• Proceedings of the PSK Conference
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• 2002.10a
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• pp.259.2-259.2
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• 2002

The purpose of the present study was to determine the effects of platycodin D and D3 on the contractile force of the isolated rat aorta and blood pressure of the anesthetized rat. and also to establish the mechanism of action. The phenylephrine (10 $\mu$M)-induced contractile responses were greatly inhibited in the presence of platycodin D (4 ∼ 24 $\mu$g/$m\ell$) in a dose-dependent fashion. (omitted)

• The Korean Journal of Pain
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• v.13 no.2
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• pp.191-195
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• 2000

Background: Vascular occlusive event is one of the etiologies of sudden sensorineural hearing loss (SNHL). Stellate ganglion block (SGB) induces dramatic and intense vasodilatation in head and neck. Based on this principle, SGB has used as one of the treatment modalities in SNHL. This study was performed to evaluate immediate response of SGB on pure tone audiogram (PTA) in SNHL. Methods: Forty patients were studied. Each patient received daily ipsilateral SGB in paratracheal approach using 0.2% bupivacaine for 2 weeks. On first, third, and fifth day of treatment, we checked their PTA twice 1 hour before (Pre-PTA) and after (Post-PTA) SGB. Pre- and Post-PTA were compared. Several factors were analyzed as a prognostic factor of therapeutic results. Results: Eleven of 40 patients revealed decreased PTA after SGB. Degree of decreased PTA were insignificant ($2.5{\pm}1.6$ dB). Initial and final PTA results was $76.2{\pm}22.5$ and $49.8{\pm}28.3$ dB, respectively. Thirty-one of 40 patients were improved their PTA over 10 dB. The recovery was mainly influenced by the severity of initial hearing loss (P<0.001) and slightly by age (P<0.05). However, the change of PTA after SGB, time interval to receive SGB, sex, site, and number of SGB were not correlated to therapeutic outcome. Conclusions: These results suggest that vasodilatation by SGB has no immediate improvement in SNHL. Therefore, we question whether SGB is beneficial to all patients with SNHL as a therapeutic modality.

• Proceedings of the Korean Society of Applied Pharmacology
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• 1994.04a
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• pp.287-287
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• 1994

In the present study, it was aimed to asses the possibility that calcitonin gene-related peptide (CGRP) released in response to transient hypotension may contribute to the reflex autoregulation of cerebral blood flow as a putative modulator. Changes in pial arterial diameter (mean, 33.0 ${\pm}$ 1.1 $\mu\textrm{m}$) with changes in systemic arterial blood pressure (mean, 101.9 ${\pm}$ 2.7 mmHg) were observed directly through a closed cranial window in anesthetized normotensive rats. Image of the pial vessels was captured with a stereoscope connected to a CCD video camera and the diameter was measured with a microscaler. In the capsaicin-treated rats (one day prior to experiment, 50 nmol capsaicin injected intracisternally), both vasodilater and vasoconstrictor responses evoked by a transient hypotension and the reverse of blood pressure were markedly attenuated or almost abolished. When changes in pial arterial diameter were plotted as a function of changes in blood pressure, the slopes of both regression lines (for vasodilators and vasoconstrictors ) were markedly reduced. Similar reductions were evidenced under treatment wi th the CGRP antibody serum (1:1,000) and following CGRP receptor desensitization. However, the autoregulatory mechanics were neither affected by treatment wi th spantide (1 ${\mu}$M), substance P antagonist, nor by substance P receptor desensitization. Suffusion wi th mock cerebrospinal fluid containing CGRP and cromakalim caused a vasodilatation in a concentration-dependent manner, respectively and their effects were antagonized by glibenclamide. Substance P produced a vasodilatation, which was, however, little affected by glibenclamide. These observations indicate that the CGRP released from the perivascular sensory fibers in response to a hypotension is implicated in the modulation of the autoregulation of cerebral blood flow.

• BMB Reports
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• v.28 no.4
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• pp.301-305
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• 1995

Considering the stimulatory effects of ginsenosides from Panax ginseng C. A. Meyer on the release of nitric oxide from bovine aortic endothelial cells in vitro and vasodilatation of rabbit pulmonary artery in vivo, the present study is designed to investigate the mechanism of nitric oxide release by ginsenosides in calf pulmonary artery endothelial cells, Nitric oxide release was determined in endothelial cells treated with ginsenosides and compared with those of the receptor-dependent agonists, bradykinin and ADP and the receptor-independent calcium ionophore $A_{23187}$. The results showed that total saponin and ginsenoside $Rg_1$, not $Rb_1$, stimulated nitric oxide release measured as conversion to L-citrulline. The nitric oxide releasing properties of total saponin and ginsenoside $Rg_1$ were different; total saponin stimulated only conversion to L-citrulline, like $A_{23187}$, while ginsenoside $Rg_1$ stimulated both L-arginine transport and conversion to L-citrulline, as bradykinin or ADP did.

• 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 Acupuncture Research
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• v.22 no.4
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• pp.179-188
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• 2005

Objectives : This study is designed to observe anaphylatic reaction In two patients, who visited Dong-Eui University Oriental Medicine Center for Bee-Venom Acupuncture. Methods : Anaphylaxis is a clinical syndrome cheracterized by the acute system reaction of multiple organ systems to an IgE-mediated immunologic mediator release in previously sensitized individuals. Anaphylatic reaction of two patients treated by Bee-Venom Acupuncture were observed in order to analysis the clinical form. Results & Conclusion : STZ One case of Anaphylatic reaction was expressed clinically hypotension drowsy mentality, dizziness muscle contraction and so on. The other case was expressed ulticaria, itching sensation, nausea and erythema. Especially ulticaria erythema are end points of increased vascular permeability and vasodilatation at the extreme of the clinical spectrum.

• Journal of Physiology & Pathology in Korean Medicine
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• v.21 no.3
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• pp.771-775
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• 2007

Licorice has been used for cure of injuries and for detoxification in East Asia. This study investigated the protective effect of licorice water extract against cadmium (CdCl$_2$, Cd)-induced nephro-toxicity in rats. To induce acute toxicity, Cd (4 mg/kg body weight) was dissolved in normal saline and then, intravenously (i.v.) injected to animals. In experiments, animals were orally administrated with vehicle or licorice water extract (50-100 mg/kg) for 3 days, exposed to a single injection of Cd after 24 h the last licorice/vehicle treatment. Licorice protected kidney injuries by Cd treatment. The number of glomeruli showing vasodilatation and thickening of Bowman's capsule was dose-dependently decreased by licorice. These results suggest that licorice might be a potent preventive protector against Cd-induced nephro-toxicity in rats.

• 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).

• Korean Journal of Veterinary Research
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• v.41 no.3
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• pp.299-304
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• 2001

The effect of the nitric oxide synthase(NOS) inhibitor, $N^{G}$-nitro-L-arginine methyl ester (L-NAME), and the prostanoid synthesis inhibitor, indomethacin, on the vasodilatation produced in response to acetylcholine(Ach) on the isolated rabbit renal artery was examined. The vasodilatory reponses to Ach($10^{-8}-3{\times}10^{-5}M$) were completely absent in thevessel which the endothelium had previous been removed. L-NAME($10^{-4}M$) significantly reduced the vasodilatory reponse to the Ach($10^{-8}-3{\times}10^{-5}M$). When L-arginine ($10^{-3}M$) was also present in the organ bath along with L-NAME($10^{-4}M$), this inhibitory effect of L-NAME ($10^{-4}M$) on the vasodilatory response to Ach ($10^{-8}-3{\times}10^{-5}M$) was significantly attenuated, Indomethacin ($10^{-6}M$) did not significantly affect the vasodilatory responses to Ach ($10^{-8}-3{\times}10^{-5}M$). The inhibition by L-NAME ($10^{-4}M$) and indomethacin ($10^{-6}M$) on vasodilatory response to Ach was significantly greater than the inhibition due to L-NAME ($10^{-4}M$) alone. The present study has established that Ach induce relaxation via and endothelium-dependent mechanism, this relaxation to Ach involves both nitric oxide(NO) and prostanoid in the isolated rabbit renal artery.

• The Journal of Korean Medicine Ophthalmology and Otolaryngology and Dermatology
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• v.1 no.1
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• pp.25-38
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• 1988

In order to evaluate the relationship between the bibliographical and clinical effectiveness of Socheongryoungtang, this study was carried out to investigate the effects of Socheongryoungtang on the respiratory system, cardiovascular system and isolated organ in the experimental animals. The following results of Socheongryoungtang were obtained; 1. The relaxing effect on the muscular contraction of isolated ileum induced by acetylcholine chloride, barium chloride and histamine${\cdot}$2HCl was recognized in mice, rat and guinea-pig. 2. The effect of direct vasodilatation was noted in rabbit. 3. The effect of hypotensor was recognized in rabbit. 4. The antihistamine effect was noted on both isolated ileum and tracheal strip-chain in guinea-pig. 5. The inhibitory effect on gastric ulcer induced by histamine${\cdot}$2HCl was noted in rat. 6. The inhibitory effect on vascular permeability was revealed in mice. 7. The antitussive effect was recognized in both dog and cat. 8. The effect of expectorant was recognized in rabbit. According to the above results, we has recognized that Socheongryoungtang has good efficacy for bibliographical and clinical diseases caused from respiratory system (especially allergic rhinitis etc.), cardiovascular system and digestive system.