• The Korean Journal of Physiology
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• 제25권2호
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• pp.147-158
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• 1991

The effects of noradrenaline on the spontaneous contraction recorded from a strip of mucosa-free antral circular muscle were studied in the guinea-pig stomach, and the changes in slow waves and membrane resistance were analyzed in order to elucidate the mechanism for the excitatory response to noradrenaline. Electrical responses of circular muscle cells were recorded using glass microelectrodes filled with 3 M KCI. Electrotonic potentials were produced to estimate membrane resistance by the partition stimulating method. All experiments were performed in tris-buffered Tyrode solution which was aerated with 100% $O_2$ and kept at $35^{\circ}C$. The results obtained were as follows: 1) The spontaneous contractions were potentiated dose-dependently by the application of noradrenaline. 2) Through the experiments using adrenoceptor-blockers, the strong excitatory effect via $[\alpha}-adrenoceptors$ and the weak inhibitory efffect via ${\beta}-adrenoceptors$ were noted. 3) Noradrenaline produced hyperpolarization of membrane potential, and increases in the amplitude and the maximum rate of rise of slow waves. 4) In the presence of apamin, Ca-dependent K channel blocker, the characteristic hyperpolarization was not developed. However, the excitatory effect of noradrenaline on spontaneous contraction remained. 5) Membrane resistance was reduced during the hyperpolarized state by the application of noradrenaline, and the change of membrane resistance and the hyperpolarized state were completely abolished by apamin. From the above results, following conclusions could be made: Excitatory responses to noradrenaline result from the dominant ${\alpha}-excitatory$, and the weak ${\beta}-inhibitory$ action of noradrenaline. Hyperpolarization of membrane potential by noradrenaline is due to the activation of Ca-dependent K channel.

• The Korean Journal of Pain
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• 제28권3호
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• pp.198-202
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• 2015

Background: Lack of proper control of acute postoperative pain often leads to lingering or chronic pain. Several studies have emphasized the role of beta-blockers in reducing postoperative pain. Esmolol is a selective short-acting beta-blocker that produces few side effects. The purpose of this study was to examine the effect of intravenous intraoperative esmolol on postoperative pain reduction following orthopedic leg fracture surgery. Methods: In a clinical trial, 82 patients between 20-65 years of age with tibia fractures and American Society of Anesthesiologists (ASA) physical status I & II who underwent surgery were divided into two groups. Group A received esmolol and group B received normal saline. Postoperative pain was measured at three time points: entering the recovery unit, and at 3 h and 6 h following surgery, using the Visual Analogue Scale (VAS). A P value of < 0.05 was considered significant. Results: Mean VAS scores at all three time points were significantly different between the two test groups (P = 0.02, P = 0.0001, and P = 0.0001, respectively). The consumption of pethidine was lower in group A than in group B (P = 0.004) and the duration of its effect was significantly longer in time (P = 0.026). Conclusions: Intravenous intraoperative esmolol is effective in the reduction of postoperative pain following leg fracture surgery. It reduced opioid consumption following surgery and delayed patient requests for analgesics.

• 분석과학
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• 제15권5호
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• pp.482-487
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• 2002

Carteolol은 국제올림픽위원회 (IOC)에서 금지약물로 규정하고 있는 ${\beta}$-차단제 중의 하나이다. 본 실험에서는 GC/MS를 사용하여 사람의 소변으로부터 carteolol의 복용여부를 확인하기 위한 검출방법 및 대사와 배설에 대해서 고찰하였다. 이를 위하여 효소 가수분해방법과 산 가수분해방법을 비교하여 보았는데 효소가수분해방법이 더 좋은 결과를 얻을 수 있었다. 효소 가수분해방법을 이용하여 실험한 결과 RSD 10%내외의 정밀도와 $0.05{\mu}g/m{\ell}$를 제외하고는 오차 5%이내의 좋은 정확도를 보여주었으며 회수율은 78.5%로 나타났다. Carteolol은 소변에서 대부분이 free carteolol과 conjugated carteolol로 존재하며 소량의 p-OH-carteolol로 대사됨을 알 수 있었으며 모 약물로 배출되는 양 중 conjugated form이 59.4%로 나타났다. 소변으로 배출된 carteolol의 양을 측정한 결과 복용양의 49%가 복용 후 72시간까지 모 약물로 배출됨을 알 수 있었다.

• Korean Circulation Journal
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• 제53권7호
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• pp.425-451
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• 2023

Most patients with heart failure (HF) have multiple comorbidities, which impact their quality of life, aggravate HF, and increase mortality. Cardiovascular comorbidities include systemic and pulmonary hypertension, ischemic and valvular heart diseases, and atrial fibrillation. Non-cardiovascular comorbidities include diabetes mellitus (DM), chronic kidney and pulmonary diseases, iron deficiency and anemia, and sleep apnea. In patients with HF with hypertension and left ventricular hypertrophy, renin-angiotensin system inhibitors combined with calcium channel blockers and/or diuretics is an effective treatment regimen. Measurement of pulmonary vascular resistance via right heart catheterization is recommended for patients with HF considered suitable for implantation of mechanical circulatory support devices or as heart transplantation candidates. Coronary angiography remains the gold standard for the diagnosis and reperfusion in patients with HF and angina pectoris refractory to antianginal medications. In patients with HF and atrial fibrillation, longterm anticoagulants are recommended according to the CHA₂DS₂-VASc scores. Valvular heart diseases should be treated medically and/or surgically. In patients with HF and DM, metformin is relatively safer; thiazolidinediones cause fluid retention and should be avoided in patients with HF and dyspnea. In renal insufficiency, both volume status and cardiac performance are important for therapy guidance. In patients with HF and pulmonary disease, beta-blockers are underused, which may be related to increased mortality. In patients with HF and anemia, iron supplementation can help improve symptoms. In obstructive sleep apnea, continuous positive airway pressure therapy helps avoid severe nocturnal hypoxia. Appropriate management of comorbidities is important for improving clinical outcomes in patients with HF.

• Journal of Chest Surgery
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• 제35권12호
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• pp.876-881
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• 2002

대동맥박리증은 사망률이 매우 높은 질환으로 조기 진단 및 치료가 되지 않으면 예후가 매우 불량한 질환이다. 최근 컴퓨터단층화촬영과 심초음파 기술의 발달로 진단률이 높아지고 조기수술이 가능하게 되었으며 술전 응급실에서 적극적인 약물투여로 사망률이 낮아지고 있는 상태이다. 따라서 이 연구는 후향적으로 응급실에서의 처치 및 수술 결과를 분석하였다. 대상 및 방법: 1991~2001년까지 외과적 교정술을 시행받은 급성 대동맥박리증 환자 42명을 대상으로 하였다. 남자가 18례, 여자가 24례였으며 연령은 평균 51.1세였다. 또한 응급실을 경유한 경우가 34례, 외래를 통한 입원이 8례였다. 결과: 수술은 상행대동맥치환술이 26례였으며 이중 대동맥판막 치환술을 병행한 경우가 7례였다. 하행대동맥치환술은 7례였으며 Bentall술식은 9례에서 시행하였다. 응급실 내원시 혈압강하제와 $\beta$-수용체차단제를 20례에서 투여하였으며 이중 6111(30%)에서 사망하였다. 이런 약물을 투여하지 않은 22례환자중 10례(45.5%)에서 사망하였다. 전체 사망은 16례(38%)였다. 결론: 대동맥박리증은 응급실이나 외래에서 조기진단이 필요하며 가능한한 비침습적 검사방법을 택하고 환자상태에 따라 적극적인 술전 약물처치가 이루어져야 할 것으로 생각된다.

• Journal of Preventive Medicine and Public Health
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• 제47권4호
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• pp.216-229
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• 2014

Objectives: This study aims to investigate trends of cardiovascular disease (CVD) risk factor profiles over 17 years in percutaneous coronary intervention (PCI) patients at the Mayo Clinic. Methods: We performed a time-trend analysis within the Mayo Clinic PCI Registry from 1994 to 2010. Results were the incidence and prevalence of CVD risk factors as estimate by the Framingham risk score. Results: Between 1994 and 2010, 25 519 patients underwent a PCI. During the time assessed, the mean age at PCI became older, but the gender distribution did not change. A significant trend towards higher body mass index and more prevalent hypercholesterolemia, hypertension, and diabetes was found over time. The prevalence of current smokers remained unchanged. The prevalence of ever-smokers decreased among males, but increased among females. However, overall CVD risk according to the Framingham risk score (FRS) and 10-year CVD risk significantly decreased. The use of most of medications elevated from 1994 to 2010, except for ${\beta}$-blockers and angiotensin converting enzyme inhibitors decreased after 2007 and 2006 in both baseline and discharge, respectively. Conclusions: Most of the major risk factors improved and the FRS and 10-year CVD risk declined in this population of PCI patients. However, obesity, history of hypercholesterolemia, hypertension, diabetes, and medication use increased substantially. Improvements to blood pressure and lipid profile management because of medication use may have influenced the positive trends.

• The Korean Journal of Physiology and Pharmacology
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• 제12권2호
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• pp.51-58
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• 2008

Cardiac fibroblasts constitute one of the largest cell populations in the heart, and contribute to structural, biochemical, mechanical and electrical properties of the myocardium. Nonetheless, their cardiac functions, especially electrophysiological properties, have often been disregarded in studies. $Ca^{2+}$-activated $K^+\;(K_{Ca})$ channels can control $Ca^{2+}$ influx as well as a number of $Ca^{2+}$-dependent physiological processes. We, therefore, attempted to identify and characterize $K_{Ca}$ channels in rat Cardiac fibroblasts. First, we showed that the cells cultured from the rat ventricle were cardiac fibroblasts by immunostaining for discoidin domain receptor 2 (DDR-2), a specific fibroblast marker. Secondly, we detected the expression of various $K_{Ca}$ channels by reverse transcription polymerase chain reaction (RT-PCR), and found all three family members of $K_{Ca}$ channels, including large conductance $K_{Ca}$ (BK-${\alpha}1-\;and\;-{\beta}1{\sim}4$subunits), intermediate conductance $K_{Ca}$ (IK), and small conductance $K_{Ca}$ (SK$1{\sim}4$ subunits) channels. Thirdly, we recorded BK, IK, and SK channels by whole cell mode patch clamp technique using their specific blockers. Finally, we performed cell proliferation assay to evaluate the effects of the channels on cell proliferation, and found that the inhibition of IK channel increased the cell proliferation. These results showed the existence of BK, IK, and SK channels in rat ventricular fibroblasts and involvement of IK channel in cell proliferation.

• 생물정신의학
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• 제21권2호
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• pp.49-56
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• 2014

Objectives Previous literature on the prescription change among patients with schizophrenia mainly focused on antipsychotics. This study investigated chronological change in the patterns of discharge medication among inpatients with schizophrenia at a psychiatric inpatient unit of a university-affiliated hospital. Methods All admission records at a psychiatric unit of Hanyang University Guri Hospital with discharge diagnosis of schizophrenia during two different five-year time frames (1996-2000 and 2006-2010) were reviewed including the demographic and clinical data and discharge medications. The data were gathered from a total of 207 patients (95 in 1990s and 112 in 2000s). Results The frequency in use of atypical antipsychotics (p < 0.01), antidepressants (p < 0.05), beta-blockers (p < 0.01), and benzodiazepine (p < 0.01) was significantly higher in 2000s. Anticholinergic drugs were less likely used in 2000s (p < 0.01). We did not find significant differences in the equivalent dose of antipsychotic drugs, the use of mood stabilizers and cholinergic drugs between two time frames. Conclusions Increased proportion of atypical antipsychotics and decreased use of anti-parkinsonian drugs are in line with literature. Our results show that more diverse classes of psychotic medications are used for schizophrenia in recent years. It is likely that psychiatrists are becoming more conscious of negative symptoms, anxiety, and depression in the pharmacotherapy of schizophrenia as well as positive symptoms of the illness.

• The Korean Journal of Physiology and Pharmacology
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• 제11권3호
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• pp.107-112
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• 2007

Gap junction protein, connexin, is expressed in endothelial cells of vessels, glomerulus, and renin secreting cells of the kidney. The purpose of this study was to investigate the role of gap junction in renin secretion and its underlying mechanisms using As 4.1 cell line, a renin-expressing clonal cell line. Renin release was increased proportionately to incubation time. The specific gap junction inhibitor, 18-beta glycyrrhetinic acid (GA) increased renin release in dose-dependent and time-dependent manners. Heptanol and octanol, gap junction blockers, also increased renin release, which were less potent than GA. GA-stimulated renin release was attenuated by pretreatment of the cells with amiloride, nifedipine, ryanodine, and thapsigargin. GA dose-dependently increased intracellular $Ca^{2+}$ concentration, which was attenuated by nifedipine, nimodipine, ryanodine, and thapsigargin. However, RP-cAMP, chelerythrine, tyrphostin A23, or phenylarsine oxide did not induced any significant change in GA-stimulated increase of intracellular $Ca^{2+}$ concentration. These results suggest that gap junction plays an important role on the regulation of renin release and intracellular $Ca^{2+}$ concentration in As 4.1 cells.

• Archives of Pharmacal Research
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• 제26권1호
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• pp.28-33
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• 2003

Ginsenosides, major active ingredients of Panax ginseng, are known to regulate excitatory ligand-gated ion channel activity such as nicotinic acetylcholine and NMDA receptor channel activity. However, it is not known whether ginsenosides affect inhibitory ligand-gated ion channel activity. We investigated the effect of ginsenosides on human recombinant $GABA_A$ receptor (${\alpha}_1{\beta}_1{\gamma}_{2s}$) channel activity expressed in Xenopus oocytes using a two-electrode voltage-clamp technique. Among the eight individual ginsenosides examined, namely, $Rb_1$, $Rb_2$, Rc, Rd, Re, Rf, $Rg_1$ and $Rg_2$, we found that Rc most potently enhanced the GABA-induced inward peak current ($I_{GABA}$). Ginsenoside Rc alone induced an inward membrane current in certain batches of oocytes expressing the $GABA_A$ receptor. The effect of ginsenoside Rc on $I_{GABA}$ was both dose-dependent and reversible. The half-stimulatory concentration ($EC_{50}$) of ginsenoside Rc was 53.2$\pm$12.3 $\mu$M. Both bicuculline, a $GABA_A$ receptor antagonist, and picrotoxin, a $GABA_A$ channel blocker, blocked the stimulatory effect of ginsenoside Rc on $I_{GABA}$. Niflumic acid (NFA) and 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS), both $CI^{-1}$ channel blockers, attenuated the effect of ginsenoside Rc on I$I_{GABA}$. This study suggests that ginsenosides regulated $GABA_A$ receptor expressed in Xenopus oocytes and implies that this regulation might be one of the pharmacological actions of Panax ginseng.