• Journal of Environmental Science International
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• v.12 no.10
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• pp.1131-1136
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• 2003

To examine whether salt stress would alter or not contractility of isolated rat aorta, under anesthesia with sodium pentobarbital(50 mg kg-1 i.p.), male Sprague Dawley rats(300-330 g) were subjected to 0, 50, and 150 mM of sodium chloride at 37$^{\circ}C$ for 60 min. where as the sham group was left at modified Krebs-bicarbonate solution. To measure contractile response of vascular ring preparation isolated from rat was determined in organ bath and was recorded on physiograph connected to isometric transducer. And the strip was checked for expression of heat shock protein(Hsp) by Western blotting. One, three and eight hours later, we measured vascular contractility of isolated rat aorta treated with KCI, phenylephrine from organ bath study. The dose-vascular responses of potassium chloride and phenylephrine showed a little augmentation by NaCl concentration in the strips exposed to NaCl for 8 hours. And the response of relaxation induced by nitroprusside and acetylcholine was not influenced by NaCl stress in isolated aorta ring for 8 hours, respectively. Expression pattern of Hsp 70 of vascular muscle in isolated rat aorta showed a little increase in 150 mM NaCl group at 8 hours after NaCl treatment but not at 3 hours, and Hsp 60 expression of rat aorta was markedly increased in 50 mM NaCl group at 8 hours after NaCl treatment. Taken together, NaCl induced dose-and time dependent accumulation of the Hsp but not affected contraction of rat aorta. These data suggest that short term high salt stress was not sufficient to induce hypertension of rat aorta.

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

• Journal of Environmental Science International
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• v.12 no.6
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• pp.651-657
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• 2003

In order to examine if arsenic, one of environmental stresses, contributes to hypertension as one of cardiovas cular pathological factors, this study was perfarmed in vivo and in vitro, using intacted or pithed rats and aorta ring preparation, respectively. And also the relationship between expression of heat shock protein (HSP) 90 and vasoactives-induced contractile response was elucidated. To measure blood pressure, the carotid arterial pressure was recorded on physiograph(Grass Co. 79E) connected to strain gauge. On the other hand, contractile response of vascular ring preparation isolated from rat was determined in organ bath and was recorded on physiograph connected to isometric transducer. And HSP was detacted by Western blotting whole cell Iysis. Preganglionic nerve stimulation was increased by 26.0% in arterial pressure of rat treated with arsenic. Vascular contractile response was monitored and HSP were measured by Western blotting of whole Iysis prepared from samples exposed with 0, 0.5, 1, 2 and 4 mM of arsenic for 8 hours. The dose-vascular responses of potassium chloride were augmented by increasing dose of arsenic in the strips exposed to arsenic for 8 hours, and were not augmented for 1, 3, 5 hours. And the response of relaxation of rat aorta induced by histamine was not influenced by arsenic stress. The increase of HSP 90 expression in rat aorta was pronounced at 8 hours after 4 mM of arsenic treatment, but HSP 60 expression was not. Arsenic stress not only increased the expression of HSP 90 in the rat aorta, but also augmented contractions to potassium chloride. These results indicated that arsenic stress was sufficient to induce heat shock protein 90, resulting in increased vascular contractility in rat aorta.

• Journal of Chest Surgery
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• v.9 no.2
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• pp.251-264
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• 1976

Forty three patients with disease of the aorta were admitted in this department during the period from beginning of 1956 to the end of 1976. They consisted of eighteen cases of aortic aneurysms, eight cases of Takayasu's arteritis, eight Leriche syndromes, six dissecting aneurysms, two aortic coarctations and one case of vascular ring. Of eighteen aortic aneurysms, twelve were operated resulting in eight survivors. Three of four mortalities were in shock preoperatively because of aneurysmal rupture. Among six dissecting aortic aneurysms, four were type III and two were type I according to DeBakey's classification. For the purpose of relief of acute arterial insufficiency in the lower extremities, a re-entry operation grafting a Y-shaped dacron vessel between abdominal aorta and common iliac arteries was performed. The patient regained consciousness soon after the operation and was well until postoperative second day, when severe convulsion developed abruptly and died. And in a chronic case of type III dissecting aneurysm, a dacron graft bypass shunt between ascending aorta and lower descending thoracic aorta with resection of the aneurysm was performed, but acute severe aortic insufficiency developed soon after the operation and fell into intractable heart failure resulting in death. The cause of the aortic insufficiency seems to be retrograde dissection from the proximal anastomosis site in the ascending aorta. Three cases were treated medically with Wheat's regimen. Two of them survived with relief of symptoms. Eight patients of Takayasu's arteritis were all females and aged between twenty and forty-four averaging twenty nine. Bypass graft operation between aortic arch and carotid arteries using Y-shaped nylon prostheses were performed in three patients resulting in death in two cases postoperatively due to severe cerebral arterial insufficiency during the procedure. All the patients with Leriche syndrome were males and over forty. In two cases, bypass graft with Y-shaped dacron vessel between terminal aorta and common iliac or femoral arteries were performed with good result. Thromboembolectomy or thromboendarterectomy was employed in three patients, of whom one was aggravated in sexual problem postoperatively. One out of two aortic coarctations and a vascular ring were treated surgically with excellent results.

• Journal of Chest Surgery
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• v.18 no.2
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• pp.305-313
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• 1985

Surgical therapy for dissection of the aorta has had a high mortality. One contributing factor has been hemorrhage from the prosthesis and the suture lines. Recently, a new method of treatment with an intraluminal graft that requires no end-to-end anastomosis has been developed. Of the four patients with dissecting aneurysm of the aorta treated by inserting sutureless ringed intraluminal graft at the Department of Thoracic and Cardiovascular Surgery, S.N.U.H., three were DeBakey type I [one with associated aortic insufficiency] and the other was DeBakey type III. Suspected etiology of the dissection was Marfan`s syndrome in one and hypertension in the others. Total cardiopulmonary bypass was utilized in repairing dissecting aneurysms of the ascending aorta [type A] and simple aortic crossclamping was used for the patient with dissecting aneurysm of the descending aorta. The basic technique consists of inserting the whole ringed graft into the true lumen of the dissected aorta and circumferentially ligating the aorta against the groove in the rings. The proximal ring of the graft effectively stabilized the flail aortic valve in patient with aortic insufficiency associated with dissection of the ascending aorta. There were no hospital deaths and one patient with type III dissecting aneurysm developed postoperative paraparesis and renal insufficiency which was resolved. Follow-up has been from 1 month to 16 months with no evidence of prosthetic problems, such as erosion, migration, or thrombosis.

• Journal of Chest Surgery
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• v.45 no.5
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• pp.338-341
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• 2012

Vascular ring, caused by Kommerell's diverticulum and ligamentum arteriosum, in a patient with right aortic arch and mirror image branching is extremely rare. A 10-month-old boy with coughing and stridor was diagnosed as having tracheo-esophageal stenosis, which is caused by a vascular ring with Kommerell's diverticulum, ligamentum arteriosum, right aortic arch, and mirror image branching. Kommerell's diverticulum was successfully resected via a left thoracotomy. The patient has been free from tracheo-esophageal stenosis for a year after the surgery.

• Journal of Chest Surgery
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• v.12 no.3
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• pp.183-190
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• 1979

A 23-year-old male patient complained dyspnea on exertion and orthopnea since December 1977. On examination, he was tall and slender. There was grade IV/VI to-and-fro murmur on the left sternal border especially on Erb`s point. The liver was descended 2 fingers breadth below right costal margin. There were no signs of Marfan`s syndrome. Echocardiography demonstrated partial closure of aortic valve and dilated aortic root with enlargement of ascending aorta. Left heart cardiac catheterization revealed moderately elevated pulmonary wedge pressure and right ventricular pressure. The left ventricular end diastolic pressure was markedly elevated to 26 mmHg. On aortography, the aortic regurgitation was severe and it was belonged to angiographically Grade IV. The aortic valve was replaced with Carpentier-Edwards valve without excision and replacement of ascending aorta, under the impression of rheumatic valvular heart disease. After closure of aortotomy, blood pressure was transiently elevated and bleeding from the site of inserting air vent needle of ascending aorta was developed. The bleeding was not controlled by any means. On postmortem microscopic study, the histologic changes were strikingly limited to the ascending aorta from the region of the aortic valve ring.

• YAKHAK HOEJI
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• v.37 no.2
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• pp.163-171
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• 1993

In order to study the functions of vascular endothelial nitric oxide(NO) generating system, we examined the effects of monomethylarginine(MMA) and dimethylarginine(DMA)(asym., sym.), arginine analogues, on modulation of vascular tone. Also, the concentrations of endogenous arginie and MMA were measured by HPLC in rat aortic tissues. The results were as follows. 1. The maximum relaxation induced by Ach (1.5$\times$10$^{-6}$M) was 80% of the contractility of rings of rat aorta induced by phenylephrine and L-Arg causes endothelium-dependent relaxation of the aorta precontracted with phenylephrine and these relaxation were concentration-dependent. 2. Endothelium-dependent contractility of rings of rat aorta induced by MMA (100 $\mu{M}$), DMA (asym., 100 $\mu{M}$) and DMA (sym., 100 $\mu{M}$) were 25.5%, 27.5% and 16.5% of that induced by phenylephrine respectively. 3. The relaxation of rat aortic ring induced by L-Arg was inhibited by MMA, DMA(asym.) and DMA(sym.). The degrees of inhibition induced by MMA, DMA(asym.) and DMA(sym.) were 45.7%, 37.1% and 18.3%, respectively. 4. The endogenous arginine and monomethylarginine contents in rat aorta were 83 pmoles/mg wet tissue, and 34.9 pmoles/mg wet tissue. After stimulation with Ach, the concentrations of L-Arg and MMA were significantly decreased. These results suggest that there are the strong relationships between the endogenous L-Arg and methylated arginines and NO-generating system.

• Nutrition Research and Practice
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• v.2 no.2
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• pp.74-79
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• 2008

Zinc plays a protective role in anti-atherosclerosis but the clear mechanism has not been proposed yet. In the present study, we evaluated whether zinc modulates atherosclerotic markers, VACM-1 and ICAM-1 and cell viability both in endothelial cells in vitro and mouse aortic cell viability ex vivo. In study 1, as in vitro model, endothelial EA.hy926 cells were treated with $TNF{\alpha}$ for 5 hours for inducing oxidative stress, and then treated with Zn-adequacy ($15\;{\mu}M$ Zn) or Zn-deficiency ($0\;{\mu}M$ Zn) for 6 hours. Pro-atherosclerosis factors, VCAM-1 and ICAM-1 mRNA expression and cell viability was measured. In study 2, as ex vivo model, mouse aorta ring was used. Mourse aorta was removed and cut in ring then, cultured in a 96-well plate. Aortic ring was treated with various $TNF{\alpha}$ (0-30 mg/ml) and intracellular zinc chelator, N, N, N', N', -tetrakis (2-pyridylmethyl) ethylenediamine (TPEN, $0-30\;{\mu}M$) for cellular zinc depletion for 2 days and then cell viability was measured. The results showed that in in vitro study, Zn-adequate group induced more VCAM-1 & ICAM-1 mRNA expression than Zn-deficient group during 6-hour zinc treatment post-5 hour TNF-$\alpha$ treatment, unexpectedly. These results might be cautiously interpreted that zinc would biologically induce the early expression of anti-oxidative stress through the increased adhesion molecule expression for reducing atherosclerotic action, particularly under the present 6-hour zinc treatment. In ex vivo, mouse aortic ring cell viability was decreased as TNF-$\alpha$ and TPEN levels increased, which suggests that mouse aortic blood vessel cell viability was decreased, when oxidative stress increases and cellular zinc level decreases. Taken together, it can be suggested that zinc may have a protective role in anti-atherosclerosis by cell viability in endothelial cells and aorta tissue. Further study is needed to clarify how pro-atherosclerosis molecule expression is modulated by zinc.

• The Korean Journal of Physiology and Pharmacology
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• v.3 no.4
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• pp.393-404
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• 1999

We have reported that hypoxia stimulates EDRF(s) release from endothelial cells and the release may be augmented by previous hypoxia. As a mechanism, it was hypothesized that reoxygenation can stimulate EDRF(s) release from endothelial cells and we tested the hypothesis via bioassay experiment. In the bioassay experiment, rabbit aorta with endothelium was used as EDRF donor vessel and rabbit carotid artery without endothelium as a bioassay test ring. The test ring was contracted by prostaglandin $F_{2a}\;(3{\times}10^{-6}\;M)$ which was added to the solution perfusing through the aorta. Hypoxia was evoked by switching the solution aerated with 95% $O_2/5%\;CO_2$ mixed gas to one aerated with 95% $O_2/5%\;CO_2$ mixed gas. Hypoxia/reoxygenation were interexchanged at intervals of 2 minutes (intermittent hypoxia). In some experiments, endothelial cells were exposed to 10-minute hypoxia (continuous hypoxia) and then exposed to reoxygenation and intermittent hypoxia. In other experiments, the duration of reoxygenation was extended from 2 minutes to 5 minutes. When the donor aorta was exposed to intermittent hypoxia, hypoxia stimulated EDRF(s) release from endothelial cells and the hypoxia-induced EDRF(s) release was augmented by previous hypoxia/reoxygenation. When the donor aorta was exposed to continuous hypoxia, there was no increase of hypoxia-induced EDRF(s) release during hypoxia. But, after the donor aorta was exposed to reoxygenation, hypoxia-induced EDRF(s) release was markedly increased. When the donor aorta was pretreated with nitro-L-arginine $(10^{-5}$ M for 30 minutes), the initial hypoxia-induced EDRF(s) release was almost completely abolished, but the mechanism for EDRF(s) release by the reoxygenation and subsequent hypoxia still remained to be clarified. TEA also blocked incompletely hypoxia-induced and hypoxia/reoxygenation-induced EDRF(s) release. EDRF(s) release by repetitive hypoxia and reoxygenation was completely blocked by the combined treatment with nitro-L-arginine and TEA. Cytochrome P450 blocker, SKF-525A, inhibited the EDRF(s) release reversibly and endothelin antgonists, BQ 123 and BQ 788, had no effect on the release of endothelium-derived vasoactive factors. Superoxide dismutase (SOD) and catalase inhibited the EDRF(s) release from endothelial cells. From these data, it could be concluded that reoxygenation stimulates EDRF(s) release and hypoxia/reoxygenation can release not only NO but also another EDRF from endothelial cells by the production of oxygen free radicals.