BACKGROUND: In spite of the clinical introduction of brachytherapy to reduce restenosis, the biologic responses of vascular smooth muscle cells(VSMCs) to radiation have not been well studied. We investigated the effects and mechanisms of gamma-irradiation on the cell cycle of VSMCs using primary cultures of rat aortic VSMCs and 137Cs as a radiation source. METHODS & RESULTS: The cell counts after irradiation with 0, 2, 8, 16 Gray (Gy) (n=, each) were 3.28, 2.34, 1.94 and 1.30 x 105/ml at 24h, and 5.10, 2.00, 1.80 and 1.20 x 105/ml at 48h, respectively. The proportions of cells in the G0/G1, S and G2/M phases, as measured by Fluorescence Activated Cell Sorter, were 61, 9 and 30% at 12 hours after 16Gy radiation (control 61, 34 and 5%), 65, 9 and 26% at 24 hours (control 70, 16 and 14%); and 67, 7 and 26% (control 78, 12 and 10%) at 48 hours, which demonstrated G1 and G2 arrest. By immunoblot analysis and kinase assay, gamma-irradiation with 8 or 16 Gy increased the expression of p21, universal cell cycle inhibitor, and decreased the expression and activity of CDK2, an important kinase during the later stages of G1/S progression, as well as the expression and activity of CDK1, which is important in the G2/M phase transition. In contrast, radiation did not affect the expression or activity of either CDK4 or CDK6. The cell-cycle inhibitors, p27 and p16 were not involved in the radiation-induced cell cycle arrest of VSMCs. CONCLUSION: Gamma-irradiation can effectively inhibit VSMC proliferation because it causes cell cycle arrest at both the G1 phase by enhancing P21 expression and suppressing CDK2, and at the G2/M phase by suppressing CDK1.
Animals ; Brachytherapy ; Cell Count ; Cell Cycle ; Cell Cycle Checkpoints ; Cyclin-Dependent Kinases* ; Fluorescence ; G1 Phase ; Muscle, Smooth, Vascular* ; Phase Transition ; Phosphotransferases ; Rats

BACKGROUND: Many studies reported that endothelium-dependent vasodilator response is impaired in patients with congestive heart failure. But the opposite results also were reported. The aim of this study was to determine the presence of endothelial dysfunction and its characteristics. METHODS AND MATERIALS: Forearm blood flow was measured in 12 patients with congestvie heart failure (7 males and 5 females, mean age 53+/-11 years old) and 10 normal control subjects (5 males and 5 females, mean age 41+/-10 years old) using strain-gauge plethysmography. The endothelium-dependent vasodilators were acetylcholine (7.5, 15, and 30 microgram/min), which uses a pertussis toxin-sensitive signal transduction pathway, and bradykinin (100, 200, and 400 ng/min), which uses a pertussis toxin-insensitive signal transduction pathway to activate nitric oxide production. Sodium nitroprusside (0.8, 1.6, and 3.2 microgram/min) was used as an endothelium-independent vasodilator. All drugs were infused into the brachial artery with random order. RESULTS: The basal forearm blood flow was similar between both groups. The maximum flow in response to acetylcholine, bradykinin, and sodium nitroprusside was also similar in two groups. CONCLUSIONS: Patients with congestive heart failure showed normal endothelium-dependent vasodilator responses to both acetylcholine and to bradykinin. This finding indicates that the endothelial vasodilator function is normal in the patients with heart failure.
Acetylcholine ; Brachial Artery ; Bradykinin ; Endothelium ; Endothelium-Dependent Relaxing Factors ; Estrogens, Conjugated (USP)* ; Female ; Forearm ; Heart Failure* ; Humans ; Male ; Nitric Oxide ; Nitroprusside ; Plethysmography ; Signal Transduction ; Vasodilation* ; Whooping Cough

No abstract available.
Echocardiography*

BACKGROUND: Myocardial infarction(MI) in the rat is a model of ventricular dysfunction which is associated with activation of compensatory neurohumoral systems. This stydy was designed to determine the temporal evolution of the regulatory factors-atrial natriuretic peptide(ANP), endothelin(ET), plasma renin activity(PRA) in rats with more than moderate sized MI at 1,4,8 weeks in comparison to normal rats. METHODS AND RESULTS: MI was created in female Sprague Dawley rats weighing 250gms to 300gms by ligating the anterior descending artery. Before sacrifice, hemodynamics were measured and blood was drawn in control rats(n=8) and rats with MI(n=7), 4(n=10), and 8 weeks(n=9) after surgery. Heart weight index increased from 329.0+/-7.3mg/gm at baseline to 380.6+/-18.4mg/gm, 441.1+/-23.2mg/gm at the 1st, 4th, and 8th weeks after MI. Plasma ANP increased in the 1st weeks and remained elevated(16+/-7, 259+/-65, 404+/-72, 494+/-73pg/ml at baseline, 1st, 4th, 8th weeks after MI respectively). Plasma endothelin was suppressed at 4th weeks but elevated at 8th week(7.8+/-0.2, 5.3+/-0.3, 11.9+/-1.3pg/ml at baseline, 4th, 8th weeks respectively). PRA, indirect index of plasma angiotensin also decreased at 4th week but elevated at 8th week(14.9+/-0.3, 9.8+/-1.0, 20.3+/-1.8ng/ml/hr at baseline, 4th, 8th weeks resepctively). CONCLUSION: These results demonstrate a biphasic response of endothelin and PRA after MI despite the inhibitory effects of ANP. These data support the important differential regulation of humoral factors in the evolution of acute MI.
Angiotensins ; Animals ; Arteries ; Atrial Natriuretic Factor ; Endothelins ; Female ; Heart Failure* ; Heart* ; Hemodynamics ; Humans ; Models, Animal* ; Myocardial Infarction ; Plasma ; Rats* ; Rats, Sprague-Dawley ; Renin ; Ventricular Dysfunction

The most feared complication of left ventricular thrombus (LVT) is the occurrence of systemic thromboembolic events, especially in the brain. Herein, we report a patient with severe sepsis who suffered recurrent devastating embolic stroke. Transthoracic echocardiography revealed apical ballooning of the left ventricle with a huge LVT, which had not been observed in chest computed tomography before the stroke. This case emphasizes the importance of serial cardiac evaluation in patients with stroke and severe medical illness.
Brain ; Echocardiography ; Heart Ventricles ; Humans ; Sepsis ; Shock, Septic* ; Stroke* ; Thorax ; Thrombosis*

A 38 year old woman presented with two week history of cough, progressive dyspnea, orthopnea and pedal edema. She had previously been in excellent health with the exception of surgery five years ago for tumor of the right thigh. The histopatihologic diagnosis was chondrosarcoma. Her clinical course was characterized by rapid aggrevation of dyspnea and eddema unresponsive to conventional managements for congestiove heart failure. Transesophageal echocardiogram showed dleft atrial mass growing from pulmonic vein. To our knowledge, cardiac metastasis from chondrosarcoma is rare and we report this is the first case of chondrosarcoma metastatic to the heart in Korea.
Adult ; Chondrosarcoma* ; Cough ; Diagnosis ; Dyspnea ; Edema ; Female ; Heart Failure ; Heart* ; Humans ; Korea ; Neoplasm Metastasis ; Thigh ; Veins

No abstract available.
Echocardiography* ; Hepatitis B virus* ; Hepatitis B* ; Hepatitis* ; Liver Cirrhosis* ; Liver*

BACKGROUND: It is well known that hypertension attenuate endothelium-dependent vasodilator response. And this finding is closely related to the development of atherosclerosis. Recently it is reported that the expression of NADPH-dependent oxidase is increased in angiotensin-induced hypertension model and superoxide (O2) produced from that might contribute to the development of vascular diseases. The possible mechanism is the degradation of endothelium-derived NO by O2. We hypothesized that SOD prevents endothelial dysfunction via prevention of the degradation of endothelium-derived NO. METHODS AND MATERIALS: We made renovascular hypertension model by constricting abdominal aorta just above the left renal artery of Sprague-Dawley female rats. The descending thoracic aorta was stuied in the organ chambers using acetylcholine as an endothelium-dependent vasodilator with or without pretreatment of SOD. RESULTS: Blood pressures of all 14 rats were significantly increased (174/123 mmHg, mean 146 mmHg). The residual tensions of the vessels precontracted by phenylephrine were similar in both groups (15.04+/-19.53 % in SOD group vs 11.84+/-18.57% in non-SOD group, p=.66). CONCLUSIONS: The endothelial dysfunctions in the rat aorta with renovascular hypertension were not improved by SOD. There is no acute effect of SOD on endothelial function in high renin/angiotensin state.
Acetylcholine ; Animals ; Aorta* ; Aorta, Abdominal ; Aorta, Thoracic ; Atherosclerosis ; Endothelium ; Female ; Humans ; Hypertension ; Hypertension, Renovascular* ; Oxidoreductases ; Phenylephrine ; Rats* ; Rats, Sprague-Dawley ; Renal Artery ; Superoxides ; Vascular Diseases

BACKGROUND: C-type natriuretic peptide (CNP), secreted from endothelial cells, dilates the vessel and increases the renal excretion of sodium and water. Plasma CNP level is not elevated in patients with congestive heart failure (CHF), but the myocardial content of CNP is increased, suggesting paracrine or autocrine role of CNP. We studied to compare the effect of ANP and CNP on vasorelaxation in CHF rat model. METHODS: Coronary artery ligation was performed in Sprague Dawley rats, resulting in CHF (n=5) and they were fed with ordinary chow for 10 weeks. After measuring hemodynamics, aorta and pulmonary artery were incised and studied in organ chamber to measure the isotonic force to KCl and to observe the relaxation response to atrial natriuretic peptide (ANP), and CNP in vessels precontracted with phenylephrine. Normal Sprague Dawley rats (n=5) were used as control. RESULTS: There were no difference in vasorelaxation responses to ANP between control and CHF rats. The response to CNP was significantly impaired in both aorta and pulmonary artery of CHF rats compared to control rats.
Animals ; Aorta* ; Atrial Natriuretic Factor ; Coronary Vessels ; Endothelial Cells ; Estrogens, Conjugated (USP)* ; Heart Failure* ; Hemodynamics ; Humans ; Ligation ; Models, Animal ; Myocardial Infarction ; Natriuretic Peptide, C-Type* ; Natriuretic Peptides ; Phenylephrine ; Plasma ; Pulmonary Artery* ; Rats* ; Rats, Sprague-Dawley ; Relaxation* ; Sodium ; Vasodilation

Preservation of the subvalvular apparatus has the merits of postoperative outcomes during mitral valve replacement for mitral regurgitation. We performed mitral valve replacement with anterior and posterior leaflet chordal preservation in a 65-year-old woman. On the 2nd postoperative day, routine postoperative trans-thoracic echocardiography showed an unknown aortic subvalvular mobile mass. We report a case of a remnant mitral subvalvular apparatus detected by echocardiography after chordal preserving mitral valve replacement which was confused with postoperative aortic valve vegetation.
Aged ; Aortic Valve ; Echocardiography ; Female ; Humans ; Mitral Valve ; Mitral Valve Insufficiency