Effects of Angiotensin II on the Growth of Vascular Smooth Muscle Cells

BACKGROUND AND OBJECTIVES: The octapeptide hormone of the renin-angiotensin system, angiotensin ii, regulates a wide variety of physiological responses including salt and water balance, blood pressure, and vascular tone. Contradictory results have been reported regarding the effects of angiotensin ii on vascular smooth mu-scle cell (VSMC) proliferation. The aim of the present study was to investigate the direct effect of angiotensin ii on the growth of VSMC. MATERIALS AND METHOD: Rat aortic smooth muscle cells were obtained by the combined collagenase and elastase methods. Cells between the 4th and 8th passages were used for the experiments. Cultures were treated daily for 3 days with either angiotensin ii alone or angiotensin ii with equimolar concentrations of saralasin. Incorporated radioactivity of [3H]thymidine and [14C]phenylalanine was measured by liquid scintillation spectrometry. RESULTS: Angiotensin ii increased [14C]phenyalanine incor-poration about 20-30%, and saralasin completely blocked the stimulation by angiotensin ii. However, there was no significant increase in [3H]thymidine incorporation by angiotensin ii stimulation in this study. CONCLUSION: These results suggest that angiotensin ii alone induces cellular hypertrophy but has no detectable mitogenic activity in cultured rat aortic VSMC.

A Case of Cardiac Chloroma Complicated by Acute Lymphocytic Leukemia

Chloroma (granulocytic sarcoma) indicates an extramedullary leukemic cell collection. It often develops in the course of, or as a presenting sign of leukemia. Cardiac chloroma is uncommon and rarely detected as a mass. We report the first case of cardiac chloroma in a patient with acute lymphocytic leukemia in Korea. A 73-year-old man was admitted because of exertional dyspnea, orthopnea and generalized weakness. Thrombocytopenia and immature leukocytes were detected in the peripheral blood. An X-ray film of the chest showed mild cardiome-galy and bilateral pleural effusion. Transthoracic and transesophageal echocardiography showed a low echogenic mass at the lateral wall of the right ventricle. The size of the mass was about 6x4 cm. MRI of the chest showed right ventricular mass with slightly increased inhomogeneous signal intensity. Bone marrow aspiration and biopsy confirmed that he had a L3 FAB subtype of acute lymphocytic leukemia. Induction chemotherapy with vincristine, prednisolone, daunorubicin resulted in hematologic complete remission. At 6 weeks after the induction chemotherapy, transesophageal echocardiography demonstrated disappearance of the right ventricular mass which suggested that it was a cardiac chloroma complicating acute lymphocytic leukemia.

Effect of Carvedilol on the Growth of Vascular Smooth Muscle Cells

Background and objectives: Carvedilol is a cardiovascular drug, beta- and alpha1-adrenoceptor antagonist, currently approved for the treatment of hypertension, angina, congestive heart failure by FDA. Carvedilol has been shown to attenuate oxygen free radical-initiated lipid peroxidation and to inhibit neointimal formation of aorta following vascular injury by balloon angioplasty. We have investigated the effect of carvedilol on DNA synthesis of vascular smooth muscle cells (VSMC) stimulated by platelet-derived growth factor (PDGF)-BB. MATERIALS AND METHOD: Rat aortic smooth muscle cells were obtained by the combined collagenase and elastase methods. Cells between the 4th and 8th passages were used for the experiments. Incorporated radioactivity of [3H]-thymidine was measured by liquid scintillation spectrometry. RESULTS: PDGF-BB (1 nM) increased [3H]-thymidine incorporation about 70-100% over basal value in cultured VSMC. PDGF-stimulated increase in DNA synthesis was significantly suppressed by simultaneous administration of carvedilol. In contrast, propranolol did not significantly affect 3[H]-thymidine uptake in rat aortic VSMC. CONCLUSION: The present study demonstrate that carvedilol significantly inhibits the proliferation of vascular smooth muscle cell in our condition. These results indicate that carvedilol may be effective in the treatment of cardiovascular diseases principally associated with abnormal vascular smooth muscle growth.

Association of Carotid Artery Intimal-Medial Thickness with Left Ventricular Hypertrophy

BACKGROUND: Atherosclerosis is a diffuse disease process that produce thickening of the vascular wall because of intimal deposition of lipid, fibrous tissue, and calcific material. Nowadays it is possible to evaluate atherosclerotic changes of carotid arteries accurately by developed noninvasive techniques such as ultrasonography. Left ventricular hypertrophy (LVH) is known to be an important risk factor for cardiovascular events in hypertension. The purpose of this study was to establish whether the carotid intimal - medial thickness (IMT) correlates with the severity of LVH. METHOD: We measured intimal-medial thickness (IMT) for 12 sites in carotid arteries (near and far walls in common carotid, bifurcation, and internal carotid arteries of both sides) by B-mode ultrasonography in both 38 normotensive and 72 hypertensive patients. Left ventricular measurements were made according to the recommendations of the American Society of Echocardiography. Left ventricular mass was derived from the formula described by Devereux et al. and each left ventricular mass value was indexed to body surface area. And then we have investigated whether hypertensive patients have significant changes of carotid IMT and IMT correlates with left ventricular mass index (LVMI). RESULTS: (1) Most hypertensive patients had diffuse thickening of the carotid artery and some had focal or multiple plaques. (2) In general, mean IMT was widest in the carotid bifurcation. (3) The mean IMT of all 12 segments increased about 40% in hypertensive patients compared with normal control group. (4) LVMI significantly correlates with IMT of carotid artery, especially bifurcation site and mean all 12 segments. CONCLUSION: The mean IMT may serve as a useful marker of the severity of atherosclerosis in hypertensive patients. The significant association between carotid IMT and LVMI suggests a simultaneous correlation of carotid atherosclerosis with left ventricular hypertrophy in hypertension.

A Case of Disseminated Mucormycosis Involving Lung, Chest Wall and Central Nervous System / 대한내과학회지

Disseminated mucormycosis is a rare but fatal fungal infection with a high mortality rate. Mucormycosis usually occurs in immunocompromised patients such as in patients with diabetes mellitus, leukemia, lymphoma and in patients undergoing anticancer therapy, prolonged immunosuppression, and antibiotic therapy. Early diagnosis and the resolution of predisposing factors, including the use of amphotericin B and wide surgical resection, are essential to make a successful outcome. We report a well-documented case of disseminated mucormycosis involving lung parenchyme, chest wall and central nervous system with the review of literatures in patients with uncontrolled diabetes and Evans' syndrome. Typical broad, branching in right angle, non-septated hyphae were observed in the biopsy of the nodular mass on the anterior chest wall. Chest CT and brain MRI found three pulmonary cavitary lesions and multiple small nodules with ring-enhancement in the cerebrum, cerebellum and the brainstem. Although 1,116mg of amphotericin B in sum was given with flucytosine, she expired due to progressive mucormycosis.

Ultrastructural Changes of the Aorta in Spontaneously Hypertensive Rats and the Effect of High Cholesterol Diet

BACKGROUND: Vascular lesions are the major cause of morbidity and mortality in hypertensive patients. However, the pathologic characteristics of gradually evolving, chronic hypertension have not been adequately studied and the mechanism by which hypertension accelerates atherosclerosis is still uncertain. This study was undertaken to invertigate the ultrastructural changes of the aorta and the effect of high cholesterol diet in spontaneously hypertensive rats(SHR). METHODS: Spontaneously hypertensive rats (n=80, male, 5 weeks old) and Wistar rats (n=40, male, 5 week old) were used. Forty SHR were fed with 2% cholestrol diete, while the remainder with control diet. Systolic blood pressure was measured weekly until 16 weeks after birth, and then biweekly until 40 weeks after birth. Transmission and scanning electron microscopy were used to evaluate ultrastrucural changes of the aorta. RESULTS: 1) The blood pressure of SHR rose stedily and progressively from the 5 weeks after birth and reached nearly 190mmHG at the 16 weeks after birth. 2) In SHR, the subendothelial component contained finely granular substances, abundant fibrillar collagen and elastin. Infiltration of the mononuclear blood leukocytes into the intima was frequently seen. 3) Endothelium from cholestrol-fed SHR did exhibit numerous pinocytotic vesicles and contained many cytoplasmic filaments. There were a number of large mononuclear lipid-filled cells in the intimal lesions. Blistering of the endothelial plasma membrane was also observed in high cholesterol diet-fed SHR. Later on, adhesion of platelets, febrin, and white blood cells as well as damage of intima shown as multiple small holes were more marked. 4) There was no significant difference in systoloic blood pressure between high cholesterol diet-fed and control diet-fed SHR. CONCLUSION: In the aorta of SHR, the most prominent change was an expansion of the subendothelial space and infiltration of the mononuclear leukocytes into the intima. The present study showed that the SHR was indeed a reliable model for the essential hypertension. In some SHR, high cholesterol diet could induce more pronounced vascular lesions, which were enhanced by hypertension.