• 약학회지
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• 제32권4호
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• pp.258-273
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• 1988

In this study attempts were made to observe the effects of guanabenz on renal function in dog, which manifests the antihypertensive action by inhibition of sympathetic tone through stimulating the presynaptic adrenoceptor (${\alpha}_2-adrenoceptor$). Guanabenz, when injected at a dose of $30.0{\mu}g/kg$, or infused at a dose of $3.0{\mu}g/kg/min$ intravenously, produced diuretic action with increased amounts of $Na^+\;and\;K^+$ in urine, and with decreased reabsorption rates of $Na^+\;and\;K^+$ in renal tubules. It was also observed that the rates of osmolar and free water clearances were increased, but the glomerular filtration rate and renal plasma flow were not changed. Guanabenz injected at a dose of $3.0{\mu}g/kg$ into a carotid artery or infused intravenously at a dose of $3.0{\mu}g/kg/min$ in a state of water diuresis elicited the diuretic action of the similar aspect as a case of guanabenz given intravenously. The diuretic action produced by guanabenz was completly blocked by pretreatment of i.v. prazosin, ${\alpha}_1-adrenoblocking$ agent, or of i.v. yohimbine, ${\alpha}_2-adrenergic$ blocking agent. Prazosin, when given into a renal artery, inhibited the diuretic action by i.v. guanabenz in only injected kidney, whereas in case of yohimbine the action was inhibited in both kidney. Guanabenz infused at a dose of $1.0{\mu}g/kg/min$ into a renal artery exhibited no significant changes of renal function in both kidney. In denervation experiments, guanabenz given intravenously produced typical diuretic action in innervated kidney, whereas in denervated kidney, it did not affect the action at initial period but exhibited the action with increase of only free water clearance at later period. These results suggest that guanabenz produced diuretic action in dog by inhibition of electrolyte reabsorption rates in renal tabules, mainly proximal tubule and of ADH release, which is mediated by stimulating of central sympathetic ${\alpha}_2-receptor$.

• 대한의생명과학회지
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• 제11권3호
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• pp.365-373
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• 2005

The aim of this study was to investigate the alterations in meningeal blood flow by stimulation of trigeminovascular system. An open cranial window was prepared on the right parietal bone of male Sprague-Dawley rats. Trigeminovascular system was stimulated by electrical stimulation of trigeminal ganglion (ETS), somatosensory (whisker) stimulation, or topical applications of capsaicin and neuropeptides including substance P and calcitonin gene-related peptide (CGRP). Neonatal capsaicin pretreatment was performed with subcutaneous administration of capsaicin (50 mg/kg) within the first 24 hours after birth. Changes in regional blood flow of dural artery (rDBF) and pial artery (rPBF) were continuously measured through the cranial window by laser-Doppler flowmetry. Both ETS and capsaicin caused a chain of alterations in rPBF and rDBF responses, i.e., an immediate transient decrease followed by rapid and marked increase in rPBF, which were significantly attenuated not only by pretreatments with L-733,060, a $NK_1$ receptor blocker, $CGRP_{8-37}$, a $CGRP_1$ receptor blocker, and 7-nitroindazole monosodium salt (7-NINA), a neuronal nitric oxide synthase inhibitor but also by neonatal capsaicin treatment. Exogenous neuropeptides including substance P and CGRP increased the meningeal blood flow, which was significantly attenuated not only by pretreatment with L-733,060 and $CGRP_{8-37}$, respectively, but also by pretreatment with 7-NINA. The rPBF response to whisker stimulation was significantly attenuated not only by trigeminovascular system injuries including nasociliary nerve denervation and neonatal capsaicin treatment but also by pretreatments with L-733,060, $CGRP_{8-37}$ and 7-NINA. These results suggest that the stimulation of trigeminovascular system causes prominent alterations in meningeal blood flow, and that neuropeptides as well as nitric oxide in the trigeminovascular system are importantly implicated in the regulation of meningeal blood flow.

• 대한후두음성언어의학회지
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• 제22권2호
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• pp.126-132
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• 2011

Background and Objectives : Vocal fold paresis is a clinical condition and considered as a continuum of neurologic dysfunction encompassing partial denervation and variable degrees and patterns of reinnervation. Its incidence, clinical presentation, significance are incompletely understood and still debated. This study describes the clinical, electromyographic findings in patients who presented with complaints of dysphonia and whose laryngoscopic finding revealed vocal fold paresis. Materials and Method : 47 patients (male : 25, female : 22) who referred to Ewha Womans University Medical Center Voice clinic for evaluation of vocal complaints were enrolled in this study. All patients had undergone a through history and physical examination including strobovideoscopic and laryngoscopic examination. Patients with in the history and/or laryngoscopic examination suggestive of vocal fold paresis were evaluated by laryngeal electromyography (LEMG). Results : Of these patients, 23 (48.9%) were found to have evidence of neuropathy on LEMG. There was no significant difference in voice symptoms and laryngoscopic findings between two groups of patients with evidence of neuropathy and who show normal findings on LEMG. Conclusion : LEMG can clinically help to guide the evaluation and management of vocal fold paresis. Due to some limitations of LEMG, laryngoscopic findings and clinical correlations should also be considered when diagnosing the vocal fold paresis.

• The Korean Journal of Physiology and Pharmacology
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• 제19권3호
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• pp.275-281
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• 2015

Orthostatic hypotension is most common in elderly people, and its prevalence increases with age. Attenuation of the vestibulo-sympathetic reflex (VSR) is commonly associated with orthostatic hypotension. In this study, we investigated the role of glutamate on the vestibulo-solitary projection of the VSR pathway to clarify the pathophysiology of orthostatic hypotension. Blood pressure and expression of both pERK and c-Fos protein were evaluated in the nucleus tractus solitarius (NTS) after microinjection of glutamate into the medial vestibular nucleus (MVN) in conscious rats with sodium nitroprusside (SNP)-induced hypotension that received baroreceptor unloading via sinoaortic denervation (SAD). SNP-induced hypotension increased the expression of both pERK and c-Fos protein in the NTS, which was abolished by pretreatment with glutamate receptor antagonists (MK801 or CNQX) in the MVN. Microinjection of glutamate receptor agonists (NMDA or AMPA) into the MVN increased the expression of both pERK and c-Fos protein in the NTS without causing changes in blood pressure. These results indicate that both NMDA and AMPA receptors play a significant role in the vestibulo-solitary projection of the VSR pathway for maintaining blood pressure, and that glutamatergic transmission in this projection might play a key role in the pathophysiology of orthostatic hypotension.

• The Korean Journal of Physiology and Pharmacology
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• 제18권4호
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• pp.353-358
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• 2014

Control of blood pressure is maintained by the interaction between the arterial baroreflex and vestibulosympathetic reflex during postural changes. In this study, the contributions of vestibular receptors and baroreceptors to the maintenance of blood pressure following acute hypotension were compared in terms of phosphorylated extracellular regulated protein kinase (pERK) expression in the nucleus tractus solitaries (NTS). Expression of pERK in the NTS was measured in conscious rats that had undergone bilateral labyrinthectomy (BL) and/or sinoaortic denervation (SAD) 5, 10, 20, and 40 min following acute hypotension induced by sodium nitroprusside (SNP) infusion. Expression of pERK increased significantly in the NTS in the control group following SNP infusion, and the expression peaked at 10 min after SNP infusion. The number of pERK positive neurons increased following SNP infusion in BL, SAD, and BL+SAD groups, although the increase was smaller than in control group. The BL group showed a relatively higher reduction in pERK expression than the SAD group, and the pERK expression in the NTS was localized to the caudal portion of the nuclei in the BL and SAD groups. These results suggest that the vestibular receptors may play a key role in maintaining blood pressure following acute hypotension; thus, the vestibular system may contribute to compensate for orthostatic hypotension.

• The Korean Journal of Physiology and Pharmacology
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• 제21권6호
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• pp.675-686
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• 2017

Orthostatic hypotension (OH) is associated with symptoms including headache, dizziness, and syncope. The incidence of OH increases with age. Attenuation of the vestibulosympathetic reflex (VSR) is also associated with an increased incidence of OH. In order to understand the pathophysiology of OH, we investigated the physiological characteristics of the VSR in the disorder. We applied sodium nitroprusside (SNP) to conscious rats with sinoaortic denervation in order to induce hypotension. Expression of pERK in the intermediolateral cell column (IMC) of the T4~7 thoracic spinal regions, blood epinephrine levels, and blood pressure were evaluated following the administration of glutamate and/or SNP. SNP-induced hypotension led to increased pERK expression in the medial vestibular nucleus (MVN), rostral ventrolateral medullary nucleus (RVLM) and the IMC, as well as increased blood epinephrine levels. We co-administered either a glutamate receptor agonist or a glutamate receptor antagonist to the MVN or the RVLM. The administration of the glutamate receptor agonists, AMPA or NMDA, to the MVN or RVLM led to elevated blood pressure, increased pERK expression in the IMC, and increased blood epinephrine levels. Administration of the glutamate receptor antagonists, CNQX or MK801, to the MVN or RVLM attenuated the increased pERK expression and blood epinephrine levels caused by SNP-induced hypotension. These results suggest that two components of the pathway which maintains blood pressure are involved in the VSR induced by SNP. These are the neurogenic control of blood pressure via the RVLM and the humoral control of blood pressure via epinephrine release from the adrenal medulla.

• The Korean Journal of Physiology
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• 제19권2호
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• pp.173-187
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• 1985

Renal compensatory adaptation caused by ablation of a part of renal mass has long been known in the field of the compensatory renal hypertrophy or hyperplasia. Many reports were found on the chronic mechanisms on the compensatory renal hyperfunction after exclusion of the contralateral kidney. However the mechanism(s) of the acute compensatory hyperfunction after contralateral exclusion has not yet been clarified. In the present experiment, we have tried to prove the possibility of the involvement of the renin-angiotensin system and/or prostaglandin system in the control mechanism of the acute compensatory renal hyperfunction after contralateral kidney exclusion. There were found different responses of the renal hyperfunction by contralateral renal pedicle or ureteral occlusion. Contralateral renal pedicle or ureteral occlusion caused a sustained increases of the urinary volume, sodium and potassium excretion, while the magnitude of the changes was different quantitatively by the maneuvers. Blood collection affected on the acute compensatory renal responses after ureteral as well as renal pedicle occlusion. Plasma prostaglandin $E_2$ level was not changed by the contralateral renal pedicle or ureteral occlusion. Urinary excretion of Prostaglandin $E_2$, the indices of renal prostaglandin biosynthesis, was not changed by the contralateral renal pedicle occlusion, but increased without significance by the contralateral ureteral occlusion. Acute renal compensatory responses after contralateral renal pedicle occlusion were blocked by the pretreatment of indomethacin. Plasma renin activity increased after contralateral ureteral occlusion, but the pattern of the increases was the same as in the time-control group. Plasma renin activity after contralateral renal pedicle occlusion did not change by the time sequence. SQ 20,881, an angiotensin I converting enzyme inhibitor, blunted the contralateral renal responses after the renal pedicle occlusion. Bilateral renal denervation abolished the contralateral renal responses after the renal pedicle occlusion. The above data suggest that there is no direct evidence to support the involvement of the renin-angiotensin system and/or prostaglandin system for the acute compensatory renal hyperfunction after contralateral kidney exclusion, and that the functional changes of the intact kidney may be caused by a humoral substances, or other mechanisms by afferent renal nerve activity originating from the treated kidney.

• 한국자원식물학회:학술대회논문집
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• 한국자원식물학회 2018년도 춘계학술발표회
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• pp.8-8
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• 2018

Muscle atrophy, known as a sarcopenia, is defined as a loss of muscle mass resulting from a reduction in muscle fiber area or density due to a decrease in muscle protein synthesis and an increase in protein breakdown. Many conditions are associated with muscle atrophy, such as aging, denervation, disuse, starvation, severe injury and inflammation, prolonged bed rest, glucocorticoid treatment, sepsis, cancer, and other cachectic diseases. On the other hand, osteoarthritis (OA) is the most common form of joint disease and is wide spread in the elderly population and is characterized by erosion of articular cartilage, osteophyte formation, and subchondral bone sclerosis. The cytokine network plays an important role in the development and progression of OA with the inflammatory cytokine. Schisandrae Fructus (SF) derived from the ripe fruit of Schisandra chinensis (Turcz.) Baill. (Magnoliaceae) has been extensively used in traditional herbal medicines in Asia. It was originally used as a tonic and has been traditionally used for the treatment of many uncomfortable symptoms, such as cough, dyspnea, dysentery, insomnia, and amnesia for a long time. Previous reports have shown that SF and its related compounds possess various biological activities such as antioxidant, anti-inflammatory, anticancer, anti-microbial, antiseptic, anti-aging, hepatoprotective and immunostimulating effects. However, the therapeutic effects of SF on muscle atrophy and OA has not yet been evaluated. In the present study, we aimed to determine whether extracts of SF, the dried fruit of S. chinensis, mitigates the development of muscle atrophy and OA.

• The Korean Journal of Pain
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• 제34권4호
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• pp.479-486
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• 2021

Background: Prior studies have reported that 40%-90% of the patients with celiac plexus-mediated visceral pain benefit from the neurolytic celiac plexus block (NCPB), but the predictive factors of response to NCPB have not been evaluated extensively. This study aimed to identify the factors associated with the immediate analgesic effectiveness of NCPB in patients with intractable upper abdominal cancer-related pain. Methods: A retrospective review was performed of 513 patients who underwent NCPB for upper abdominal cancer-related pain. Response to the procedure was defined as (1) a decrease of ≥ 50% or ≥ 4 points on the numerical rating scale (NRS) in pain intensity from the baseline without an increase in opioid requirement, or (2) a decrease of ≥ 30% or ≥ 2 points on the NRS from the baseline with simultaneously reduced opioid consumption after NCPB. Logistic regression analysis was performed to determine the factors associated with successful responses to NCPB. Results: Among the 513 patients included in the analysis, 255 (49.8%) and 258 (50.2%) patients were in the non-responder and responder group after NCPB, respectively. Multivariable logistic regression analysis showed that diabetes (odds ratio [OR] = 0.644, P = 0.035), history of upper abdominal surgery (OR = 0.691, P = 0.040), and celiac metastasis (OR = 1.496, P = 0.039) were the independent factors associated with response to NCPB. Conclusions: Celiac plexus metastases, absence of diabetes, and absence of prior upper abdominal surgery may be independently associated with better response to NCPB for upper abdominal cancer-related pain.

• Clinical Pain
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• 제18권1호
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• pp.52-57
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• 2019

Spinal accessory neuropathy (SAN) is commonly caused by an iatrogenic procedure, and that caused by tumors is very rare. We present a case of a 49-year-old man suffering from weakness in the right trapezius and sternocleidomastoid muscle. An electrophysiology study confirmed proximal SAN. Fluorodeoxyglucose (FDG)-positron emission tomography (PET)/computed tomography (CT) revealed a diffuse large B-cell lymphoma compressing the right spinal accessory nerve. Ultrasonography showed definite atrophy on the trapezius and sternocleidomastoid muscles. In addition, post-chemotherapy FDG-PET/CT showed increased FDG uptake in the right upper trapezius, suggestive of denervation. This is the first report of SAN caused by direct compression by a diffuse large B-cell lymphoma, comprehensively assessed by an electrophysiology study, ultrasonography, and FDG-PET/CT.