BACKGROUND: To evaluate the safety and the efficacy of amlodipine, a dihydropyridine calcium antagonist, monotherapy in the treatment of moderate essential hypertension. METHOD: Amlodipine 5mg once a day was administered as a starting dose in 30 patients with essential hypertension in the morning and a one step upward titration was performed (amlodipine 10 mg once a day) was done at the end of 4weeks treatment. Final evaluation was done at 12weeks with laboratory test and echocardiogram. RESULT: Within 4weeks treatment with dose of 5mg amlodipine once a day, the systolic blood pressure (SBP) was decreased(184.5+/-23.3/150.5+/-16.0mmHg,p<0.000), and the diastolic blood pressure(DBP) was also decreased significantly (109.9+/-04.6/92.3+/-11.5mmHg, P<0.001). After 12 weeks of treatment with a mean dosage of 6.6mg once a day, SBP and DBP was maintained comparing with basal level (147.0+/-15.8/88.1+/-0.9mmHg, respectively). The efficacy of amlodipine treatment was noted an excellent in 16 patients(53.3%), good in 4 patient(13.3%), fair in 4 patients(13.3%), and failed in 2 patients(6.7%). There was no significant change in heart rate before and after amlodipine treatment. (80.0+/-2.3/80.9+/-10.4 beats/minute n.s). Amlodipine had not significant effects on laboratory findings such as serum creatinine, BUN, ALT/AST, hemoglobin, leukocyte count,platelet and lipid profiles. There was facial flushing 2 patients, but no need to discontinue administration of amlodipine and all patients completed for 12weeks therapy. CONCLUSION: It is concluded that amlodipine is an effective antihypertensive agent, as monotherapy once a day in patients with moderate essential hypertension.
Amlodipine ; Blood Pressure ; Calcium ; Creatinine ; Flushing ; Heart Rate ; Humans ; Hypertension* ; Leukocytes

BACKGROUND: The effective ventricular function during ejection and filling is likely to depend on the coordinated action of the longitudinally and circumferentially orientated myocardial fibers and the function of these longitudinal fibers has not been extensively studied. METHODS: The role of longitudinally and circumferentially orientated fibers in left ventricular wall motion was evaluated by M-mode echocardiograms of the mitral ring(whose motion reflect long axis change) and the standard minor axis(left ventricular posterior wall), simultaneous recordings of phonocardiograms and electrocardiograms on the paper (speed 100mm/sec), in 24 healty individuals, 17 patients with mitral stenosis, 11 patients with open mitral commissurotomy and 17 mitral valve replaced patients. RESULTS: In the controls long axis shortening significantly preceded minor axis shortening (phase difference between two axes : 20+/-3 msec, mean+/-SEM) during early systole, indicating left ventricle become more spherical. This phase difference was also observed in the patients with mitral stenosis and in those with open mitral commissurotomy. In patients with mitral valve replacement(MVR) whose papillary muscles had been sectioned, the onset of long axis shortening was more delayed during early systole than that of short axis(-33+/-6msec) and the end of shortening was also prolonged to early diastole more than that of normal controls (54+/-3 msec vs 90+/-8 msec, mean+/-SEM, p<0.01 by t-test). CONCLUSION: We observed the time relations between long and short axis motion in normal controls. It can be concluded that the reversed time relation in patients with MVR is one of the important factors which may effect negatively on ventricular function and long-term prognosis, thus the surgical procedures to preserve papillary annular continuity should be considered in patients with mitral valvular disease. And the controlled, prospective, clinical trials with homogenous groups of patients are needed to evaluate the potential benefits of papillary annular continuity in preserving atrio-ventricular interaction in patients undergoing mitral valvular surgery.
Axis, Cervical Vertebra* ; Diastole ; Echocardiography ; Electrocardiography ; Heart Valve Diseases* ; Heart Ventricles ; Humans ; Mitral Valve ; Mitral Valve Stenosis ; Papillary Muscles ; Prognosis ; Systole ; Ventricular Function

No abstract available.
Echocardiography* ; Electrocardiography*

BACKGROUND: This study was designed to evaluate the safety and the efficacy of fosinopril(Monopril(R)) in the treatment of mild to moderate essential hypertension. METHOD: Fosinopril(10mg) once a day was administrated as a starting dose in 20 patients with essential hypertension in the morning and a one step upward titration was performed(fosinopril 20mg once a day, after 4 weeks treatment). RESULT: After 2 weeks treatment with dose of 10mg, the systolic blood pressure(SBP) was decreased(183.8+/-28.5 vs, 161.5+/-25.9mmHg, p<0.05) and the diastolic blood pressure(DBP) was also decreased significantly(108.3+/-9.3 vs, 96.6+/-10.3mmHg, p<0.05). The effect of fosinopril were maintained. The SBP an DBP were decreased in 14 out of 20 patients till 8 weeks. There was no significant change in heart rate before and after fosinopril treatment(74.3+/-10 vs, 76.4+/-7.9beats/min). Fosinopril had no significant effects on laboratory findings such as serum creatinin, BUN, AST/ALT, WBC, Platelet and lipid profiles. Mild dry coughing was noticed only in 5 patients and it did not disturb continuing medication. CONCLUSION: Fosinopril is an effective antihypertensive agent, as monotherapy once a day in patients with mild to moderate hypertension.
Blood Platelets ; Cough ; Fosinopril* ; Heart Rate ; Humans ; Hypertension*

BACKGROUND: In previous study, hypertensive patients with left ventricular diastolic dysfunction showed delayed relaxation time intervals and increased relaxation nonuniformity of regional wall motion. In this point of view, the effects of amlodipine on the regional wall motion and mitral flow patterns were evaluated. METHODS: Before and 32weeks after the antihypertensive medication of amlodipine, M-mode & Doppler echocardiogram were performed in 14 patients with moderate hypertension. We measured A2 to the peak thinning rate point of left ventricular(LV)posterior wall [A2-(-)dpw/dt] and the peak lengthening rate point of mitral annulus [A2-dL/dt] on M-mode echocardiogram and we defined nonuniformity as the time interval, (-)dpw/dt-dL/dt. RESULTS: 1) Mitral flow velocity E/A ratio was increased (0.95+/-0.4 vs 1.42+/-0.6, p<0.05) after amlodipine medication. 2) Heart rate and LV posterior wall thickness was decreased (79+/-9.3 vs 72+/-10.8 beats/min, 10.7+/-1.5 vs 9.4+/-2.0mm, p<0.05 respectively). 3) Long axis relaxation was improved (A2-dL/dt ; 165+/-44 vs 140+/-23msec, p<0.05) and nonuniformity index was decreased ((-)dpw/dt-dL/dt ; 63+/-49 vs 41+/-30msec p=0.07). CONCLUSION: Amlodipine improved E/A ratio of mitral flow (E/A ratio) in hypertensive patients with diastolic dysfunction, which could be attributed to the decreased heart rate, the decrease in wall thickness and the improvement in relaxation movement of LV long axis.
Amlodipine* ; Axis, Cervical Vertebra ; Heart Rate ; Humans ; Hypertension* ; Relaxation

BACKGROUND: Viral myocarditis is considered as a cause of dilated cardiomyopathy. At present, two pathogenic mechanisms may be involved in the pathogenesis of viral myocarditis and subsequent cardiomyopathy. First, the virus infection of myocyte may directly lead to either cell death or persistent metabolic dysfunction. Second, virus-induced immune or autoimmune mechanism may play a role. METHODS: To test the therapeutic efficacy of immunosuppression with cyclophophamide(CYP) on coxsackievirus B3(CB3) myocarditis, 10-14 week-old Balb/c mice were inoculated with 4000 plaque-forming units of CB3. In experiment 1, CYP (100mg/kg/day subcutaneous injection, s.c) was administrated daily on days 1-7(group 2, n=16). In experiment 2, CYP 30mg/kg/day s.c(group 3, n=32) or CYP 100mg/kg/day s.c(group 4, n=32) were administrated on days 8-14. The animals of infected controls(group 1, n=26) and group 2, 3, 4 were dissected at days 4, 7, 15, 22 and spleen, heart, thymus and body weights were measured. RESULTS: In experiment 1. survival rate in group 2 on day 7, 15 were low compared with group 1(85%, 0% vs 100%, p<0.05). and myocardial virus titers in group 2 on day 4 was 50 times, and on day 7, 1000 times higher compared with group 1, Histologically, on day 7, focal cellular infiltrations were prominent findings in group 1, but diffuse myocardial necrosis without cellular infiltration were observed in group 2. In experiment 2, survival rate, cardiac histopathology myocardial virus titer and serum neutralizing antibody titers did not differ among groups 1, 3 and 4. In experiment 1 and 2, the spleen-to-body-weight and thymus-to-body-weight ratios were significantly lower in CYP treated groups than those in controls and marked cellular depletions in spleens and thymus were observed in CYP treated groups. CONCLUSIONS: As the results of above, it can be concluded that the immunosuppression during viremic phase of murine viral myocarditis aggravated the myocardial necrosis, and during aviremic phase, the administration of CYP didnot affect the process of viral myocarditis. Thus, direct viral mechanisms in the production of cardiomyocyte injury in CB3-infected mice appear to bo more important than cell mediated immune mechanism. To understand relevant pathogenic mechanisms of clinical myocarditis and dilated cardiomyopathy resulting from viral infection, the experimental study expanding into nonmurine animals and into various models using other infectious agents may be required.
Animals ; Antibodies, Neutralizing ; Body Weight ; Cardiomyopathies ; Cardiomyopathy, Dilated ; Cell Death ; Cyclophosphamide* ; Heart ; Immunosuppression ; Injections, Subcutaneous ; Mice ; Muscle Cells ; Myocarditis* ; Myocytes, Cardiac ; Necrosis ; Spleen ; Survival Rate ; Thymus Gland ; Viral Load

No abstract available.
Blood Flow Velocity*

Brown adipose tissue is specialized to burn lipids for thermogenesis and energy expenditure. Second-generation antipsychotics (SGA) are the most commonly used drugs for schizophrenia with several advantages over first-line drugs, however, it can cause clinically-significant weight gain. To reveal the involvement of brown adipocytes in SGA-induced weight gain, we compared the effect of clozapine, quetiapine, and ziprasidone, SGA with different propensities to induce weight gain, on the differentiation and the expression of brown fat-specific markers, lipogenic genes and adipokines in a mouse brown preadipocyte cell line. On Oil Red-O staining, the differentiation was inhibited almost completely by clozapine (40 microM) and partially by quetiapine (30 microM). Clozapine significantly down-regulated the brown adipogenesis markers PRDM16, C/EBPbeta, PPARgamma2, UCP-1, PGC-1alpha, and Cidea in dose- and time-dependent manners, whereas quetiapine suppressed PRDM16, PPARgamma2, and UCP-1 much weakly than clozapine. Clozapine also significantly inhibited the mRNA expressions of lipogenic genes ACC, SCD1, GLUT4, aP2, and CD36 as well as adipokines such as resistin, leptin, and adiponectin. In contrast, quetiapine suppressed only resistin and leptin but not those of lipogenic genes and adiponectin. Ziprasidone (10 microM) did not alter the differentiation as well as the gene expression patterns. Our results suggest for the first time that the inhibition of brown adipogenesis may be a possible mechanism to explain weight gain induced by clozapine and quetiapine.
Adipocytes, Brown/drug effects ; Adipogenesis/drug effects ; Adipokines/metabolism ; Animals ; *Antipsychotic Agents/administration & dosage/adverse effects ; Cell Differentiation/drug effects ; Cell Line ; Cell Survival/drug effects ; *Clozapine/administration & dosage/adverse effects ; *Dibenzothiazepines/administration & dosage/adverse effects ; Gene Expression Regulation/drug effects ; Humans ; Mice ; *Piperazines/administration & dosage/adverse effects ; Schizophrenia/drug therapy ; *Thiazoles/administration & dosage/adverse effects ; Weight Gain/*drug effects

BACKGROUND: Endotracheal intubation often results in hypertension and tachycardia. Desflurane and nitrous oxide (N2O) are known to augment the sympathetic nervous activity. We examined whether N2O and desflurane affect the cardiovascular responses to the intubation. METHODS: One hundred-fifty patients were assigned randomly to receive one of six treatment regimens (n = 25 each): 2% sevoflurane (control), 6% desflurane or 12% desflurane with and without 75% N2O, respectively. General anesthesia was induced with intravenous thiopental (5-7 mg/kg), and tracheal intubation was facilitated with intravenous vecuronium (0.12 mg/kg). N2O was started 3 min before and desflurane soon after the intubation. Systolic arterial blood pressure (SAP), heart rate (HR), and plasma catecholamine concentrations were determined. RESULTS: The intubation increased SAP and HR in all groups within 1 min. A second increase was noted with 12% desflurane at 3 to 5 min after the intubation. N2O did not affect the tachycardiac response, but attenuated the pressor response to both intubation and 12% desflurane. The plasma concentrations of norepinephrine increased significantly at 1 min after the intubation in all groups with more pronounced rise in N2O groups, and increased further at 5 min in the 12% desflurane groups. CONCLUSIONS: A biphasic increase of SAP and HR was noted with 12% desflurane. The first increase may be related with the mechanical stimulus of the tracheal intubation and the second with the desflurane itself. Although N2O did not affect the tachycardiac responses and augmented norepinephrine release, it suppressed the pressor responses.
Anesthesia, General ; Arterial Pressure ; Heart Rate ; Humans ; Hypertension ; Intubation ; Intubation, Intratracheal* ; Nitrous Oxide* ; Norepinephrine ; Plasma ; Tachycardia ; Thiopental ; Vecuronium Bromide

Hepatic portal venous gas (HPVG) is a rare disease presenting as acute abdomen. The presence of the air in the portal vein has been associated with a mortality rate of more than 75%. Because of high mortality rate, most HPVG requires emergent surgical interventions and intensive medical management. HPVG is most commonly caused by mesenteric ischemia but may have a variety other causes. Clostridium perfringens is the most common pathogen of gas forming bacteria that can cause of HPVG, but Clostridium perfringens blood stream infection with HPVG is not yet reported in Korea. We experienced a case of HPVG caused by Clostridium perfringens blood stream infection at mesenteric venous hemangioma with portal hypertension due to mesenteric arteriovenous malformation.
Abdomen, Acute ; Arteriovenous Malformations ; Bacteria ; Clostridium perfringens* ; Hemangioma ; Humans ; Hypertension, Portal* ; Ischemia ; Korea ; Mortality ; Portal Vein ; Rare Diseases ; Rivers