• Title/Summary/Keyword: cardiovascular toxicity

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The Risk Factors of Acute Cardiovascular and Neurological Toxicity in Acute CO Poisoning Patients and Epidemiologic Features of Exposure Routes (급성 일산화탄소 중독 환자에서 급성 심혈관계, 신경학적 독성의 위험요인과 노출 경로의 역학적 특성)

  • Park, Jinsoo;Shin, Seunglyul;Seo, Youngho;Jung, Hyunmin
    • Journal of The Korean Society of Clinical Toxicology
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    • v.18 no.1
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    • pp.34-41
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    • 2020
  • Purpose: This study evaluated aggressive hyperbaric oxygen therapy (HBOT) by understanding various exposure routes of acute carbon monoxide (CO) poisoning, the risk factors causing acute cardiovascular, and neurological toxicity caused by poisoning. Methods: A retrospective study was conducted based on the medical records of 417 acute CO poisoning patients who visited the emergency care unit from March 2017 to August 2019. The exposure routes, HBOT performance, age, sex, medical history (hypertension, diabetes mellitus, ischemic heart disease, heart failure), intentionality, loss of consciousness (LOC), intake with alcohol or sedatives, and initial test results (carboxyhemoglobin (COHb), troponin-I, electrocardiography, echocardiography, brain MRI) were examined. Comparative analysis of the clinical information was conducted between the groups that showed acute cardiovascular toxicity and neurological toxicity, and groups that did not. Results: Among 417 patients diagnosed with acute CO poisoning, 201 cases (48.2%) were intentional, and charcoal briquette was the most common route (169 patients (40.5%)). Two hundred sixteen cases (51.8%) were accidental, and fire was the most common route (135 patients (32.4%)). The exposure route was more diverse with accidental poisoning. Three hundred ninety-nine patients were studied for acute cardiovascular toxicity, and 62 patients (15.5%) were confirmed to be positive. The result was statistically significant in intentionality, LOC, combined sedatives, initial COHb, HTN, and IHD. One hundred two patients were studied for acute neurological toxicity, which was observed in 26 patients (25.5%). The result was statistically significant in age and LOC. Conclusion: Active HBOT should be performed to minimize damage to the major organs by identifying the various exposure routes of CO poisoning, risk factors for acute cardiovascular toxicity (intentionality, LOC, combined sedatives, initial COHb, HTN, IHD), and the risk factors for acute neurological toxicity (age, LOC).

Anti-VEGF Therapy with Bevacizumab - Limited Cardiovascular Toxicity

  • Yu, Jing;Cao, Xu-Fen;Zheng, Ye;Zhao, Rong-Cheng;Yan, Li-Qiu;Zhao, Lei;Wang, Jia-Wang
    • Asian Pacific Journal of Cancer Prevention
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    • v.15 no.24
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    • pp.10769-10772
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    • 2015
  • Purpose: This analysis was conducted to evaluate cardiovascular toxicity of commonly used anti-VEGF therapeutic agent, bevacizumab, in treating patients with cancer. Methods: Clinical studies evaluating the efficacy and safety of bevacizumab-based regimens on response and safety for patients with cancer were identified using a predefined search strategy, allowing cardiovascular toxicity and other side effects of treatment to be estimated. Results: In bevacizumab based regimens, 4 clinical studies including 282 patients with advanced cancer (including gliomas, cervical, breast and ovarian cancer) were considered eligible for inclusion. These bevacizumab-based regimens included docetaxel, irinitecan and carboplatin. Systematic analysis suggested that, of 282 patients treated by bevacizumab based regimens, hypertension and thrombo-embolism occurred in 2.5% (7/282), while only 3 patients reported cardiovascular events (1.1%). No treatment related death occurred in bevacizumab based treatment. Conclusion: This systemic analysis suggests that bevacizumab based regimens are associated with reasonable and accepted cardiovascular toxicity when treating patients with gliomas, cervical, breast and ovarian cancer.

Spontaneous Pneumomediastinum Accompanied by Bleomycin-Induced lung Toxicity (Bleomycin 유도 폐독성에 동반된 자연성 종격동 기종)

  • Do, Young-Woo;Cho, Suk-Ki;Lee, Young-Ok;Lee, Eung-Bae
    • Journal of Chest Surgery
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    • v.41 no.6
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    • pp.791-794
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    • 2008
  • Pneumomediastinum is a rare, but well recognized complication of bleomycin-induced lung toxicity. Spontaneous pneumomediastinum has to be considered as one of the causes when the dyspnea becomes aggravated in patients with bleomycin induced lung toxicity. We describe here two patients who suffered with germ cell tumor and they developed spontaneous pneumomediastinum without pneumothorax, and this was caused by bleomycin-induced lung toxicity.

Identification of Marker Genes Related to Cardiovascular Toxicity of Doxorubicin and Daunorubicin in Human Umbilical Vein Endothelial Cells (HUVECs)

  • Kim, Youn-Jung;Lee, Ha-Eun;Ryu, Jae-Chun
    • Molecular & Cellular Toxicology
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    • v.3 no.4
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    • pp.246-253
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    • 2007
  • Doxorubicin and daunorubicin are excellent chemotherapeutic agents utilized for several types of cancer but the irreversible cardiac damage is the major limitation for its use. The biochemical mechanisms of doxorubicin- and daunorubicin- induced cardiotoxicity remain unclear. There are many reports on toxicity of doxorubicin and doxorubicin in cardiomyocytes, but effects in cardiovascular system by these drugs are almost not reported. In this study, we investigated gene expression profiles in human umbilical vein endothelial cells (HUVECs) to better understand the causes of doxorubicin and doxorubicininduced cardiovascular toxicity and to identify differentially expressed genes (DEGs). Through the clustering analysis of gene expression profiles, we identified 124 up-regulated common genes and 298 down-regulated common genes changed by more than 1.5-fold by all two cardiac toxicants. HUVECs responded to doxorubicin and doxorubicin damage by increasing levels of apoptosis, oxidative stress, EGF and lipid metabolism related genes. By clustering analysis, we identified some genes as potential markers on apoptosis effects of doxorubicin and doxorubicin. Six genes of these, BBC3, APLP1, FAS, TP53INP, BIRC5 and DAPK were the most significantly affected by doxorubicin and doxorubicin. Thus, this study suggests that these differentially expressed genes may play an important role in the cardiovascular toxic effects and have significant potential as novel biomarkers to doxorubicin and doxorubicin exposure.

Cardiovascular Manifestations and Clinical Course after Acute Carbon Monoxide Poisoning (급성 일산화탄소 중독에 의한 심혈관계 독성의 임상 양상 및 경과)

  • Lee, In Soo;Jung, Yoon Seok;Min, Young Gi;Kim, Gi Woon;Choi, Sang Cheon
    • Journal of The Korean Society of Clinical Toxicology
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    • v.10 no.2
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    • pp.103-110
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    • 2012
  • Purpose: The aim of this study was to evaluate the cardiovascular manifestations and clinical course in patients with acute carbon monoxide poisoning. Methods: A retrospective study was conducted over a 36 month period on consecutive patients who visited an emergency medical center and were diagnosed with acute carbon monoxide poisoning. A standardized data extraction protocol was performed on the selected patients. Results: A total of 293 patients were selected during the study period. Cardiac manifestations were observed in 35.2% (n=103) of the patients: hypotension in 11 patients (3.8%), ECG abnormalities in 44 patients (15.0%) and cardiac enzyme abnormalities in 103 patients (35.2%). Echo cardiography was performed on 56 patients with cardiac toxicity: 12 patients had abnormal results (5 patients with global hypokinesia and 7 patients with regional wall akinesia). Five patients died within 3 hours after ED admission, and the remaining patients were discharged alive. At 3 months after discharge, none of these patients had died.The SOFA scores in the severe cardiac toxicity group and non-severe cardiac toxicity group at the time of arrival were $2.53{\pm}2.29$ and $2.19{\pm}2.12$, respectively (p=0.860). Conclusion: Cardiovascular manifestations occur after acute CO poisoning at arateof 35.2%. Even those with severe cardiovascular toxicity recovered well within 10 days after admission. Therefore, the importance of cardiac toxicity after acute CO poisoning is not significant in itself in the clinical course, and the short-term prognosis of cardiac toxicity is unlikely to be unfavorable in acute CO poisoning.

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Methylated Organic Metabolites of Arsenic and their Cardiovascular Toxicities

  • Bae, Ok-Nam;Lim, Kyung-Min;Noh, Ji-Yoon;Kim, Keun-Young;Lim, Eun-Kyung;Chung, Jin-Ho
    • Toxicological Research
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    • v.24 no.3
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    • pp.161-167
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    • 2008
  • Recently, arsenic-toxicity has become the major focus of strenuous assessment and dynamic research from the academy and regulatory agency. To elucidate the cause and the mechanism underlying the serious adverse health effects from chronic ingestion of arsenic-contaminated drinking water, numerous studies have been directed on the investigation of arsenic-toxicity using various in vitro as well as in vivo systems. Neverthless, some questions for arsenic effects remain unexplained, reflecting the contribution of unknown factors to the manifestation of arsenic-toxicity. Interestingly, very recent studies on arsenic metabolites have discovered that trivalent methylated arsenicals show stronger cytotoxic and genotoxic potentials than inorganic arsenic or pentavalent metabolites, arguing that these metabolites could play a key role in arsenic-associated disorders. In this review, recent progress and literatures are summarized on the metabolism of trivalent methylated metabolites and their toxicity on body systems including cardiovascular system in an effort to provide an insight into the future research on arsenic-associated disorders.

carbofuran Induces Cardiovascular Dysfunction in Rat (휜쥐의 심혈관 기능에 대한 carbofuran독성작용)

  • 정이숙;이수환;백은주;문창규;문창현
    • YAKHAK HOEJI
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    • v.45 no.6
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    • pp.739-745
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    • 2001
  • Of all pesticides, carbamates are known to be most common, since alternatives such as organophosphates have long lifetime and are extremely toxic to produce a delayed neurotoxic effect. Although a number of studies about toxicity of carbofuran, a most widely used carbamate, have been reported, its cardiovascular toxicity has not yet been studied. In the present study, we investigated its cardiovascular toxic effect in anesthetized rat in vivo and in isolated Langendorff rat heart, In anesthetized rat model, carbofuran (10 mg/kg) significantly reduced heart rate, and transiently increased blood pressure. In isolated rat heart, carbofuran (10${\mu}{\textrm}{m}$) caused a significant depression in the left ventricular developed pressure (LVDP), indicating contractile dysfunction by carbofuran. Carbofuran (10${\mu}{\textrm}{m}$) also decreased coronary flow rate (CFR) in isolated heart, indicating carbofuran-induced coronary dysfunction. These results suggest that carbofuran can cause cardiac dysfunction in rat in vivo and vitro.

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Single-Dose Oral Toxicity Test of Woohwangchungshim-won in Mice (우황청심원의 마우스 단회 경구투여 독성시험 연구)

  • Lee, Je Won;Baek, Kyung Min;Chang, Woo Seok
    • Journal of Physiology & Pathology in Korean Medicine
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    • v.28 no.2
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    • pp.186-194
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    • 2014
  • The object of this study was to obtain acute toxicity information (single-dose oral toxicity) of Woohwangchungshim-won (WHCSW), a pill type herbal medicine used in Korean Medicine (KM) for treating stroke. In order to obtain the 50% lethal dose (LD50), approximate lethal dosage (ALD) and target organs, WHCSW powders were once orally administered to female and male ICR mice at dose levels of 2,000, 1,000, 500 and 0 (control) mg/kg (body weight.) according to the recommendation of Korea Food and Drug Administration (KFDA) Guidelines (Notification No. 2009-116). The mortality and changes in the body weight, clinical signs and gross observation were monitored for 14 days after single-dose oral administration of WHCSW according to KFDA Guidelines with organ weights and histopathological changes were observed in 12 principle organs. After single-dose oral administration of WHCSW, we could not find any mortality and toxicological evidences up to 2,000 mg/kg-administered group, except for some accidental findings and dose-independent increases of body weight gains in female 1,000 and 500 mg/kg-administered female mice. The results obtained in this study suggest that the LD50 and ALD of WHCSW in both female and male mice after single-dose oral administration were considered as over 2,000 mg/kg because no mortalities were detected up to 2,000 mg/kg that was the highest dose recommended by KFDA and Organization for Economic Co-Operation and Development (OECD), and can be safely used in clinics.

Norflurazon causes developmental defects including cardiovascular abnormalities in early-stage zebrafish (Danio rerio)

  • An, Garam;Park, Hahyun;Hong, Taeyeon;Song, Gwonhwa;Lim, Whasun
    • Journal of Animal Reproduction and Biotechnology
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    • v.37 no.3
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    • pp.176-182
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    • 2022
  • Norflurazon is widely used on agricultural lands and has a high potential to pollute water sources. However, its effects on fish have not been fully elucidated. The purpose of our study was to determine whether norflurazon adversely affects the developmental stage of zebrafish, which are frequently used as a model system to evaluate the environmental impact of pollutants. Norflurazon interfered with the hatching of zebrafish embryos and induced several sublethal deformities including body length reduction, increased yolk sac volume, and enlargement of the pericardial region. We further examined the cardiotoxicity of norflurazon in the flk1:eGFP transgenic zebrafish line. The vascular network, mainly in the brain region, was significantly disrupted in norflurazon-exposed zebrafish. In addition, due to the failure of cardiac looping, norflurazon-exposed zebrafish had an abnormal cardiac structure. These developmental abnormalities were related to the apoptotic process triggered by norflurazon. Overall, the present study demonstrated the non-target toxicity of norflurazon by analyzing the hazardous effects of norflurazon on developing zebrafish.

Mecoprop-p interrupts the development of zebrafish via apoptosis and vascular damage

  • Park, Junho;An, Garam;Park, Hahyun;Hong, Taeyeon;Song, Gwonhwa;Lim, Whasun
    • Journal of Animal Reproduction and Biotechnology
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    • v.37 no.3
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    • pp.162-168
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    • 2022
  • Mecoprop-p, a chlorophenoxy herbicide, has been widely used since the 1980s. Due to its high water solubility, it could be detected in the aquatic environment, as it has already been detected in the surface water or groundwater in several countries. The toxicity of other chlorophenoxy herbicides has been reported; however, there are few studies on the toxicity of mecoprop-p, one of the chlorophenoxy herbicides, on aquatic organisms. Here, we investigated the toxic effects of mecoprop-p using zebrafish. After mecoprop-p exposure, we observed that the zebrafish larvae eyes did not form normally, heart edema was generated, and the body length was shortened. The number of cells undergoing apoptosis also increased in the anterior part including head, heart, and yolk sac of the mecoprop-p-treated zebrafish compared to the untreated controls. Moreover, cardiovascular structures, including the heart and aortic arches, were also malformed after exposure to mecoprop-p. Therefore, our results suggest that mecoprop-p could cause abnormal development in zebrafish larvae and there is also a high possibility that mecoprop-p would be toxic to other aquatic organisms.