Heart failure is a recognized, although uncommon, cause of massive liver cell necrosis, the clinical consequence of which are intermingled with those of cardiac insufficiency in most case. But, hepatic coma is rerely caused by hepatic congestion only. We report the three cases with heart failure resulted in massive liver cell necrosis and fulminant hepatic failure. The manifestations of fulminant hepatic failure were hepatic encephalopathy, jaundice, marked increase of prothrombin time and serum transaminase and there were no evidences of viral hepatitis and toxic hepatitis as a cause of liver failure.
Drug-Induced Liver Injury ; Estrogens, Conjugated (USP)* ; Heart Failure* ; Hepatic Encephalopathy ; Hepatitis ; Jaundice ; Liver ; Liver Failure ; Liver Failure, Acute* ; Necrosis ; Prothrombin Time

The authors reported here a 23 years-old female patient with acute renal failure and anaphylaxis induced by rifampicin, who was suffered from exudative pericarditis. The diagnosis was made by its reproducibility with rifampicin. The pathogenesis of acute renal failure and anaphylaxis in this case was thought to be immunologic mechanism, because of elevated IgE and depressed complements. Relevant literature was also reviewed.
Acute Kidney Injury* ; Anaphylaxis* ; Complement System Proteins ; Diagnosis ; Female ; Humans ; Immunoglobulin E ; Pericarditis ; Rifampin ; Young Adult

No abstract available.
Amlodipine* ; Humans ; Hypertension*

No abstract available.
Doxazosin* ; Hypertension*

No abstract available.
Humans ; Hypercholesterolemia* ; Lovastatin*

Left ventricular false tendon, also called moderator bands, anomalous cords, accessory bands or false chordae tendinae, has been known as simple anatomical without clinical importance. But the possible relationship with Still's type murmur and ventricular arrhythmia were reported recently. The incidence of false tendon was known as 0.5-6.1% variably. In Korea, there are no reports about left ventricular false tendon till now. The authors examined 2,052 patients' echocaediograms and clinical manifestations retrospectively to find the incidence and potent clinical significance of false tendons. The incidence in present study was 1.02% and there was no specific relationship between false tendon and cardiovascular diseases. The authors observed Still's type musical murmur in 5 patients out of 21 and ventricular premature beats in 2 patients out of 10 without other cardiovascular diseases. One of them showed nonsustained ventricular tachycaedia during Holter ECG monitoring. The most frequent echocardiographic site of attachment was from basal inter-ventricular septum to lelft ventricular free wall and false tendon attached to papillary muscle was least frequently observed.
Arrhythmias, Cardiac ; Cardiac Complexes, Premature ; Cardiovascular Diseases ; Echocardiography ; Electrocardiography ; Humans ; Incidence ; Korea ; Music ; Papillary Muscles ; Retrospective Studies ; Tendons*

In single atrial and ventricular cells isolated from the guinea-pig and the rabbit heart, action potentials and membrane currents were recorded by using the whole cell voltage clamp technique. In rabbit atrial cells the repolarization showed two distinctive phases, referred as the early and late phases(early and late plateau phase), but in guinea-pig atrial cells there was a maintained plateau and less distinctive two phases of repolartization. Increasing intracellular sodium or reducing external sodium by replacement with lithium suppressed the late phase of the action potential in rabbit atrial cells and shortened the plateau of action potential in rabbit ventricle and guinea-pig atrial cells. Reducing external sodium decreased Ca-current and late inward current in voltage clamp. Ouabain in the concentration of 10(-5)M shortened the duration of action potential and shifted the holding current level to outward direction, decreased Ca-current and moved late inward current to outward direction. Ryanodine 10(-6)M which is known to be an inhibitor of Ca-release in the intracellular store, suppressed the late phase of action potential in rabbit atrial cells and shortened the plateau of action potential in rabbit ventricular cells. Ryanodine also decreased Ca-current and shifted late inward current to outward direction. It is concluded that an inward current activated by intracellular calcium contributes to the late Phase of the action potential in rabbit atrial cells and to the late plateau in rabbit ventricular cells and in guinea-pig atrial cells. It may be carried by the Na-Ca exchange precess and/or by calcium-activated non-specific channels but preferably Na-Ca exchange machanism.
Action Potentials* ; Calcium ; Heart* ; Lithium ; Membranes* ; Myocytes, Cardiac ; Ouabain ; Ryanodine ; Sodium

Left ventricular hypertrophy is a compensatory response to hemodynamic overload secondary to an increased systemic resistance. This increase, however, is not the only cause of hypertrophy, and there are other factors which can have a significant effect on its incidence. To determine whether chronic antihypertensive therapy by enalapril modifies the cellular and subcellular changes of left ventricular hypertrophy observed in spontaneously hypertensive rats(SHR), 20-weeks-old SHR were treated for 22 weeks with enalapril(2mg/kg) and compared with normotensive Wister-Kyoto rats and not-treated SHR. Systolic blood pressure in enalapril-treated SHR was significantly lowered after 22 weeks compared with that of untreated control SHR group. Myocytes were reduced in size and fibrination seen in cardiac muscle fibers of control SHR was decreased in treated SHR group. Myofibrils appeared to be irregular in shape and myofilaments are decreased in control SHR but in enalapril-treated SHR the diameter and length of the myofilament became turned to regular forms. These results suggest that, enalapril, angiotensin converting enzyme inhibitor, may regress hypertrophy and some subcellular changes may be modified by enalapril.
Animals ; Blood Pressure ; Enalapril* ; Fibrin ; Hemodynamics ; Hypertrophy ; Hypertrophy, Left Ventricular* ; Incidence ; Muscle Cells ; Myocardium ; Myofibrils ; Peptidyl-Dipeptidase A ; Rats ; Rats, Inbred SHR*

This study attempted to clarify the morphological changes of the uriniferous tubules in the postobstructed kidneys of rabbits by electron microscopy. A total of l3 rabbits weighing about 2.5 kg were used. Under penthothal sodium anesthesia, complete ureteral obstruction was accomplished by ligation on the left ureter 1 cm above the ureterovesical junction. The experimental animals were sacrificed at the second and fourth week after the unilateral ureteral ligation. Tissue specimens taken from the renal cortex and medulla were fixed in a mixture of 2% paraform-aldehyde-2.5% glutaraldehyde (phosphate buffer, pH 7.2 ) prior to fixation in 1% osmium tetroxide (phosphate buffer, pH 7.2), and embedded in Epon 8l2. The sections were cut with LKB-III ultratome. Ultra thin sections were contrasted with uranyl acetate and lead citrate, and examine with a JEM-100B electron microscope. The results were as follows: 1. In the 2 weeks group of postobstruction, the abnormal morphology of the uriniferous tubules was: diminution in microvilli and basal invaginations, widening of intercellular space, focal necrosis of the epithelium, desquamation of tubular cells and splitting of the basal lamina. The degenerative changes were severe in the distal tubule, loop of Henle and collecting duct. However, the changes were mild in the proximal tubules. 2. In the 4 weeks group of postobstruction, the degenerative changes were more severe and generalized in all portions of the uriniferous tubules, and focal necrosis and desquamation of the epithelial cells were prominent in the distal tubules and collecting ducts. 3. In both groups of postobstruction, the epithelial cells with mild deformity, such as a decrease of microvilli and basal invaginations, were still preserved in all portions of the uriniferous tubules. From these findings in the obstruct nephropathy, degenerative changes are progressively expedited and partially produced in the urinary tubules.
Anesthesia ; Animals ; Basement Membrane ; Citric Acid ; Congenital Abnormalities ; Epithelial Cells ; Epithelium ; Extracellular Space ; Glutaral ; Hydrogen-Ion Concentration ; Kidney ; Ligation* ; Loop of Henle ; Microscopy, Electron ; Microvilli ; Necrosis ; Osmium Tetroxide ; Rabbits* ; Sodium ; Ureter* ; Ureteral Obstruction

Electrocardiography* ; Pain, Postoperative*