• Biomolecules & Therapeutics
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• 제24권4호
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• pp.363-370
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• 2016

Cardiovascular disease is the most common cause of death in diabetic patients. Hyperglycemia is the primary characteristic of diabetes and is associated with many complications. The role of hyperglycemia in the dysfunction of human cardiac progenitor cells that can regenerate damaged cardiac tissue has been investigated, but the exact mechanism underlying this association is not clear. Thus, we examined whether hyperglycemia could regulate mitochondrial dynamics and lead to cardiac progenitor cell dysfunction, and whether blocking glucose uptake could rescue this dysfunction. High glucose in cardiac progenitor cells results in reduced cell viability and decreased expression of cell cycle-related molecules, including CDK2 and cyclin E. A tube formation assay revealed that hyperglycemia led to a significant decrease in the tube-forming ability of cardiac progenitor cells. Fluorescent labeling of cardiac progenitor cell mitochondria revealed that hyperglycemia alters mitochondrial dynamics and increases expression of fission-related proteins, including Fis1 and Drp1. Moreover, we showed that specific blockage of GLUT1 improved cell viability, tube formation, and regulation of mitochondrial dynamics in cardiac progenitor cells. To our knowledge, this study is the first to demonstrate that high glucose leads to cardiac progenitor cell dysfunction through an increase in mitochondrial fission, and that a GLUT1 blocker can rescue cardiac progenitor cell dysfunction and downregulation of mitochondrial fission. Combined therapy with cardiac progenitor cells and a GLUT1 blocker may provide a novel strategy for cardiac progenitor cell therapy in cardiovascular disease patients with diabetes.

• 대한의용생체공학회:의공학회지
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• 제30권5호
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• pp.355-361
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• 2009

Mitochondria play a key role in maintaining life by producing ATP and heat. Recent researches have demonstrated that degenerative diseases such as heart failure, obesity/diabetes, cardiovascular disease, and psychiatric diseases are accompanied by mitochondria dysfunction. In this sense, mitochondria medicine considers the significance of mitochondria in human pathology and tries to explain degenerative diseases as a fatal consequence of mitochondria dysfunction. Here, I introduce the fundamentals of mitochondria physiology and present examples showing the relationship between mitochondria dysfunction and chronic complex diseases. Although mitochondria medicine uses a molecular biological approach predominantly, a biomedical engineering approach might play a critical role in unveiling the complexity of mitochondria medicine and in its application to the diagnosis and treatment of chronic diseases. Thus, I also briefly review the prospects of research using biomedical engineering methods.

• Journal of Chest Surgery
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• 제49권3호
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• pp.203-206
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• 2016

Patients with venoarterial extracorporeal membrane oxygenation (ECMO) frequently suffer from pulmonary edema due to left ventricular dysfunction that accompanies left heart dilatation, which is caused by left atrial hypertension. The problem can be resolved by left atrium (LA) decompression. We performed a successful percutaneous LA decompression with an atrial septostomy and placement of an LA venting cannula in a 38-month-old child treated with venoarterial ECMO for acute myocarditis.

• Clinical and Experimental Pediatrics
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• 제46권6호
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• pp.585-590
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• 2003

목 적 : 심혈관계 자율신경 기능이상은 청소년기 당뇨병 환자의 7.7-28%에서 동반되며, 당뇨병성 자율신경병증은 심장 교감 신경계 이상으로 인한 돌발성 부정맥 및 돌연사를 초래할 수 있는 것으로 보고되었다. 본 연구는 소아 및 청소년기 당뇨병 환자에서 심혈관계 자율신경 기능이상의 빈도 및 이에 영향을 미치는 인자들을 파악하여 당뇨병성 자율신경병증의 조기진단 및 치료에 도움이 되고자 시행하였다. 방 법 : 8-26세의 1형 당뇨병 환자 80명(남자 27명, 여자 53명)과 2형 당뇨병 환자 12명(남자 4명, 여자 8명)을 대상으로, 발살바 동작시 R-R 간격의 변화(발살바 비), 심호흡시 심박수의 변화, 기립시 R-R 간격의 변화(30 : 15 비), 기립성 저혈압의 4가지 항목에 대하여 검사를 시행하여 환자의 연령, 유병기간, 당화혈색소, 소변 알부민 배설량, 신경전달속도 이상 및 당뇨병성 망막증 유무와의 연관성을 분석하였다. 결 과 : 검사 당시 연령 및 평균 유병기간은 1형과 2형 당뇨병 환자간에 의미있는 차이가 없었으나, 당뇨병의 발병연령은 2형에서 더 높았다. 체질량지수는 1형에 비해 2형에서 의미있게 높았으며, 혈압 및 당화혈색소는 두 군간에 차이가 없었다. 1형 당뇨병 환자의 22.5%에서 조기, 8.7%에서 중등도, 1.3%에서 심한 자율신경병증에 해당하였으며, 2형의 경우 16.7%에서는 조기, 8.3%에서 중등도, 8.3%에서 심한 자율신경병증에 해당하였다. 전체적으로, 심혈관계 자율신경 기능 이상은 1형의 32.5%에서, 2형의 33.3% 에서 나타나 빈도에 있어서 두 군간에 차이는 보이지 않았다. 1형에서는 발살바 비와 유병기간 간에 의미있는 상관관계가 있었으며, 2형에서는 발살바 비와 연령, 심호흡시 심박수 변화와 당화혈색소, 그리고 기립성 저혈압과 유병기간 간에 의미있는 상관관계가 관찰되었다. 1형과 2형 당뇨병 환자 전체를 대상으로 시행한 로지스틱 회귀분석상, 연령(OR=1.133(1.003-1.279), P<0.05) 및 유병기간(OR=1.148(1.009-1.307), P<0.05)만이 자율신경 기능 이상의 의미있는 예측인자로 나타났으며, 당화혈색소, 혈압, 소변 알부민 배설량, 신경전달속도 이상 및 당뇨병성 망막증 유무와는 관련이 없었다. 검사항목 중 발살바 비는 31.5%의 환자에서, 심호흡시 심박수의 변화는 41.3%의 환자에서 경계역 또는 이상소견을 보인 반면, 30 : 15 비 및 혈압변화는 각각 14.1%, 9.8%에서 경계역 또는 이상소견을 보였다. 발살바 비(OR=0.001(0.000-0.083), P<0.01)와 심호흡시 심박수의 변화(OR=0.840(0.754-0.934), P<0.01)는 자율신경 기능이상 유무에 의미있게 영향을 미쳤으나, 30 : 15 비 및 기립성 저혈압은 영향을 미치지 못하였다. 결 론 : 심혈관계 자율신경 기능이상은 소아 및 청소년 당뇨병 환자의 32.6%에서 동반되었으며, 중등도 이상의 뚜렷한 자율신경 기능이상도 10.8%에서 관찰되었다. 혈당 조절이 양호한 환자에서도 자율신경계 합병증의 가능성은 배제할 수 없으며 연령 및 유병기간이 증가할수록 그 위험은 더욱 증가하였다. 소아 및 청소년기 당뇨병 환자에서 자율신경 기능검사시, 발살바 비와 심호흡시 심박수의 변화가 가장 유용한 검사 항목으로 사료된다.

• Journal of Chest Surgery
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• 제21권1호
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• pp.164-168
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• 1988

Between November, 1984, and May, 1986, 93 patients underwent combined valvular and coronary artery operation. They were 70 male and 23 female, the age ranging from 29 to 82. From this population 89 patients underwent single valve replacement and 4 patients underwent double valve replacement. Patients with mitral valve disease were in the majority present in the age group between 50 till 70, where as in the group after 60 years, patients with aortic valve disease were dominant. The main indication for aortic valve replacement was aortic stenosis and the indication for mitral valve replacement was equal between mitral stenosis and mitral incompetence, the later was due to papillary dysfunction after myocardial infarction. Dyspnea was a very frequent symptom and it was found in nearly all patients. 28 patients had a previous myocardial infarction and severe left ventricular dysfunction. The grafts were placed prior to valve replacement and periods of myocardial ischemia were kept at a minimum by maintaining coronary perfusion throughout the operation. It is our opinion that simultaneous valve replacement and myocardial revascularization does not increase the risk of cardiac valve replacement substantially.

• 수면정신생리
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• 제4권2호
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• pp.129-139
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• 1997

수면 무호흡을 포함한 다양한 원인의 수면과 관련된 호흡장애를 동반한 환자들에서는 여러가지 심혈관계 기능부전이 초래되어 이들 환자의 임상경과에 중대한 영향을 미친다. 수면 무호흡증후군, 특히 폐쇄성 수면 무호흡증후군은 수면장애의 여러 가지 원인 중 임상영역에서 가장 흔히 볼수 있는 질환으로 전신성 고혈압, 심부정맥, 폐동맥 고혈압 및 우심실 부전, 협심증 및 심근경색증, 뇌졸증등의 발병률이 정상인에 비하여 현저히 높은 것으로 알려져 있다. 폐쇄성 수면 무호흡과 달리 중추성 수면 무호흡은 수면중에 호흡중추를 불안정하게 하는 다양한 원인에 의해 발생하며 역시 심혈관계의 기능에 영향을 미칠 수 있다. 수면중에 환기장애가 더욱 악화될 수 있는 호흡기계 질환이 있는 환자들은 수면 무호흡증후군과 달리 만성적인 저산소증과 고탄산증이 동반되며 이로 인해 심부정맥, 폐동맥 고혈압, 우심실 부전(폐성심) 등의 심혈관계 이상이 초래될 수 있다. 따라서 수면 무호흡을 포함한 수면과 관련된 호홉 장애의 진단과 치료에 있어서는 호흡기계 질환에 대한 정확한 평가와 더불어 동반될 수 있는 심혈관계의 기능부전에 대한 정밀한 분석이 반드시 필요하며, 이들 자료를 바탕으로 기관절개술, 기계적 호흡, 지속적 양압공급치료, 적절한 산소요법 등의 적극적이고도 효과적인 치료법을 적용함으로서 심혈관계 합병증의 발생과 이로 인한 사망률을 감소시킬 수 있을 것으로 생각된다.

• Journal of Chest Surgery
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• 제46권3호
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• pp.185-191
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• 2013

Background: Cardiopulmonary bypass (CPB) induces variable systemic inflammatory reactions associated with major organ dysfunction via polymorphonuclear neutrophils (PMNs). Ulinastatin, a urinary trypsin inhibitor, inhibits PMN activity and reduces systemic inflammatory responses. The aim of this study is to evaluate the effect of ulinastatin on postoperative blood loss and laboratory changes in patients undergoing open heart surgery. Materials and Methods: Between January 2008 and February 2009, 110 patients who underwent atrioventricular valve surgery through right thoracotomy were divided into two groups. Patients received either 5,000 U/kg ulinastatin (ulinastatin group, n=41) or the equivalent volume of normal saline (control group, n=69) before aortic cross clamping. The primary end points were early coagulation profile changes, postoperative blood loss, transfusion requirements, and duration of intubation and intensive care unit stay. Results: There were no statistically significant differences between the two groups in early coagulation profile, other perioperative laboratory data, and postoperative blood loss with transfusion requirements. Conclusion: Administration of ulinastatin during operation did not improve the early coagulation profile, postoperative blood loss, or transfusion requirements of patients undergoing open heart surgery. In addition, no significant effect of ulinastatin was observed in major organs dysfunction, systemic inflammatory reactions, or other postoperative profiles.

• Asian Journal of Atmospheric Environment
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• 제1권1호
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• pp.28-35
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• 2007

Accumulated epidemiological and animal studies have suggested that prolonged exposure to ambient particulate matter (PM) is associated with an increased risk of cardiovascular disease and pulmonary dysfunction. While diesel exhaust particles (DEP) contain large variety of compounds, polycyclic aromatic hydrocarbons (PAHs) are a dominant component contaminated in DEP. This article reviews effects of two PAH quinones, 9,10-phenanthraquinone (9,10-PQ) and l,2-naphthoquinone (l,2-NQ), on vascular and respiratory systems.

• Journal of Chest Surgery
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• 제18권4호
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• pp.746-752
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• 1985

A retrospective clinical observation was made of 40 patients with postoperative cerebral dysfunction among 2634 patients who underwent open-heart operations in Severance Hospital. Yonsei University between 1962, the year the first successful open heart operation was done, and June 1985. Suspected causes of brain damage were reviewed. Brain CT findings were evaluated in 24 patients. There were 15 cerebral infarcts, 4 intracerebral bleedings, 3 ischemic brain damages, 1 infarction with intracerebral hemorrhage and 1 diffuse cortical atrophy from unknown cause. The most frequent site of cerebral infarction was the middle cerebral artery area with no predilection on the right of left.

• Clinical and Experimental Pediatrics
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• 제57권11호
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• pp.472-478
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• 2014

Kawasaki disease (KD), an acute vasculitis that primarily affects young children, is the most common acquired paediatric cardiovascular disease in developed countries. While sequelae of arterial inflammation in the acute phase of KD are well documented, its late effects on vascular health are increasingly unveiled. Late vascular dysfunction is characterized by structural alterations and functional impairment in term of arterial stiffening and endothelial dysfunction and shown to involve both coronary and systemic arteries. Further evidence suggests that continuous low grade inflammation and ongoing active remodeling of coronary arterial lesions occur late after acute illness and may play a role in structural and functional alterations of the arteries. Potential importance of genetic modulation on vascular health late after KD is implicated by associations between mannose binding lectin and inflammatory gene polymorphisms with severity of peripheral arterial stiffening and carotid intima-media thickening. The changes in cholesterol and lipoproteins levels late after KD further appear similar to those proposed to be atherogenic. While data on adverse vascular health are less controversial in patients with persistent or regressed coronary arterial aneurysms, data appear conflicting in individuals with no coronary arterial involvements or only transient coronary ectasia. Notwithstanding, concerns have been raised with regard to predisposition of KD in childhood to accelerated atherosclerosis in adulthood. Until further evidence-based data are available, however, it remains important to assess and monitor cardiovascular risk factors and to promote cardiovascular health in children with a history of KD in the long term.