• Journal of Industrial Convergence
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• v.20 no.7
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• pp.131-137
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• 2022

In the study, we endeavored to assess the convergence effect of Silybum marianum-derived silymarin and epidemiologically-correlated alcohol intake on vascular contractility and to determine the mechanism involved. There were few reports addressing the question whether thin or thick filament modulation is included in ethanol and silymarin-induced regulation. We hypothesized that ethanol at a low concentration and silymarin play a role in agonist-dependent regulation of vascular contractility. Denuded arterial muscles of Sprague-Dawley male rats were suspended in organ baths and isometric tensions were transduced and recorded using isometric transducers and an automatic data acquisition system. Interestingly, both silymarin and ethanol didn't encourage silymarin alone-induced inhibition in agonists-induced contraction suggesting that endothelial nitric oxide synthesis might be involved in ethanol or silymarin-induced modulation of vascular contractility and additional pathways besides endothelial nitric oxide synthesis such as ROCK inactivation might be involved in the silymarin-induced modulation of vascular contractility.

• Journal of Cardiovascular Imaging
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• v.31 no.2
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• pp.71-82
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• 2023

BACKGROUND: Cardiac magnetic resonance fingerprinting (cMRF) enables simultaneous mapping of myocardial T1 and T2 with very short acquisition times. Breathing maneuvers have been utilized as a vasoactive stress test to dynamically characterize myocardial tissue in vivo. We tested the feasibility of sequential, rapid cMRF acquisitions during breathing maneuvers to quantify myocardial T1 and T2 changes. METHODS: We measured T1 and T2 values using conventional T1 and T2-mapping techniques (modified look locker inversion [MOLLI] and T2-prepared balanced-steady state free precession), and a 15 heartbeat (15-hb) and rapid 5-hb cMRF sequence in a phantom and in 9 healthy volunteers. The cMRF_5-hb sequence was also used to dynamically assess T1 and T2 changes over the course of a vasoactive combined breathing maneuver. RESULTS: In healthy volunteers, the mean myocardial T1 of the different mapping methodologies were: MOLLI 1,224 ± 81 ms, cMRF_15-hb 1,359 ± 97 ms, and cMRF_5-hb 1,357 ± 76 ms. The mean myocardial T2 measured with the conventional mapping technique was 41.7 ± 6.7 ms, while for cMRF_15-hb 29.6 ± 5.8 ms and cMRF_5-hb 30.5 ± 5.8 ms. T2 was reduced with vasoconstriction (post-hyperventilation compared to a baseline resting state) (30.15 ± 1.53 ms vs. 27.99 ± 2.07 ms, p = 0.02), while T1 did not change with hyperventilation. During the vasodilatory breath-hold, no significant change of myocardial T1 and T2 was observed. CONCLUSIONS: cMRF_5-hb enables simultaneous mapping of myocardial T1 and T2, and may be used to track dynamic changes of myocardial T1 and T2 during vasoactive combined breathing maneuvers.

• Journal of Chest Surgery
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• v.32 no.5
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• pp.461-464
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• 1999

Background: Thoracoscopic T2 sympathicotomy is an effective method for the treatment of palmar hyperhidrosis. Not only are the symptoms of hyperhidrosis abolished but also the temperature of the ipsilateral palm is elevated due to the sympatholytic vasodilation after the completion of the sympathicotomy on the first side. However little is known about the temperature changes in the contralateral palm. This study was performed to evaluate the changes in both palmar temperatures during the thoracoscopic T2 sympathicotomy for palmar hyperhidrosis. Material and Method: Thoracoscopic T2 sympathicotomy was performed in 15 patients with primary palmar hyperhidrosis. Surface temperatures of both palms were monitored continuously and were recorded simultaneously during the 7 different stages of the operation. Result: When T2 sympathicotomy was performed on the first(left) side, an ipsilateral increase with a contralateral decrease of temperature was observed. The difference in the temperature of both palms was greatest just before the sympathicotomy on the contralateral(right) side(Lt. 34.6$\pm$0.9$^{\circ}C$ vs. Rt. 31.6$\pm$1.3$^{\circ}C$, P<0.0001). After the sympathicotomy on the second(right) side, temperature of the right palm was elevated. The difference in the temperature of both palms was abolished at the end of the operation(Lt.34.7$\pm$0.9$^{\circ}C$ vs. Rt.34.4$\pm$1.$0^{\circ}C$, P=0.415). Conclusion: When T2 sympathicotomy was performed on the first side, an ipsilateral palmar temperature increased due to the sympatholytic vasodilation. However contralateral palmar temperature decreased due to a vasoconstriction. Although the mechanism of vasoconstriction is still unknown, it is postulated that there may be a cross- inhibitory effect by the post-ganglionic neurons innervating blood vessels of the palm.

• Journal of Chest Surgery
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• v.41 no.5
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• pp.541-549
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• 2008

Background: Vasoconstrictor-induced reduction in arterial graft diameter can cause significant flow deprivation. The aim of this study was to evaluate the effect of vasodilator pretreatment on vasoconstrictor-induced blood vessel spasm in vitro. Material and Method: Rabbit brachial arteries (BA) and celiac arteries (CA) were cut into rings $(3{\sim}4mm)$ and suspended with a force displacement transducer (TSD $125C^{(R)}$, Biopac Inc. USA) in a tissue bath filled with 5 mL modified Krebs solution bubbled with 5% $CO_2$ and 95% $O_2\;at\;38^{\circ}C$. The rings were contracted with vasoconstrictors, and the developed tension changes were considered control values. The rings were then pre- treated with $30{\mu}M$ nitroglycerin, nicardipine, verapamil, and papaverine, respectively, for 40 minutes and rinsed with the physiologic buffered salt solution three times every 15 min. The vasoconstrictor-induced tension changes after the previous procedure were considered experimental values. Data are expressed as the percentage tension induced by vasoconstrictors before and after pretreatment with vasodilators. Result: Nicardipine depressed vasoconstriction induced by norepinephrine, angiotensin II (All), and U46619 in both the BA and the CA more significantly than did nitroglycerin (p<0.01) and verapamil (p<0.05). Verapamil depressed vasoconstriction induced by 5-hydroxytryptamine (5HT), All, and U46619 in the BA and by 5HT in the CA more significantly than did nitroglycerin (p<0.01). Conclusion: These findings suggest that both nicardipine and verapamil effectively depressed vasoconstrictor action. Nicardipine is thought to be more effective than verapamil for the prevention of vasoconstrictor action.

• Tuberculosis and Respiratory Diseases
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• v.62 no.5
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• pp.421-426
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• 2007

Portopulmonary hypertension (PPHTN) is a clinically and pathophysiologically distinct complication of advanced liver disease. PPHTN is characterized by the development of pulmonary arterial hypertension in association with advanced hepatic disease-related portal hypertension. A characteristic feature of PPHTN is an obstruction to the pulmonary artery flow caused by vasoconstriction, the proliferation of the endothelium and smooth muscle components of the vascular wall, as well as in situ thrombosis. This disorder is commonly underdiagnosed but the clinical implications are significant because it has substantial effects on survival and requires special treatment. We report a case of portopulmonary hypertension in a 53-year-old woman with primary biliary cirrhosis who presented with exertional dyspnea.

• The Korean Journal of Pharmacology
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• v.31 no.1 s.57
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• pp.27-37
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• 1995

In anesthetized rats, we examined the possibility that endothelium-derived relaxing factor (EDRF) or nitric oxide (NO) released in response to cholinergic mechanism may contribute to the reflex autoregulation of cerebral blood flow. Suffusion with mock cerebrospinal fluid (CSF), containing acetylcholine (ACh, $10^{-9}{\sim}10^{-6}M$) evoked concentration-dependent vasodilatation of the resting pial artery (mean, $19.3{\pm}1.7{\mu}m$, n=36), which was significantly inhibited not only by $N{\omega}$-nitro-L-arginine (L-NNA, $10^{-5}M$) but also by methylene blue ($10^{-6}M$) and oxyhemoglobin ($10^{-6}M$). The muscarinic receptors in the endothelium of pial artery implicated in the release of EDRF were considered to be $M_1\;and\;M_3$ subtypes. When suffused with mock CSF containing L-arginine it caused a transient vasodilatation, which was strongly inhibited by LY 83583 ($10^{-5}M$), but not by L-NNA ($10^{-5}M$). Additionally, both ACh- and L-arginine-induced vasodilation were significantly inhibited by glibenclamide, a specific ATP-sensitive $K^+$ channel blocker. On the other hand, changes in pial arterial diameter were plotted as a function of changes in systemic arterial blood pressure. The slopes of regression lines for vasodilation and vasoconstriction were not affected by pretreatment with $10^{-5}M$ L-NNA, but significantly reduced by $3{\times}10^{-6}M$ glibenclamide. Thus it is suggested that the reflex vasodilation of rat pial arteries in response to a transient hypotension is not mediated by EDRF (NO).

• The Korean Journal of Nuclear Medicine Technology
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• v.22 no.1
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• pp.84-89
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• 2018

Purpose Renin is a proteolytic enzyme synthesized and secreted from epidermal(juxtaglomerular) cells in kidney. Renin acts on the renin substrate angiotensinogen to produce angiotensin I, and then angiotensin II is produced by the action of angiotensin converting enzyme. This causes the adrenal glands to boost blood pressure (vasoconstriction) and promote aldosterone secretion. While Plasma renin activity (PRA) is to test angiotensin I, the active renin concentration (ARC) is a renin test directly. They have different test methods and their own substrates. However, these two methods are sometimes interpreted as the same as a result. The purpose of this study was to evaluate the usefulness of the ARC test by comparing the results between PRA and ARC. Materials and Methods For the diversity of the experiment, 26 samples were requested to test with PRA(TFB company) and ARC(Cisbio company) to other institution. We compared and analyzed PRA(Immunotech company) and ARC(Cisbio company) tests using 28 samples from September $15^{th}$ to October $13^{th}$ in 2017. The statistical analysis method for PRA/ARC evaluated the usefulness using Microsoft Excel program by verifying a correlation analysis of Aldosterone/PRA ratio and a correlation analysis of Aldosterone/ARC ratio and conducting T-test. Results The regression equation of the PRA(Immunotech company)/ARC(Cisbio company), which was tested in the department, was y = 0.0619x + 0.4615 and the correlation coefficient was 0.73. The regression equation of the PRA(TFB company)/ARC(Cisbio company), which was tested in the other institution, was y = 0.0888x + 0.3316 and the correlation coefficient was 0.91. In addition, The regression equation of Aldosterone / PRA ratio and Aldosterone / ARC ratio was y = 0.875x - 11.688 and the correlation coefficient was 0.87. Plus T - test showed no significant difference (P>0.05). Conclusion Both tests showed a strong positive correlation, but this only represents the strength and direction of the relationship between the two tests. Furthermore, the actual results showed somewhat differences. It is presumed that the measured value was influenced by the endogenous renin group mass in the plasma, the condition of the enzyme reaction and the kind of the inhibitor. When the active renin concentration (ARC) test is performed, it is useful to distinguish between the two tests as they are complementary.

• Biomolecules & Therapeutics
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• v.3 no.1
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• pp.21-27
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• 1995

The only compounds with antagonistic activity via AT$_1$receptor, one of two subtypes of angiotensin II (AII) receptor, have been demonstrated to block the vasoconstriction effects of AII and thereby provide therapeutic potential. This initiated the search for compounds with high specific affinity to AT$_1$receptor and their effective screening methods. The radioligand binding assay for the AII receptor is regarded as the primary method for the evaluation of AT$_1$receptor antagonists for their activity. In this paper, we characterized the liver AT$_1$receptor and describe the efficient method of the radioligand binding assay using rat liver as a source of AT$_1$receptor. Equilibrium binding studies with rat adrenal cortex, adrenal medulla, liver and bovine adrenal showed that the specific bindings of [$^3$H] AII were saturable in all tissues and the Scatchard plots of those data were linear, suggesting a single population of binding sites. Hill slopes were very near to the unity in all tissues. Kinetic studies of [$^3$H) AII binding in rat liver homogenates yielded two association rate constants, 4.10$\times$10$^{7}$ M$^{-1}$ min$^{-1}$ and 4.02$\times$10$^{9}$ M$^{-1}$ min$^{-1}$ , with a single dissociation rate constant, 7.07$\times$10$^{-3}$ min-$^{-1}$ , possibly due to the partial dissociation phenomenon. The rank order of inhibition potencies of [$^3$H] AII binding in rat liver was AII>Sarile>Losartan>PD 123177. Rat liver homogenates revealed to have very high density of homogeneous population of the AT$_1$receptor subtype, as the specifically bound [$^3$H] AII was not inhibited by PD 123177, the nonpeptide antagonist of AT$_2$. The results of this study demonstrated that the liver homogenates from rats could be the best receptor preparation for the AT$_1$receptor binding assay and provide an efficient system for the screening of newly synthesized candidate compounds of AT$_1$receptor antagonist.

• Journal of Physiology & Pathology in Korean Medicine
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• v.27 no.5
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• pp.602-610
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• 2013

This study was aimed to evaluate the cavernosal relaxation effect of Crataegii fructus(CF) in the contracted rabbit penile corpus cavernosum by agonists.In order to study the effect of CF on the vasoconstriction of rabbit penile corpus cavernosum, isolated rabbit penile corpus cavernosum tissues were used for the experiment using organ baths containing Krebs solution.To investigate the cavernosal relaxation of CF, CF extract at $0.01{\sim}3.0mg/m{\ell}$ was added after penile corpus cavernosum were contracted by norepinephrine(NE) $1{\mu}M$. To analyze the mechanism of CF's vasorelaxation, CF extract infused into contracted penile tissues by NE after each treatment of indomethacin(IM), $N{\omega}$-nitro-L-arginine(L-NNA), methylene blue(MB), tetraethylammonium chloride(TEA).To study the effect of CF on influx of extracellular calcium chloride($Ca^{2+}$) in penile tissues, in $Ca^{2+}$-free krebs solution, $Ca^{2+}$ 1 mM infused into contracted penile tissues by NE after pretreatment of CF. Cytotoxic activity of CF on human umbilical vein endothelial cell(HUVEC) was measured by MTT assay, and nitric oxide(NO) prodution was measured by Griess reagent. CF relaxed cavernosal strip with endothelium contracted by NE, but in the strips without endothelium, CF-induced relaxation was significantly inhibited. The pretreatment of L-NNA, MB, TEA decreased significantly on the cavernosal relaxation than not-treatment of them. But the pretreatment of IM had no significant effect on the cavernosal relaxation. In $Ca^{2+}$-free krebs solution, when $Ca^{2+}$ infused into contracted penile tissues by NE, pretreatment of CF inhibit contraction induced by adding $Ca^{2+}$.NO production wasn't increased by treatment of CF on HUVEC. This findings showed that CF is effective for the relaxation of rabbit penile corpus cavernosum, and we suggest that CF relax rabbit corpus cavernosal smooth muscle through multiple action mechanisms that include increasing the release of nitric oxide from corporal sinusoidal endothelium, inhibition of $Ca^{2+}$ mobilization into cytosol from the extracellular fluid, and maybe a hyperpolarizing action.

• The Korean Journal of Physiology and Pharmacology
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• v.20 no.6
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• pp.605-611
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• 2016

Ketamine is an anesthetic with hypertensive effects, which make it useful for patients at risk of shock. However, previous ex vivo studies reported vasodilatory actions of ketamine in isolated arteries. In this study, we reexamined the effects of ketamine on arterial tones in the presence and absence of physiological concentrations of 5-hydroxytryptamine (5-HT) and norepinephrine (NE) by measuring the isometric tension of endothelium-denuded rat mesenteric arterial rings. Ketamine little affected the resting tone of control mesenteric arterial rings, but, in the presence of 5-HT (100~200 nM), ketamine ($10{\sim}100{\mu}M$) markedly contracted the arterial rings. Ketamine did not contract arterial rings in the presence of NE (10 nM), indicating that the vasoconstrictive action of ketamine is 5-HT-dependent. The concentration-response curves (CRCs) of 5-HT were clearly shifted to the left in the presence of ketamine ($30{\mu}M$), whereas the CRCs of NE were little affected by ketamine. The left shift of the 5-HT CRCs caused by ketamine was reversed with ketanserin, a competitive 5-$HT_{2A}$ receptor inhibitor, indicating that ketamine facilitated the activation of 5-$HT_{2A}$ receptors. Anpirtoline and BW723C86, selective agonists of 5-$HT_{1B}$ and 5-$HT_{2B}$ receptors, respectively, did not contract arterial rings in the absence or presence of ketamine. These results indicate that ketamine specifically enhances 5-$HT_{2A}$ receptor-mediated vasoconstriction and that it is vasoconstrictive in a clinical setting. The facilitative action of ketamine on 5-$HT_{2A}$ receptors should be considered in ketamine-induced hypertension as well as in the pathogenesis of diseases such as schizophrenia, wherein experimental animal models are frequently generated using ketamine.