• 대한중풍순환신경학회지
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• 제8권1호
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• pp.52-57
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• 2007

Drug eruption is a relatively commin dermatological disorder and may cause significant problems. The treatment is to stop using a drug that may cuase a drug eruption. In some cases, steroids and antihistamines can be used supportively. According to some reports, Onchungeum(溫淸飮) has steroid-like effects and antihistaminic effects. We administered Onchungeum(溫淸飮) a patient with severe itching because of a drug eruption. After administration of Onchungeum(溫淸飮), itching decreased to much degrees. It can be suggested that Onchungeum(溫淸飮) can be used to treat symptoms of allergic skin disease like a drug eruption.

• Biomolecules & Therapeutics
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• 제23권4호
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• pp.386-389
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• 2015

Sibutramine is an anorectic that has been banned since 2010 due to cardiovascular safety issues. However, counterfeit drugs or slimming products that include sibutramine are still available in the market. It has been reported that illegal sibutramine-contained pharmaceutical products induce cardiovascular crisis. However, the mechanism underlying sibutramine-induced cardiovascular adverse effect has not been fully evaluated yet. In this study, we performed cardiovascular safety pharmacology studies of sibutramine systemically using by hERG channel inhibition, action potential duration, and telemetry assays. Sibutramine inhibited hERG channel current of HEK293 cells with an $IC_{50}$ of $3.92{\mu}M$ in patch clamp assay and increased the heart rate and blood pressure ($76{\Delta}bpm$ in heart rate and $51{\Delta}mmHg$ in blood pressure) in beagle dogs at a dose of 30 mg/kg (per oral), while it shortened action potential duration (at $10{\mu}M$ and $30{\mu}M$, resulted in 15% and 29% decreases in $APD_{50}$, and 9% and 17% decreases in $APD_{90}$, respectively) in the Purkinje fibers of rabbits and had no effects on the QTc interval in beagle dogs. These results suggest that sibutramine has a considerable adverse effect on the cardiovascular system and may contribute to accurate drug safety regulation.

• Restorative Dentistry and Endodontics
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• 제38권4호
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• pp.187-193
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• 2013

Epinephrine is one of the most widely-used vasoconstrictors in dental treatment including endodontic microsurgery. However, the systemic safety of epinephrine has been in debate for many years because of its potential risk to cause cardiovascular complications. The purpose of this review was to assess the cardiovascular effect of epinephrine use in endodontic microsurgery. Endodontic microsurgery directly applies epinephrine into the bone cavity, and the amount is reported to be much larger than other dental surgeries. Moreover, when considering that systemic potency of intraosseous application is reported to be comparable to intravenous application, the systemic influence of epinephrine could be increased in endodontic microsurgery. Besides, pre-existing cardiovascular complications or drug interactions can enhance its systemic influence, resulting in increased susceptibility to cardiovascular complications. Although clinical studies have not reported significant complications for patients without severe systemic complications, many epinephrine-induced emergency cases are warning the cardiovascular risk related with pre-existing systemic disease or drug interactions. Epinephrine is a dose-sensitive drug, and its hypersensitivity reaction can be fatal to patients when it is related to cardiovascular complications. Therefore, clinicians should recognize the risk, and the usage of pre-operative patient evaluation, dose control and patient monitoring are required to ensure patient's safety during endodontic microsurgery.

• 한국임상약학회지
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• 제22권1호
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• pp.41-46
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• 2012

Adverse drug reaction (ADR) is a global problem of major concern in health care. ADRs can be accrued in any organs or systems. However, cardiovascular ADRs could be a more serious problem if they are irreversible or severe. For this reason, this study was conducted to analyze pattern and severity of cardiovascular ADRs, and suspicious medication. Total 646 reports including cardiovascular ADRs reported to the KFDA between January and June 2010 were analyzed. Amlodipine besylate (36 reports, 3.3%), iopromide (29 reports, 2.7%), tramadol HCl (28 reports, 2.6%) were most suspicious drugs that occurred cardiovascular ADRs. The most common cardiovascular ADRs were hypotension( 236 reports, 33.1%), palpitation (134 reports, 18.8%), and hypertension (89 reports, 12.5%). The most frequent ADRs were occurred in the age group of more than 60. This result could be of help to prescribers and other healthcare providers to predict and prevent cardiovascular ADRs. Also this study suggested that patients with cardiovascular ADR risk factors should be intensively monitored during the medications.

• Journal of Ginseng Research
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• 제48권4호
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• pp.405-416
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• 2024

Background: Hypoxic pulmonary hypertension (HPH) is the main pathological change in vascular remodeling, a complex cardiopulmonary disease caused by hypoxia. Some research results have shown that ginsenoside Rg1 (Rg1) can improve vascular remodeling, but the effect and mechanism of Rg1 on hypoxia-induced pulmonary hypertension are not clear. The purpose of this study was to discuss the potential mechanism of action of Rg1 on HPH. Methods: C57BL/6 mice, calpain-1 knockout mice and Pulmonary artery smooth muscle cells (PASMCs) were exposed to a low oxygen environment with or without different treatments. The effect of Rg1 and calpain-1 silencing on inflammation, fibrosis, proliferation and the protein expression levels of calpain-1, STAT3 and p-STAT3 were determined at the animal and cellular levels. Results: At the mouse and cellular levels, hypoxia promotes inflammation, fibrosis, and cell proliferation, and the expression of calpain-1 and p-STAT3 is also increased. Ginsenoside Rg1 administration and calpain-1 knockdown, MDL-28170, and HY-13818 treatment showed protective effects on hypoxia-induced inflammation, fibrosis, and cell proliferation, which may be associated with the downregulation of calpain-1 and p-STAT3 expression in mice and cells. In addition, overexpression of calpain 1 increased p-STAT3 expression, accelerating the onset of inflammation, fibrosis and cell proliferation in hypoxic PASMCs. Conclusion: Ginsenoside Rg1 may ameliorate hypoxia-induced pulmonary vascular remodeling by suppressing the calpain-1/STAT3 signaling pathway.

• 대한한방내과학회지
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• 제16권1호
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• pp.181-196
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• 1995

The present experiments were designed to investigate the effects of BangPoongSan on the cardiovascular system in the experimental Animals. And thus the change of blood pressure, auricular blood flow, artery contraction, death rate, platelet aggregation repression, plasma coagulation factor activity, plasma antithrombin activity, whole blood viscosity and plasma viscosity were studied. The result were summarized as the followings: 1. BangPoongSan dropped the blood pressure in the spontaneous hypertensive rat. 2. The drug increased the auricular blood flow in rabbit. 3. The drug relaxed the artery contraction by pretreated norepinephrine in white rat. 4. The drug inhibited the death rate of mouse which was led to thromboembolism by serotonin and collagen. 5. The drug inhibited the platelet aggregation in rat. 6. The drug prolonged the prothrombin time and activated partial thromboplastin time on the test of plasma coagulation factor activity in rat, but was not valuable. 7. The drug presented the antithrombin activity in rat. 8. The drug reduced the whole blood viscosity and plasma viscosity in rat, but the latter was not valuable. According to the results, Bangpoongsan increased the blood flow and dropped the blood pressure by dilatation of blood vessel smooth muscle. And the drug presented the antithrombin acivity, inhibited the platelet aggregation and reduced blood viscosity. Therefore these effects are assumed to improve the cardiovascular circulation disorder and prevent thrombosis.

• Journal of Ginseng Research
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• 제45권6호
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• pp.683-694
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• 2021

Background: Ginsenoside Rg1 (Rg1) has been well documented to be effective against various cardiovascular disease. The aim of this study is to evaluate the effect of Rg1 on mechanical stress-induced cardiac injury and its possible mechanism with a focus on the calcium sensing receptor (CaSR) signaling pathway. Methods: Mechanical stress was implemented on rats through abdominal aortic constriction (AAC) procedure and on cardiomyocytes and cardiac fibroblasts by mechanical stretching with Bioflex Collagen I plates. The effects of Rg1 on cell hypertrophy, fibrosis, cardiac function, [Ca²⁺]_i, and the expression of CaSR and calcineurin (CaN) were assayed both on rat and cellular level. Results: Rg1 alleviated cardiac hypertrophy and fibrosis, and improved cardiac decompensation induced by AAC in rat myocardial tissue and cultured cardiomyocytes and cardiac fibroblasts. Importantly, Rg1 treatment inhibited CaSR expression and increase of [Ca²⁺]_i, which similar to the CaSR inhibitor NPS2143. In addition, Rg1 treatment inhibited CaN and TGF-b1 pathways activation. Mechanistic analysis showed that the CaSR agonist GdCl₃ could not further increase the [Ca²⁺]_i and CaN pathway related protein expression induced by mechanical stretching in cultured cardiomyocytes. CsA, an inhibitor of CaN, inhibited cardiac hypertrophy, cardiac fibrosis, [Ca²⁺]_i and CaN signaling but had no effect on CaSR expression. Conclusion: The activation of CaN pathway and the increase of [Ca²⁺]_i mediated by CaSR are involved in cardiac hypertrophy and fibrosis, that may be the target of cardioprotection of Rg1 against myocardial injury.

• 한국독성학회:학술대회논문집
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• 한국독성학회 2005년도 추계학술대회
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• pp.124-132
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• 2005

• 한국응용약물학회:학술대회논문집
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• 한국응용약물학회 1995년도 춘계학술대회
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• pp.21-27
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• 1995

This document collects Center for Drug Evaluation and Research (CDER) and Center for Devices and Radiological Health (CDRH) guidance documents, citations to the primary literature, and other published and unpublished documents relevant to development and approval of drug/device combinations collected by the CDRH Division of Cardiovascular, Respiratory and Neurological Devices (DCRND). Since the Master Bibliography number represents an accession number, an alphabetical (by author) listing appears at the end of the document, Any citation marked with a, is on file in the DCRND offices, 340B, in the Piccard Building (HFZ-450), 1390 Piccard Avenue, Rockville, MD 20850.

• Journal of Medicine and Life Science
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• 제21권3호
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• pp.62-71
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• 2024

The incidence of diabetes is continuously increasing worldwide, resulting in a considerable socioeconomic burden. Glycemic control using traditional diabetes medications prevents microvascular complications; however, there is no objective evidence that it prevents macrovascular complications. In the 21st century, concerns have arisen that strict glycemic control and the diabetes drug rosiglitazone might increase mortality. This led the United States Food and Drug Administration to establish guidelines that require that cardiovascular outcome trials (CVOTs) with 3-point major adverse cardiovascular events (3-P MACE) as the primary endpoints be performed for new diabetes drugs. Since then, 20 CVOTs have been reported. Dipeptidyl peptidase 4 inhibitors do not increase the incidence of cardiovascular disease; however, saxagliptin increases the risk of heart failure. Sodium-glucose cotransporter inhibitors (SGLT2is) and glucagon-like peptide 1 receptor agonists (GLP-1RAs) not only have proven cardiovascular safety but also have shown results beyond expectations by reducing the incidence of cardiovascular diseases. Additionally, SGLT2is have been reported to markedly prevent heart failure and kidney disease. The reduction in 3-P MACE by GLP-1RAs was observed only with long-acting agents; long-acting GLP-1RAs also markedly reduced renal endpoints. However, no preventive effect against heart failure was observed with GLP-1RAs. The preventive effects of both drug types against cardiovascular and kidney diseases appear to be independent of glycemic control. In conclusion, based on CVOT results, it is necessary to actively prescribe SGLT2is and GLP-1RAs to prevent cardiovascular disease in patients with diabetes, regardless of glycemic control.