• The Korean Journal of Physiology
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• v.24 no.1
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• pp.77-90
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• 1990

There have been conflicting reports concerning the effect of Panax ginseng on the contractility of vascular smooth muscle, i.e., Panax ginseng extract has been reported to cause relaxation, contraction or to have no effect on the tension of vascular smooth muscle. A further investigation of $Ca^{++}$ stores which supply $Ca^{++}$ for contraction of vascular smooth muscle is needed to understand the underlying mechanisms of this conflicting effect of ginseng alcohol extract (GAE). The present study was intended to examine the sources of calcium mobilized for contraction of vascular smooth muscle by GAE. Aortic ring preparations were made from the rabbit thoracic aorta and endothelial cells were removed from the ring. The contractility of the aortic ring was measured under various experimental conditions and $Ca^{++}$ flux across the membrane of aortic ring and the sarcoplasmic reticulum and mitochondria were measured with a calcium selective electrode. The result were summarized as follows; 1) At low concentration of extracellular $Ca^{++}$, GAE increased the contractility of vascular smooth muscle in dose-dependent fashion except high concentration $Ca^{++}$ (1 mM). 2) In the presence of ryanodine, GAE still increased contractility of vascular smooth muscle as much as control group, but in the presence of caffeine, GAE increased it significantly. i.e. Their effects seemed to be additive. 3) In the presence of verapamil+lanthanum, and verapamil+lanthanum+ryanodine, the contractility of the vascular smooth muscle was decreased, but a dose dependent increase in vascular tension was still demonstrated by GAE although total tension was low. 4) GAE increased $Ca^{++}$ efflux from vascular smooth muscle cells, but have no effect on $Ca^{++}$ influx. 5) GAE increased $Ca^{++}$ efflux from sarcoplasmic reticulum and mitochondria vesicles. From the above results, it may be concluded that GAE increased the release of $Ca^{++}$ from sarcoplasmic reticulum, mitochondria or other intracellular $Ca^{++}$ stores of vascular smooth muscle, but it does not increase $Ca^{++}$ influx across the plasma membrane.

• Journal of Chest Surgery
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• v.48 no.1
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• pp.78-81
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• 2015

This study reports our early experience with thoracoscopic division of vascular rings. Three patients were reviewed; their ages at surgery were 25 months, 4 years, and 57 years. All patients were suffering from complete vascular rings involving combinations of the right aortic arch, left ligamentum arteriosum, Kommerell's diverticulum, and retroesophageal left subclavian artery. The median surgical time was 180.5 minutes, and the patients showed immediate recovery. Three complications, namely chylothorax, transient supraventricular tachycardia, and left vocal cord palsy, were observed. Our early experience indicates that thoracoscopic division of a vascular ring may provide early recovery and could be a promising operative choice.

• Preventive Nutrition and Food Science
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• v.20 no.4
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• pp.221-229
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• 2015

Hesperidin has been shown to possess a potential inhibitory effect on vascular formation in endothelial cells. However, the fundamental mechanism for the anti-angiogenic activity of hesperidin is not fully understood. In the present study, we evaluated whether hesperidin has anti-angiogenic effects in mouse embryonic stem cell (mES)-derived endothelial-like cells, and human umbilical vascular endothelial cells (HUVECs), and evaluated their mechanism via the AKT/mammalian target of rapamycin (mTOR) signaling pathway. The endothelial cells were treated with several doses of hesperidin (12.5, 25, 50, and $100{\mu}M$) for 24 h. Cell viability and vascular formation were analyzed using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide and tube formation assay, respectively. Alteration of the AKT/mTOR signaling in vascular formation was analyzed by western blot. In addition, a mouse aortic ring assay was used to determine the effect of hesperidin on vascular formation. There were no differences between the viability of mES-derived endothelial-like cells and HUVECs after hesperidin treatment. However, hesperidin significantly inhibited cell migration and tube formation of HUVECs (P<0.05) and suppressed sprouting of microvessels in the mouse aortic ring assay. Moreover, hesperidin suppressed the expression of AKT and mTOR in HUVECs. Taken together, these findings suggest that hesperidin inhibits vascular formation by blocking the AKT/mTOR signaling pathways.

• Preventive Nutrition and Food Science
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• v.19 no.4
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• pp.299-306
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• 2014

Hesperetin has been shown to possess a potential anti-angiogenic effect, including vascular formation by endothelial cells. However, the mechanisms underlying the potential anti-angiogenic activity of hesperetin are not fully understood. In the present study, we evaluated whether hesperetin has anti-angiogenic effects in human umbilical vascular endothelial cells (HUVECs). HUVECs were treated with 50 ng/mL vascular endothelial growth factor (VEGF) to induce proliferation as well as vascular formation, followed by treatment with several doses of hesperetin (25, 50, and $100{\mu}M$) for 24 h. Cell proliferation and vascular formation were analyzed using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide and tube formation assay, respectively. In addition, cell signaling related to cell proliferation and vascular formation was analyzed by western blot. Furthermore, a mouse aorta ring assay was performed to confirm the effect of hesperetin on vascular formation. Hesperetin treatment did not cause differences in HUVECs proliferation. However, hesperetin significantly inhibited VEGF-induced cell migration and tube formation of HUVECs (P<0.05). Moreover, hesperetin suppressed the expression of ERK, p38 MAPK, and PI3K/AKT in the VEGF-induced HUVECs. In an ex vivo model, hesperetin also suppressed microvessel sprouting of mouse aortic rings. Taken together, the findings suggest that hesperetin inhibited vascular formation by endothelial cells via the inhibition of the PI3K/AKT, ERK and p38 MAPK signaling.

• 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 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.

• Journal of Chest Surgery
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• v.39 no.12 s.269
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• pp.943-945
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• 2006

An 11-month old girl with a feeding difficulty and recurrent aspiration pneumonia received surgical correction of complete vascular ring, which was formed by right aortic arch, aberrant left subclavian artery(LSCA) originating from Kommerell's diverticulum(KD) and ligamentum arteriosum. Through left posterolateral thoracotomy, the ligamentum arteriosum was divided to relieve the tracheo-esophageal bundle. KD was separated from the right descending aorta, and the left subclavian artery was severed from KD at its origin and trasfered to the side wall of left common carotid artery. Postoperative course was uneventful, and the patient has been followed up with a clinical improvement.

• Journal of the Korean Orthopaedic Association
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• v.54 no.6
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• pp.557-561
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• 2019

Most low-energy pelvic ring fractures in elderly patients are treated conservatively so that an initial evaluation for complications such as vascular injury is usually overlooked. An 81-year-old female, who was taking regular aspirin, visited the emergency room and was diagnosed with a simple non-displaced pubic ramus fracture from a low-energy fall from standing, which was complicated by massive hemorrhage from the overlooked injury of the corona mortis. Elderly patients with pelvic ring fractures can have a delayed presentation of vascular injuries, regardless of the degree of displacement of the fractures, which highlights the need for a careful physical examination and close monitoring.

• Journal of Korean Neurosurgical Society
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• v.29 no.4
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• pp.451-460
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• 2000

Objective : This experiment is aimed at clarifying the characteristics of spasmodic basilar arteries in the rabbits of subarachnoid hemorrhage(SAH) with observation of vascular response to nitric oxide(NO) and endothelin-1. Material and Methods : Seventy-nine New Zealand white rabbits were divided into 4 groups : control(n=17), sham operation(n=13), postictal-2-day(n=25), and postictal-7-day group(n=24). Rabbits in the postictal-2-day group and postictal-7-day group underwent transfemoral vertebral angiography 2 days and 7 days after SAH respectively. A vascular ring of spasmodic basilar artery was harvested and suspended in organ chamber($37^{\circ}C$) to observe isometric tension changes in response to NO and endothelin-1 under both high(95% $O_2$/5% $CO_2$) and low(95% $N_2$/5% $CO_2$) $O_2$ tension. To investigate the vascular response to NO, acetylcholine from $10^{-7}M$ to $3{\times}10^{-4}M$ concentration was applied to basilar artery ring precontracted with histamine $10^{-6}-10^{-5}M$ in the organ chamber. The vascular response to endothelin-1 was observed by applying endothelin-1 from $10^{-11}M$ to $3{\times}10^{-8}M$ concentration into organ chamber. Results : Seven of 15 live rabbits which underwent angiography 2 days after SAH, were confirmed to develop vasospasm($64.3{\pm}11.2%$) whereas seven of 13 live rabbits which underwent angiography 7 days after SAH, were confirmed to develop vasospasm($64.9{\pm}10.9%$). In all groups, hypoxia significantly reduced the vascular relaxation of basilar arteries to NO. However, hypoxia made no influence on the vascular contraction of basilar arteries to endothelin-1 in all groups. In vascular relaxation of basilar arteries to NO under high $O_2$ tension between groups, the maximum relaxation of basilar arteries in the postictal-7-day group was significantly reduced compared to the postictal-2-day group. In vascular contraction of basilar arteries to endothelin-1 under high $O_2$ tension between groups, the maximum contraction of basilar arteries in the postictal-7-day group was significantly reduced compared to the postictal-2-day group. Conclusions : This experiment suggests that the characteristics of vascular response to NO and endothelin-1 in the spasmodic basilar arteries of rabbits observed 2 days after SAH is different from those observed 7 days after SAH.

• Proceedings of the Korea Society of Environmental Biology Conference
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• 2003.11a
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• pp.86-91
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• 2003

In this study, in order to examine whether salt and heat shock stress would alter or not contraction and relaxation of isolated rat aorta. Under anesthesia with sodium pentobarbital(50 mg Kg$^{-1}$ i.p.), male Sprague Dawley rats weighing 300-330 g were subjected to 0, heat shock combined salt stress, 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(Hsps) by means of western blotting. The combination group of heat and 50 mM NaCl group increased vascular contractility, and the heat and 150 mM NaCl group decreased vascular contractility for 5 hours, and then recovered for 8 hours compared to that of control. Expressin of Hsp 70 of vascular muscle of rat aorta more increased by combination of heat and NaCl treatment than those of single treatment of heat or NaCl treatment, and vascular Hsp 70 showed a little decrease at 8 hours compared at 5 hours. These result indicate that mixed environmental stress either increased or decreased in vascular contractility by combination of heat and NaCl concentration.