respiratory Diseases
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• v.42 no.6
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• pp.913-922
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• 1995

Background: When we define the pressure of pulmonary vasculature in which a recruitment of blood flow occurs as $P_I$ and the proportion of change in pulmonary artery to that in cardiac output as IR and then we compare PI and IR with pulmonary vascular resistance, we would find some problems in pulmonary vascular resistance. In other words, it is the theory that, IR should be increased mainly in pulmonary embolism in which decreases the cross sectional area of pulmonary vasculature. But there are many contradictory reports resulted from various researches and the fact is known widely that any difference exists between PVR and PI, IR. For this reason, the purpose of this study is to observe how PI and IR change at the time of the outbreak and during treatment of the pulmonary embolism, and to find out the meaning of these new indicators and the difference from the pulmonary vascular resistance used generally when we subdivide the pulmonary vascular resistance into PI and IR. Method: After making AV fistula in experimental dog, we controlled cardiac output at the intervals of 15 minute in case of three kinds(all AV fistula are obstructed, only one of fistula is open and all of fistula is open), and after evoking massive pulmonary embolism with radioactive autologous blood clots, we measured the mean pulmonary artery pressure, and calculated PI and IR. We observed the pattern of change in PI and IR, without giving the control group any specific treatment and with injecting intravenously rtPA in the Group 1 and Group 2 at the dose of 1mg per kg, for 15 minutes fot the former and 3 hours for the latter. Result: 1) Pulmonary vascular resistance showed a change similar to that of pulmonary artery pressure and in all three group, PVR increased significantly, but group 1 and group 2 showed tendency that PVR keeps on decreasing after treatment, and the rate of decrease in group 1 is more rapid than group 2 significantly. 2) Both intersection(PI) and degree(IR) are proved statistically significant, in view of the straight line relationship between cardiac output and pulmonary artery pressure, calculated by minimal regression method. 3) PI changed similarly to pulmonary vascular resistance, while in the IR which is theoretically more similar to PVR, there was no significant difference or change after rtPA infusion. Conclusion: In the pulmonary embolism, Both change in IR which means real resistance of pulmonary vasculature and PI which was developed due to secondary vasoconstriction by pulmonary embolism are reflected same time.

• Journal of Chest Surgery
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• v.14 no.1
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• pp.9-16
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• 1981

Twenty eight patients with conpnital heart disuse underwent lung biopsy to assets pulmonary obstructive vascular disease at cardiac surpry. Thirteen patients had patent ductus arteriosus, 10, ventricular septal defects and S, atrial septal defects. The aaes were between 2 and 30 years. In patients with patent ductus arteriosus lung biopsy was performed from the IIngular Hlment. The anterior seament of the right upper lobe was blopsled in cases with ventricular septal defect and atrial septal defect. Grading of pulmonary obstructive vascular disease could not be assessed In 9 cases. In 2 cases poor quality of the slides made us impossible to evaluate and In 7 cases there were no suitable small muscular arteries to evaluate in the slides of lung tissue especially taken from the IIngular seament. Nineteen cases were evaluated pulmonary obstructive vascular disease. Among them 17 cases had Heath-Edwards changes of grade 1 and 2 patients had that of grade 3. The thickness of media was measured. It was expressed as percentage of medial thickness to outer diameter of artery. The medial thickness was correlated proportionally with elevation of pulmonary arterial pressure and pulmonary vascular resistance to systemic vascular resistance ratio. There were no complications related to the procedure of lung biopsy.

• Journal of Chest Surgery
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• v.17 no.3
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• pp.339-345
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• 1984

Thirty four patients with a ventricular septal defect, aged 2 months to 24 years [median 2.33 years], had lung biopsies during open heart procedures to assess the degree of pulmonary vascular disease. The patients were divided into two groups according to their age; group 1 - under 2 years of age [15 patients], and group 2- over 2 years of age [19 patients]. The, pathologic change of the pulmonary arterioles was correlated with pre-operative hemodynamic data in 34 patients. There was no significant correlation between the severity of pulmonary vascular disease according to Heath-Edwards classification and the patients age [X2=1.8381, P=0.1751 ]. There was a significant correlation between degree of medial wall thickness and arteriolar diameter and the level of preoperative peak pulmonary artery pressure and peak systemic artery pressure [Pp/Ps]. Also, there was a good correlation between the preoperative pulmonary vascular resistance and systemic vascular resistance [Rp/Rs]. There was no significant correlation between wall thickness and Pp/Ps, and Rp/Rs below the age of 2 years. We conclude that, in patients over 2 years of age, there was a significant correlation between the medial wall thickness of the pulmonary arteriole and elevation of Pp/Ps and Rp/Rs. This is not true in patients under 2 years of age.

• Journal of Chest Surgery
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• v.23 no.4
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• pp.659-666
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• 1990

We evaluated 68 patients with mitral valve disease who underwent mitral valve replacement from April, 1986, to December, 1988. Among them 20 patients showed increased systolic pulmonary arterial pressure greater than 60 mmHg and postoperative hemodynamic data were obtained in 19 patients average 13 months after mitral valve replacement. The results were as followings. 1. Average pulmonary systolic pressure decreased from 84.8$\pm$4.5 preoperatively to 33. 0$\pm$1.9mmHg postoperatively[P<0.001]. 2. Average pulmonary vascular resistance index decreased from 1425$\pm$148 preoperatively to 287+35.8 dyne * sec * cm2 * m postoperatively[P<0.001]. 3. Average cardiac index rose from 1.927$\pm$0.169 preoperatively to 2.625$\pm$0.159 L/min/m2 postoperatively [P <0.005]. This study shows that pulmonary hypertension and the increased pulmonary vascular resistance index due to mitral valve disease can regress significantly after mitral valve replacement.

• The Korean Journal of Physiology and Pharmacology
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• v.20 no.6
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• pp.641-647
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• 2016

Pulmonary arterial hypertension (PAH) is a progressive disease characterized by vascular remodeling of pulmonary arteries (PAs) and increased vascular resistance in the lung. Monocrotaline (MCT), a toxic alkaloid, is widely used for developing rat models of PAH caused by injury to pulmonary endothelial cells; however, characteristics of vascular functions in MCT-induced PAH vary and are not fully understood. Here, we investigated hypoxic pulmonary vasoconstriction (HPV) responses and effects of various vasoconstrictors with isolated/perfused lungs of MCT-induced PAH (PAH-MCT) rats. Using hematoxylin and eosin staining, we confirmed vascular remodeling (i.e., medial thickening of PA) and right ventricle hypertrophy in PAH-MCT rats. The basal pulmonary arterial pressure (PAP) and PAP increase by a raised flow rate (40 mL/min) were higher in the PAH-MCT than in the control rats. In addition, both high $K^+$ (40 mM KCl)- and angiotensin II-induced PAP increases were higher in the PAH-MCT than in the control rats. Surprisingly, application of a nitric oxide synthase inhibitor, L-$N^G$-Nitroarginine methyl ester (L-NAME), induced a marked PAP increase in the PAH-MCT rats, suggesting that endothelial functions were recovered in the three-week PAH-MCT rats. In addition, the medial thickening of the PA was similar to that in chronic hypoxia-induced PAH (PAH-CH) rats. However, the HPV response (i.e., PAP increased by acute hypoxia) was not affected in the MCT rats, whereas HPV disappeared in the PAH-CH rats. These results showed that vascular contractility and HPV remain robust in the MCT-induced PAH rat model with vascular remodeling.

• Clinical and Experimental Pediatrics
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• v.57 no.10
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• pp.461-463
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• 2014

Decreased exercise capacity after Fontan surgery is relatively common and the failure of the Fontan state gradually increases with age. However, there is no further treatment for patients with Fontan circulation. Pulmonary vasodilation therapy is an effective method to solve this problem because pulmonary vascular resistance is a major factor of the Fontan problem. Inhaled iloprost is a chemically stable prostacyclin analogue and a potent pulmonary vasodilator. We experienced two cases of Fontan patients treated with inhaled iloprost for 12 weeks. The first patient was an 18-year-old female with pulmonary atresia with an intact ventricular septum, and the second patient was a 22-year-old male with a double outlet right ventricle. Fifteen years have passed since both patients received Fontan surgery. While the pulmonary pressure was not decreased significantly, improved exercise capacity and cardiac output were observed without any major side effects in both patients. The iloprost inhalation therapy was well tolerated and effective for the symptomatic treatment of Fontan patients.

• Journal of Chest Surgery
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• v.13 no.3
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• pp.237-242
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• 1980

This is a case report of spontaneous regression of elevated pulmonary vascular resistance after the age of 6 years in a patient with partial endocardial cushion defect. The patient was first evaluated and considered to be highly risky for surgical correction because of obstructive type of pulmonary hypertension and presisting congestive heart failure at the age of 6 years, during which time medical treatment for congestive heart failure and sufferring from respiratory infection were only provided. Finally the patient was reevaluated at the age of 16 years, in January of 1980 when cardiac catheterization was revealed markedly reduced pulmonary vascular resistance and pulmonary hypertension as well. The patient was operated upon with uneventful postoperative recovery. So we report this case with review of the literatures regarding natural history regarding natural history of partial endocardial cushion defect.

• Neonatal Medicine
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• v.28 no.1
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• pp.1-6
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• 2021

Persistent pulmonary hypertension of the newborn (PPHN) is a consequence of the failure of a decrease in the elevated pulmonary vascular resistance after birth. Pulmonary vasodilators, including inhaled nitric oxide (iNO), have been the mainstream of targeted therapy for PPHN, but no drugs have been proven to be effective in preterm infants with PPHN. The fetus remains hemodynamically stable despite lower arterial oxygen tension and pulmonary blood flow as compared to full-term newborns. This adaptation is due to the lower oxygen requirement and high oxygen-carrying capacity of fetal circulation. The immature lungs of preterm infants are more vulnerable to reactive oxygen species, and the response of pulmonary vascular dilatation to blood oxygen tension is blunted in preterm infants. Recently, iNO has been reported to be effective in a selected group of preterm infants, such as those with prolonged preterm rupture of membrane-oligohydramnios-pulmonary hypoplasia sequence. PPHN in preterm infants, along with maximum supportive treatment based on fetal physiology and meticulous assessment of cardiovascular function, is in dire need of new treatment guidelines, including optimal dosing strategies for pulmonary vasodilators.

• Journal of Chest Surgery
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• v.33 no.1
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• pp.1-6
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• 2000

Background: TNF-$\alpha$ plays a major role in producing left ventricular dysfunction cardio-myopathy pulmonary edema and inhibits the compensatory mechanism of congestive heart failure. IL-6 is an acute reactant of immune reaction and also known to control immune reaction but its function in the myocyte was not clearly investigated. Author's performed this experiment to investigate the contents of TNF-$\alpha$ and IL-6 on the assumption that TNF-$\alpha$ and IL-6 may reside in nonfailing heart that has gone cardiac surgery and play some role in cardiac function. Material and Method : Right auricular tissues were sampled from 12 patients who had undergone total corrective surgery for both congenital and acquired heart diseases from January 1998 to June 1998 in Kosin Universcfy Gospel hospital. The quantitive analysis of TNF-$\alpha$ and IL-6 were assessed by ELISA method in right auricular tissue. Hemodynamic values about the pressure of ventricle atrium aorta pulmonary artery and cardiac index pulmonary and systemic vascular resistance and cardiac output were measured by echocardiography and cardiac catheterization and biochemical analyses of LDH & AST were done before operation. statistical analysis was by Paired Student t-test. Patients were divided into children(under 15 years olds) and adults groups and the data was compared beween two groups. Conclusion: Mild pulmonary hypertension and increased pulmonary vascular resistance were existed in both group. The contents of tissue TNF-$\alpha$ IL-6 in each group were independent of each data.