• Journal of Oral Medicine and Pain
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• v.21 no.1
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• pp.79-87
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• 1996

The purpose of this study was to assess the vascular changes after thermophysical therapies using ice pack and ultrasound, investgate the mechanism of peripheral vasodilation by sympathetic nerve, and to observe the effects of the ergotamine to the thermophysical therapy. The author had used 16 healthy rabbits which were divided into 2 groups : with and without administration of ergotamine. Experimental animals were sacrificed 5, 10, 20 minutes after experiment, and were examined with gross and stereoscope of resin casting blood vessel models. The results were as follows : 1. Vasodilation was not remarkably found in the group with administration of egrotamine after thermophysical therapy. 2. Vasodilation was remarkably found in the group without administration of ergotamine after thermophysical therapy. 3. Vasodilation was increased in the group without administration of ergotamine, but not remarkably found in the group with administration of ergotamine in lapse of time 4. Thermophysical therapy was most effective to arterioles. Our data suggest that the dilation of peripheral blood vessels from thermophysical therapy was controlled by sympathetic nerve, because the blood vessels did not changed after administration of ergotamines which was a sympathetic nerve blocker.

• The Korean Journal of Physiology
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• v.24 no.1
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• pp.115-121
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• 1990

The interaction between a calcium channel blocker nifedipine and atrial natriuretic peptide (ANP) was examined in normotensive and renal hypertensive rats. The infusion of either ANP or nifedipine produced a significant decrease in mean arterial pressure (MAP). The combined infusion of ANP with nifedipine resulted in a greater fall of MAP than did the infusion of each drug alone. ANP significantly increased urinary volume and excretion of sodium, while nifedipine was without effects. The diuretic/natriuretic effects of ANP were potentiated by the combined infusion with nifedipine. The vasodepressor and renal effects of ANP or nifedipine were qualitatively similar between the normotensive and hypertensive rats. Nifedipine caused an upward and leftward shift of the ANP dose-relaxation curve of the phenylephrine-precontracted thoracic aortic rings isolated from the normotensive rats , suggesting that the vasodilation sensitivity to ANP is increased in the presence of nifedipine. These results indicate that nifedipine enhances the vasodepressor effect of ANP, the likely mechanisms being attributable to a contraction of effective intravascular volume as a consequence of potentiated renal excretion and a greater peripheral vasodilation.

• The Korean Journal of Physiology
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• v.23 no.1
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• pp.139-149
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• 1989

Although tail flick reflex (TFR) in rats has been used as a classic model of the nociceptive test to evaluate the action of analgesics, there have been few studies on the origin of the latent period of TFR. Present study was performed to elucidate the mechanism of increase in latency of TFR by morphine in anesthetized rats. Tail skin and dorsolateral tail nerve were stimulated electrically and EMG activities were recorded from abductor caudae dorsalis muscle participating in tail flick reflex. In the case of noxious radiant heat stimulation to tail, the tail flick tension was recorded before and after administration of morphine. Then changes in latency and conduction velocity of peripheral nerve were evaluated. The results obtained were as follows: 1) The latencies of TFR evoked by the electrical stimulation of tail skin and dorsolateral tail nerve were all within 40 ms and were elongated by several milliseconds from control after the administration of morphine. Peripheral conduction velocities of tail flick afferent nerve were within the range of 10-25 m/s. 2) The conduction velocity of peripheral nerve was significantly reduced after morphine administration, therefore the afferent time (utilization time+conduction time to spinal cord) was significantly increased. But the time for central delay and efferent time was not affected by morphine. 3) The conduction velocity under room temperature $(20-25^{\circ}C)$ was significantly reduced after morphine while that under vasodilation state $(40{\sim}42^{\circ}C)$ increased, 30 min and 45 min after morphine. The conduction velocity under vasodilation state without treatment of morphine increased continuously 4) The latency in tension response of TFR evoked by electrical stimulation was elongated by several milliseconds from control while the latency evoked by noxious radiant heat was elongated by several seconds compared with that of control. From the above results, it could be concluded that: 1) the increased latency of TFR evoked by electrical stimulation of the tail after morphine administration was due to the reducton in conduction velocity of peripheral nerve, which was the secondry effect of morphine on the peripheral vasomotion and 2) increased latency of TFR evoked by noxious radiant heat was also due to the same effect of morphine and the increase in cutaneous insulation to the noxious heat.

• Journal of Korean Physical Therapy Science
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• v.1 no.1
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• pp.121-127
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• 1994

The purpose of this study was to determine whether vasodilation occurs when interferential current is applied to the cervical sympathetic chain and peripheral sympathetic nerves. A digital thermometer was used to record skin temperature change. The protocols used for interferential stimulation were 90-100 Hz, applied for 20 minutes via two pairs of electrodes 1) to the throat and 2) to the forearm. Forty subjects were stimulated at each of the two sites. There was no significant correlation between inital skin temperature, sex or age and temperature change. Even though there was a statistically significant temperature increase with cervical sympathetic chain stimulation, this had no clinical vasodilatory effect. More research on interferential current stimulation is needed so that the potential benefits to normal subjects and patients is better understood.

• Journal of Life Science
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• v.18 no.6
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• pp.891-896
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• 2008

The function of mast cells as effector cells in allergy has been extensively studied. Mast cells activated through high affinity IgE-receptor ($Fc{\varepsilon}RI$) release diverse mediators, and lead to smooth muscle constriction, vasodilation, increase of vascular permeability, leukocyte recruitment and activation, mucus secretion, and tissue proliferation and remodeling. However, various other immunological and non-immunological signals can lead to the activation of mast cells. In resent years, mast cells have been identified to be involved in a complex range of immune functions. Mast cells can be important as key players in the regulation of innate as well as adapted immune responses, and may influence the development of allergy, autoimmune disorder and peripheral tolerance. This review summarizes the recent advances in the understanding of effector functions of mast cells in immune responses.

• Journal of Haehwa Medicine
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• v.15 no.2
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• pp.263-272
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• 2006

Purpose Brain vessles have autoregulation function, so even when perfusion pressure drops, cerebral blood flow remain stable by vasodilation. Latest research on this reserve of cerebral vessels is being done using TCD, which measures the reserve of the vessels. We did a research comparing cerebral vessel and peripheral vessel reserve between Taeumin, who are more likely to suffer CVA, and the normal. We observed blood flow of Internal carotid artery siphon and radial indicis artery of the two group with TCD. Method We picked 20 people out of patients diagnosed as cerebral infarction at Cheon-An Oriental hospital of Daejeon University. They were diagnosed as Taeumin with QSCCII questionnaire and constitutional differentiation. Using TCD, we measured highest blood flow rate, mean blood flow and asymmetric counting blood flow of Internal carotid artery siphon and radial indicis artery at rest. And then we measured again after stimulating cerebral vessels, by triggering hypercapnia by self apnea and peripheral vessels by palm heating. Result At rest, mean blood flow rate of Internal carotid artery siphon showed significant decrease compared to control group. Blood flow rate of Internal carotid artery siphon after hypercapnia showed significant decline in highest blood flow rate and mean blood flow compared to control group. Cerebral vessel reaction after the hypercapnia induction showed great change in experiment group than the control group. Peripheral vessel reaction after palm heating showed significant decline in experiment group compared to control group. Conclusion In conclusion, measuring the alteration of blood flow used in diagnosing cerebral infarction, is more sensitive when vessel stimulation is done. Non-invasive TCD is effective especially in case of Taeumin who are more likely to suffer vascular disorder than others.

• Archives of Reconstructive Microsurgery
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• v.6 no.1
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• pp.1-8
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• 1997

Recently prostaglandin $E_1(PGE_1)$ has been shown to ensure flap survival by producing vasodilation of the peripheral vessels and platelet disaggreation. However, direct observation and detailed quantitative studies of the effects of $PGE_1$ on the cutaneous microcirculation have not been reported. In the present study, we investigated cutaneous microcirculatory changes in the rabbit ear chamber(REC) with an intravital microscope following intravenous administration of $PGE_1$. The results obtained in this study indicate that $PGE_1$ administered intravenously at a rate of 200ng/kg/min might act directly on the vessels and cause dilatation of metarterioles and capillaries without affecting vasomotion and systemic blood pressure. Clinically in order to evaluate the effect of an intravenous administration of $PGE_1$ on the cutaneous microcirculation, cutaneous blood flow, skin temperature and transcutaneous $Po_2$ in the pedicle or free flap of operated patients were evaluated by the combination of several measurements following the administration of $PGE_1$. The present study suggests that improvement of cutaneous microcirculation by $PGE_1$ may enhance the survival rate of flap or replantation. Both vessel arterial ischemia and venous congestion are main factors of tissue necrosis in the flap surgery. Vasodilatory or antithrombotic agents have been used in salvage of flap necrosis. However, the therapeutic effects of those drugs are still not well elucidated. Recently prostaglandin $E_1(PGE_1)$ has been shown to ensure flap survival by producing vasodilatation of the peripheral vessels and platelet disaggregation[1-3]. Emerson and sykes[4] have obtained significant improvement in the flap survival in the rat using $PGI_2$. Suzuki et al.[5] have reported prolonged flap survival length by using $PGE_1$ in the rabbit and concluded that $PGE_1$ improved the microcircuration in the flap. However, direct observation and detailed quantitative studies of the effects of $PGE_1$ on the cutaneous microcirculation have not been reported. In the present study, we investigated microcirculatory changes in the rabbit ear chamber[6,7] with an intravital microscope following intravenous administration of $PGE_1$.

• The Korean Journal of Pharmacology
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• v.11 no.1 s.17
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• pp.33-38
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• 1975

The clinical efficacy of Ethaverine, a peripheral vasodilator, was studied according to a double-blind, non-cross over method in 29 diabetic patients with peripheral arterial diseases. The clinical improvement was assessed from the history of patients including the incidence and frequency of intermitten claudication. Ethaverine, after 4 weeks of therapy, was not effective in improving clinical symptoms compared to placebo. Ethaverine, however, was an efective vasodilator than placebo. The quality of vasodilation induced by Ethaverine, was similar to that of alcohol. A new clinical method of studying peripheral vasodilator was presented. The clinical symptoms of peripheral vascular arterial disease in the lower extrimities include reduced intensity of palpable pulses, coldness, and discoloration of the skin. Intermittent claudication may be present. Pathologic changes in vessel architecture precede the symptoms, and recognition of impending vascular insufficiency is a determining factor in selecting vasodilating therapy or surgical management. Also, post-operative patients who have chronic peripheral vascular arterial disease may be candidates for subsequent vasodilating therapy. Peripheral vasodilators, according to the series of reports, may be indicated in vasospastic peripheral vascular condition rather than an occlusive vascular disease and the vessel responds best when a relatively large vascular beds are involved rather than a small, capillary beds. Recently, the clinical efficacy of peripheral vasodilators have been challanged by many clinical investigators and clinicians. In this study, we have re-evaluated the efficacy of Ethaverine HCl as peripheral vasodilator in patients with vasospastic peripheral arterial disease. Ethaverine is claimed to be two to four times as potent a spasmolytic agent as papaverine in a variety of laboratory and clinical work.

• Proceedings of the Korean Society of Applied Pharmacology
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• 1998.11a
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• pp.176-176
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• 1998

An enhanced formation of nitric oxide (NO) is an important mediator of hypotention, peripheral vasodilation and vascular hyporeactivity to vasoconstrictor agents in endotoxaemia. And tumor necrosis factor (TNF${\alpha}$), as a primary mediator of circulatory shock has been known to induce inducible nitric oxide synthase (i-NOS), leading to excessive production of NO. We isolated two sesquiterpene lactone compounds from Saussurea lappa and their structures were elucidated as dehydrocostus lactone and costunolide. These compounds inhibit the production of both NO and TNF${\alpha}$ by LPS (1 $\mu\textrm{g}$/$m\ell$)-activated Raw 264.7 cells. NO was measured spectropho-tometrically as nitrite by the Griess reagent and TNF${\alpha}$ by ELISA. Dehydrocostus lactone (IC$\sub$50/ : 3.0 ${\mu}$M) and costunolide (IC$\sub$50/ : 4.5 ${\mu}$M) inhibited the production of NO in LPS-activated Raw 264.7 cells by suppressing inducible nitric oxide synthase enzyme expression. These compounds also decreased the TNF${\alpha}$ levels in LPS-activated system in vitro and in vivo.

• Asian Pacific Journal of Cancer Prevention
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• v.17 no.2
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• pp.575-579
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• 2016

The aim of this research is to determine the characteristics of endothelial factors and the hemostatic system conditions with malignant neoplasms patients, which were exposed to ionizing radiation. Total number of examined people is 223, 153 of them are patients with gastrointestinal tract oncopathology. The article presents the results of the analysis of numerical indicators of endothelial condition and platelet hemostasis of patients, who had cancer. They lived in the regions of Kazakhstan, subjected to contamination of radionuclides as a result of nuclear weapons tests, which took place in this region from 1949 to 1989. These results then were compared to cancer patients and healthy individuals with no radiation risk. The study revealed the presence of higher levels of endothelial dysfunction and following trigger of the hemostatic system in patients with malignant tumors of the gastrointestinal tract. In particular, the defined high degree of endothelial dysfunction include endothelium-dependent vasodilation, content desquamated endothelial cells in peripheral blood and von Willebrand factor. These indicators have a clear correlation with the degree of disorder of studied parameters of the hemostasis, which can cause the development of thrombotic complications.