• 대한두개안면성형외과학회지
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• 제19권4호
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• pp.243-247
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• 2018

Vascular anomalies are disorders of the endothelium and surrounding cells that can affect the vasculature and involve any anatomical structure. The most common problem associated with vascular anomalies is psychological distress related to disfigurement as well as functional defects, as many lesions affect the head and neck. This article provides an overview of the current clinical features that distinguish the major types of vascular anomalies that affect the head and neck.

• 동의생리병리학회지
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• 제16권1호
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• pp.67-71
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• 2002

This study investigated the relaxation effects of Crataegi Fructus(CF, Crataegus pinnatifida Bunge) on the contraction evoked by phenylephrine in rabbit carotid artery, and also analyzes antioxidative status in vitro. CF revealed siginificant relaxation on phenylephrine-induced arterial contraction. It's relaxant effect statistically significant in both in the presence of endothelium and absence of endothelium, but statistically exerted more strong relaxation in the presence of endothelium. CF increased in vitro nitric oxide(NO) production in dose-dependent manner. Also, they reduced malondiaidehyde(MDA) concentrations, phosphatidyl choline-liposome(PCOOH) contents, linoleic acid-induced lipid peroxidation and exerted 1,1-diphenyl-2- picryl-hydrazyl(DPPH) radical scavenging effect, in vitro. These results indicate that Crataegi Fructus would be effective in relaxing arterial contraction and it's antioxidative effects may be involved in endothelium-dependent relaxation of artery via vascular protective properites.

• 동의생리병리학회지
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• 제22권1호
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• pp.148-154
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• 2008

The butanol extract of Euonymus alatus (BEA) induced dose-dependent relaxation of phenylephrine-precontracted aorta, which was abolished by removal of functional endothelium. Pre-treatment of the endothelium-intact aortic tissues with $N^G-nitro-L-arginine methylester$ (L-NAME), and 1 H-[1,2,4]-oxadiazole- [$4,3-{\alpha}$]-quinoxalin-1-one (ODQ) inhibited the relaxation induced by BEA, respectively. BEA-induced vascular relaxation was not blocked by glibenclamide, tetraethylammonium (TEA), indomethacin, atropine, propranolol, verapamil, and diltiazem, respectively. Moreover, BEA inhibits phenylephrine-induced vascular constriction in a dose-dependent manner. These results suggest that BEA relaxes vascular smooth muscle via endothelium-dependent nitric oxide/cGMP signaling.

• The Korean Journal of Physiology and Pharmacology
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• 제20권5호
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• pp.441-447
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• 2016

Despite the complex vascular effects of dexmedetomidine (DEX), its actions on human pulmonary resistance arteries remain unknown. The present study tested the hypothesis that DEX inhibits vascular tension in human pulmonary arteries through the endothelial nitric oxide synthase (eNOS) mediated production of nitric oxide (NO). Pulmonary artery segments were obtained from 62 patients who underwent lung resection. The direct effects of DEX on human pulmonary artery tension and changes in vascular tension were determined by isometric force measurements recorded on a myograph. Arterial contractions caused by increasing concentrations of serotonin with DEX in the presence or absence of L-NAME (endothelial nitric oxide synthase inhibitor), yohimbine (${\alpha}_2$-adrenoceptor antagonist) and indomethacin (cyclooxygenase inhibitor) as antagonists were also measured. DEX had no effect on endothelium-intact pulmonary arteries, whereas at concentrations of $10^{-8}{\sim}10^{-6}mol/L$, it elicited contractions in endothelium-denuded pulmonary arteries. DEX (0.3, 1, or $3{\times}10^{-9}mmol/L$) inhibited serotonin-induced contraction in arteries with intact endothelium in a dose-dependent manner. L-NAME and yohimbine abolished DEX-induced inhibition, whereas indomethacin had no effect. No inhibitory effect was observed in endothelium-denuded pulmonary arteries. DEX-induced inhibition of vasoconstriction in human pulmonary arteries is mediated by NO production induced by the activation of endothelial ${\alpha}_2$-adrenoceptor and nitric oxide synthase.

• 동의생리병리학회지
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• 제20권5호
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• pp.1166-1173
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• 2006

The aqueous extracts of Cortex Caryophylli (AEC) induced dose-dependent relaxation of phenylephrine-precontracted aorta, which was abolished by removal of functional endothelium. Pretreatment of the endothelium-intact aortic tissues with N$^G$_nitro-L-arginine methyl ester (L-NAME) or 1 H-[1,2,4]-oxadiazole-[4,3-${\alpha}$l-quinoxalin-1-one (ODQ) inhibited the relaxation induced by AEC. AEC-induced vascular relaxations were also markedly attenuated by addition of verapamil, diltiazem and glibenclamide, tetraethylammonium (TEA), respectively, while the relaxation effect of AEC was not blocked by indomethacin, atropine, or propranolol. Moreover, incubation of endothelium-intact aortic rings with AEC increased the production of cGMP. These results suggest that AEC dilates vascular smooth muscle via endothelium-dependent nitric oxide/cGMP signaling, which seems to be causally related with L-type Ca$^{2+}$ and K$^+$ channels.

• The Korean Journal of Physiology
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• 제30권1호
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• pp.21-31
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• 1996

To investigate the mechanisms of increased endothelium-dependent contraction by acetylcholine in hypertensive rats, the relationship between endothelium-dependent contraction by acetylcholine and blood pressure was studied in spontaneously hypertensive rats (SHR), one-kidney, one clip Goldblatt hypertension (1K,1C-GBH) rats, and Wistar-Kyoto rats (WKY). SHR were treated orally with enalapril or nicardipine in order to prevent development of hypertension or suppress the developed hypertension. 1K,1C-GBH rats were made by renal artery stenosis with contralateral nephrectomy in 8 week-WKY. 1. Endothelium-dependent contractions by acetylcholine $(10^{-6}{\sim}10^{-5}\;M)$ in SHR were significantly greater than those in WKY. 2. Chronic treatment with enalapril or nicardipine reduced the endothelium-dependent contraction in SHR 3. The degree of reduction of endothelium-dependent contraction was greater in SHR which was prevented from developing hypertension than in SHR of which high blood pressure was suppressed. 4. In aortic rings from 1K,1C-GBH rats, endothelium-dependent contractions by acetylcholine were augmented as compared with WKY. 5. There is good relationship between the value of blood pressure and magnitude of endothelium-dependent contraction. Thus, it is suggested that increased endothelium-dependent contraction in hypertensive rats may he due to the high blood pressure and endothelium-dependent contraction may not be a cause of the initiation of hypertension in SHR.

• 생명과학회지
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• 제13권5호
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• pp.634-641
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• 2003

외부에서 가해진 비소 스트레스가 내피유무에 따른 흰쥐 대동맥의 수축력 증가와 이완반응에 미치는 영향을 알아보고자 본 실험을 실시하였다. 혈압의 측정은 생리기록계를 이용하였고, 내피 유무에 따른 혈관의 수축력은 Organ bath에 조직을 걸고 자동조절 생리기록계를 이용하여 측정하였다. 중추신경계를 파괴시킨 흰쥐의 생체 내 실험에서 비소처리로 vasopressin과 phenylephrine에 의한 혈관 수축력은 대조군에 비해 각각 19.1%와 46.6%로 대동맥의 혈압은 상승되었다. 0, 0.5, 1, 2 및 4 mM As을 처리한 적출 대동맥 실험에서 phenylephrine $(10^{-6}M)$을 가했을 때 5시간까지는 혈관 수축력의 변화가 미미했으나 8시간째 비소 처리군은 대조군에 비해 39% 증가된 값을 보여 수축력이 더욱 유의하게 증가되었다. 내피 제거 시 저농도 비소처리에서 다소 신속한 수축반응을 보였으나 고농도 비소 처리시에는 내피유무에 따른 차이가 유의적이지 않았다. 이완제 sodium nitroprusside와 acetylcoline를 처리했을 때 대조군에 비해 다소 증가된 이완력을 보였고, 시간경과에 따라 내피 비의존적인 nitroprusside와 달리 내피 의존적인 acetylcholine에서 이완력이 대조군에 비해 다소 촉진되었다. 이상의 결과에서 4 mM As처리시 혈관의 수축력은 증가되었으나 내피유무에 따른 차이는 유의적이지 않았고, 내피가 혈관의 이완력을 다소 촉진시킨 것으로 나타났다. 결론적으로 비소처리한 혈관은 내피유무와 무관하게 수축력이 증가되어 장기간 고농도 비소에 노출 시 고혈압을 유발할 우려가 있을 것으로 여겨진다.

• Biomolecules & Therapeutics
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• 제26권4호
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• pp.374-379
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• 2018

In this study, we investigated the effects of pelargonidin, an anthocyanidin found in many fruits and vegetables, on endothelium-independent vascular contractility to determine the underlying mechanism of relaxation. Isometric contractions of denuded aortic muscles from male rats were recorded, and the data were combined with those obtained in western blot analysis. Pelargonidin significantly inhibited fluoride-, thromboxane A2-, and phorbol ester-induced vascular contractions, regardless of the presence or absence of endothelium, suggesting a direct effect of the compound on vascular smooth muscles via a different pathway. Pelargonidin significantly inhibited the fluoride-dependent increase in the level of myosin phosphatase target subunit 1 (MYPT1) phosphorylation at Thr-855 and the phorbol 12,13-dibutyrate-dependent increase in the level of extracellular signal-regulated kinase (ERK) 1/2 phosphorylation at Thr202/Tyr204, suggesting the inhibition of Rho-kinase and mitogen-activated protein kinase kinase (MEK) activities and subsequent phosphorylation of MYPT1 and ERK1/2. These results suggest that the relaxation effect of pelargonidin on agonist-dependent vascular contractions includes inhibition of Rho-kinase and MEK activities, independent of the endothelial function.

• The Korean Journal of Physiology and Pharmacology
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• 제20권5호
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• pp.539-545
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• 2016

Nafamostat mesilate (NM), a synthetic serine protease inhibitor, has anticoagulant and anti-inflammatory properties. The intracellular mediator and external anti-inflammatory external signal in the vascular wall have been reported to protect endothelial cells, in part due to nitric oxide (NO) production. This study was designed to examine whether NM exhibit endothelium dependent vascular relaxation through Akt/endothelial nitric oxide synthase (eNOS) activation and generation of NO. NM enhanced Akt/eNOS phosphorylation and NO production in a dose- and time-dependent manner in human umbilical vein endothelial cells (HUVECs) and aorta tissues obtained from rats treated with various concentrations of NM. NM concomitantly decreased arginase activity, which could increase the available arginine substrate for NO production. Moreover, we investigated whether NM increased NO bioavailability and decreased aortic relaxation response to an eNOS inhibitor in the aorta. These results suggest that NM increases NO generation via the Akt/eNOS signaling pathway, leading to endothelium-dependent vascular relaxation. Therefore, the vasorelaxing action of NM may contribute to the regulation of cardiovascular function.

• The Korean Journal of Physiology
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• 제29권2호
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• pp.279-289
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• 1995

This study was designed 1) to develop a hypertensive animal model in which the blood pressures (BPs) of symmetric regions (right and left upper extremities) are significantly different and 2) to test the effect of BP per se on the contractility and endothelium-dependent relaxation of vascular smooth muscle. Rabbits were anesthetized with sodium pentobarbital and ventilated with room air via animal respirator. The transverse aorta was exposed through the left second intercostal space and the lumen of the aorta was narrowed partially by ligation using 3-0 silk and a probe at a point between the origins of the brachiocephalic trunk and the left subclavian artery. Four to eight weeks postoperatively, BPs were measured in the carotid artery as the high BP area (proximal to coactation site) and in the femoral artery as the low BP area (distal to coarctation site). In the animal model, pressure-overload hypertension was developed and the BP of the right subclavian artery was higher than that of the left subclavian artery. The concentrations of circulating epinephrine, norepinephrine, angiotensin I, and angiotensin II were measured. The right and left subclavian arteries and their branches were used for isometric tension recording in organ baths and their responsiveness to phenylephrine, serotonin, acetylcholine, and sodium nitroprusside were examined. The BPs of carotid and femoral artery in control animals were $116{\pm} 12/75{\pm}9\;mmHg (mean ${\pm}SEM$) and $130{\pm}16/68{\pm}9\;mmHg$ respectively, while those of carotid and femoral artery in the hypetensive animals were $172{\pm}6/111{\pm}10\;mmHg$ and 136{\pm} 4/100 {\pm}9\;mmHg$ respectively. There were no significant differences in the concentrations of circulating epinephrine, norepinephrine, angiotensin I, and angiotensin II between controls and the animal models. No significant differences were found in the vascular sensitivities to phenylephrine and serotonin between the high pressure-exposed vessels and the low pressure-exposed vessels. However, the endothelium-dependent relaxation to acetylcholine and nitroprusside-induced relaxation showed significant differences between the high pressure-exposed and the low pressure-exposed subclavian arteries. From the above results, we suggest that the contractility of vascular smooth muscle is unchanged by the elevated pressure per se. However, the endothelium-dependent relaxation to acetylcholine and the nitroprusside-induced relaxation are attenuated by pressure.