• Biomolecules & Therapeutics
• /
• v.24 no.5
• /
• pp.523-528
• /
• 2016

Urotensin II (UII) is a potent vasoactive peptide and mitogenic agent to induce proliferation of various cells including vascular smooth muscle cells (VSMCs). In this study, we examined the effects of a novel UII receptor (UT) antagonist, KR-36676, on vasoconstriction of aorta and proliferation of aortic SMCs. In rat aorta, UII-induced vasoconstriction was significantly inhibited by KR-36676 in a concentration-dependent manner. In primary human aortic SMCs (hAoSMCs), UII-induced cell proliferation was significantly inhibited by KR-36676 in a concentration-dependent manner. In addition, KR-36676 decreased UII-induced phosphorylation of ERK, and UII-induced cell proliferation was also significantly inhibited by a known ERK inhibitor U0126. In mouse carotid ligation model, intimal thickening of carotid artery was dramatically suppressed by oral treatment with KR-36676 (30 mg/kg/day) for 4 weeks compared to vehicle-treated group. From these results, it is indicated that KR-36676 suppress UII-induced proliferation of VSMCs at least partially through inhibition of ERK activation, and that it also attenuates UII-induced vasoconstriction and vascular neointima formation. Our study suggest that KR-36676 may be an attractive candidate for the pharmacological management of vascular dysfunction.

• Journal of Chest Surgery
• /
• v.25 no.12
• /
• pp.1399-1403
• /
• 1992

The evaluation of the effectivess of ongoing cardiopulmonary resucitation efforts is dependent on the commonly used methods, such as the presence of femoral or carotid artery pulsations, arterial blood gas determinations, peripheral arterial pressure and intracardiac pressure monitoring. But recent studies suggest that end-tidal carbon dioxide tension serves as a non-invasive measurement of pulmonary blood flow and therefore cardiac output under constant ventilation. A prospective clinical study was done to determine whether end-tidal carbon dioxide monitoring in open heart surgery under cardiopulmonary bypass could be used as a prognostic indicator of bypass weaning. We monitored end-tidal PCO2 values continuously during cardiopulmonary bypass in 30 patients. "Ohmeda 5210 CO-2 monitor" under infrared absorption method were incorperated into the ventilator circuit by means of a side point adaptor between endotracheal tube and ventilator tubing. 18 patients[Group I ] were res-ucitated from partial bypass followed by aorta cross clamp off and 12 patients[Group II ] from aorta cross clamp off followed by partial bypass. But there was no difference between two groups[p>0.05]. The value of end-tidal carbon dioxide tension during ventricular fibrillation or nearly arrest state was 6.6$\pm$2.9 mmHg, and at the time of spontaneous beating was 19.3$\pm$5.6 mmHg[Mean$\pm$Standard deviation], In conclusion end-tidal carbon dioxide tension monitoring provides clinically useful, continous, noninvasive and supplementary prognostic indicator during cardiopulmonary bypass weaning procedures.rocedures.

• Journal of Chest Surgery
• /
• v.37 no.1
• /
• pp.80-83
• /
• 2004

The aortic coarctation is located in the distal thoracic aorta or abdominal aorta, or both and is often called ‘middle aortic syndrome’ or ‘mid-aortic dyspastic syndrome’. Etiology is controversial and most cases are seen in young female women. Severe complication such as cardiac or renal dysfunction as well as cerebral hemorrhage may occur, so aggressive surgical intervention may take effect. Lately we experienced a middle aortic syndrome which was not typical because of the patient's advanced age at the time of clinical presentation. The Axillo-femoral artery bypass graft with 6 mm PTFE vascular graft was done.

• Journal of Chest Surgery
• /
• v.37 no.1
• /
• pp.88-91
• /
• 2004

Aortic regurgitation is not a rare complication of Takayasu's disease. Aortic regurgitation may aggravate cerebral ischemic syndrome like syncope in patients with stenotic or occlusive lesions in cerebral branches of aorta secondary to acute or progressive inflammation. In a 34-yrs-old male patient who complained of syncope and exertional dyspnea with occlusion of both carotid arteries and severe stenoses of both subclavian arteries, occlusion of right coronary artery, and aortic regurgitation, his symptom was improved with perioperative aggressive steroid therapy, stent insertion in both subclavian arteries, and aortic valve replacement.

• Journal of Chest Surgery
• /
• v.31 no.4
• /
• pp.402-408
• /
• 1998

A 56-year old female underwent total aortic arch replacement March 1995, because of an expanding chronic Debakey type I aortic dissection. This aortic dissection had an intimal tear at the origin of the right carotid artery. Retrograde and antegrade propagation of dissection resulted in aortic arch blood flow separation and expanding pseudolumen to the abdominal aorta. Sudden anuria(ARF) developed 3 hours later postoperatively and renal doppler ultrasonography and aortography showed diminished blood flow of renal arteries. We performed balloon aortic dilatation but failed. She could be restored good renal flow after intimal flap fenestration resection and thrombectomy of the abdominal aorta. This patient could be discharged in a state of mild CRF after 2 months of ICU care for respiratory and renal failure.

• Journal of Chest Surgery
• /
• v.39 no.4 s.261
• /
• pp.275-280
• /
• 2006

Background: Aortopulmonary window (APW) is a very rare congenital heart anomaly, often associated with other cardiac anomalies. It causes a significant systemic to pulmonary artery shunt, which requires early surgical correction. Accurate diagnosis and surgical correction will bring good outcomes. The purpose of this study was to describe our 20-year experience of aortopulmonary window. Material and Method: Between March 1985 and January 2005, 16 patients with APW underwent surgical repair. Mean age at operation was $157.8{\pm}245.3$ ($15.0{\sim}994.0$) days and mean weight was $4.8{\pm}2.5$ ($1.7{\sim}10.7$) kg. Patent ductus arteriosus (8), atrial septal defect (7), interruptedaortic arch (5), ventricular septal defect (4), patent foramen ovate (3), tricuspid valve regurgitation (3), mitral valve regurgitation (2), aortic valve regurgitation (1), coarctation of aorta (1), left superior vena cavae (1), and dextrocardia (1) were associated. Repair methods included 1) division of the APW with primary closure or patch closure of aorta and pulmonary artery primary closure or patch closure (11) and 2) intra-arterial patch closure (3). 3) Division of the window and descending aorta to APW anastomosis (2) in the patients with interrupted aortic arch or coarctation. Result: There was one death. The patient had 2.5 cm long severe tracheal stenosis from carina with tracheal bronchus supplying right upper lobe. The patient died at 5th post operative day due to massive tracheal bleeding. Patients with complex aortopulmonary window had longer intensive care unit and hospital stay and showed more morbidities and higher reoperation rates. 5 patients had reoperations due to left pulmonary artery stenosis (4), right pulmonary artery stenosis (2), and main pulmonary artery stenosis (1). The mean follow-up period was $6.8{\pm}5.6$ (57.0 days$\sim$16.7 years)years and all patients belonged to NYHA class 1. Conclusion: With early and prompt correction of APW, excellent surgical outcome can be expected. However, optimal surgical method needs to be established to decrease the rate of stenosis of pulmonary arteries.

• Journal of Chest Surgery
• /
• v.38 no.3 s.248
• /
• pp.241-244
• /
• 2005

A 57-year-old man with numbness and paresthesia of left arm is presented. There was no pulse in the left arm was absent and his chest radiograph suggested right-sided aortic arch. The aortogram showed right-sided aortic arch with Kommerell's diverticulum. The proximal portion of left subclavian artery was totally occluded and blood was being supplied through vertebral arteries to distal subclavian artery. He underwent bypass grafting between both subclavian arteries by an expanded polytetrafluoroethylene graft. Because the size of Kommerell's diverticulum was small, it need to be observed closely.

• Tuberculosis and Respiratory Diseases
• /
• v.39 no.6
• /
• pp.548-553
• /
• 1992

The Unilateral absence of a pulmonary artery (UAPA) is an uncommon congenital anomaly. Approximately 160 cases have been reported in the literature since Frantzel's first report in 1968. Most of the patients with UAPA are asymptomatic but some patients may suffer from recurrent respiratory infections, hemoptysis, or pulmonary hypertension. The diagnosis could be suspected from the chest roentgenogram and lung scan, and definitely confirmed by pulmonary angiography. We experienced a case of UAPA in a 39-year-old male with the recurrent hemoptysis. Chest X-ray revealed that the left lung volume was moderately decreased and the heart and mediastinum were displaced to the left side. Lung perfusion scan showed that the left lung was not perfused. Pulmonary angiography revealed the absence of the left main pulmonary artery. Aortic arch and descending aorta on aortogram were right sided. Blood supply to the left lung was originated from numerous systemic collaterals from intercostal and brachiocephalic origin. No other intrinsic or internal abnormalities of the cardiac chambers were noted.

• Archives of Plastic Surgery
• /
• v.38 no.4
• /
• pp.508-511
• /
• 2011

Purpose: Blue toe syndrome consists of blue or purplish toes in the absence of a history of obvious trauma, serious cold exposure, or disorders producing generalized cyanosis. It is a life-threatening and still underrecognized disease. It can be commonly occurred by vascular surgery, invasive cutaneous procedures or anticoagulant therapy. Our case is presented of blue toe syndrome related to atheromatous embolization that was presumably triggered by angio CT. Methods: A 69-year-old man presented with the suddenly developed pain, cyanosis and livedo reticularis of the toes in right foot. Dorsalis pedis pulses were palpable. He had been performed a diagnostic angio CT 1 month earlier. Angio CT revealed diffuse aortic atheromatous plaque in lower abdominal aorta and both common iliac artery. One month after angio CT, he visited our clinic. There was no visible distal first dorsal metatarsal artery and digital artery of right first toe in lower extremity arteriography. A diagnosis was established of blue toe syndrome. Because his symptom was aggravated, we performed the exploration of the right foot. After exposure of first dorsal metatarsal artery, microsurgical atheroembolectomy was done. Results: There were no postoperative complications. After three months the patient had no clinically demonstrable problems. Conclusion: Patient with blue toe syndrome is at high risk of limb loss and mortality despite treatment. Blue toe syndrome produces painful, cyanosed toes with preserved pedal pulses. It needs to be aware of blue toe syndrome. Careful history should reveal the diagnosis. Treatment is controversial, however, most believe that anticoagulation therapy should be avoided.

• The Korean Journal of Physiology and Pharmacology
• /
• v.2 no.2
• /
• pp.209-216
• /
• 1998

The present study was designed: (1) to determine whether or not hypoxia stimulates the release of endothelium-derived relaxing factors (EDRFs) from endothelial cells, and (2) to examine whether or not the hypoxia-induced EDRFs release is further augmented by previous hypoxia-reoxygenation, using bioassay system. In the bioassay experiment, rabbit aorta with endothelium was used as EDRFs donor vessel and rabbit carotid artery without endothelium as a bioassay test ring. The test ring was contracted by prostaglandin $F_{2{\alpha}}$ $(3{\times}10^{-6}\;M/L)$, which was added to the solution perfusing through the aortic segment. Hypoxia was evoked by switching the solution aerated with 95% $O_2/5%\;CO_2$ mixed gas to one aerated with 95% $N_2/5%\;CO_2$ mixed gas. When the contraction induced by prostaglandin $F_{2{\alpha}}$ reached a steady state, the solution was exchanged for hypoxic one. And then, hypoxia and reoxygenation were interchanged at intervals of 2 minutes (intermittent hypoxia). The endothelial cells were also exposed to single 10-minute hypoxia (continuous hypoxia). When the bioassay ring was superfused with the perfusate through intact aorta, hypoxia relaxed the precontracted bioassay test ring markedly. Whereas, when bioassay ring was superfused with the perfusate through denuded aorta or polyethylene tubing, hypoxia relaxed the precontracted ring slightly. The relaxation was not inhibited by indomethacin but by nitro-L-arginine or methylene blue. The hypoxia-induced relaxation was further augmented by previous hypoxia-reoxygenation and the magnitude of the relaxation by intermittent hypoxia was significantly greater than that of the relaxation by continuous hypoxia. The results suggest that hypoxia stimulates EDNO release from endothelial cells and that the hypoxia-induced EDNO release is further augmented by previous hypoxia-reoxygenation.