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Biomedical subjects

R Kojima

Publications and source records attributed to R Kojima.

At least 91 records · Page 5Linked to original sources
PubMed1986

[SAM sound studied by pulsed Doppler echocardiography].

The occurrence of a systolic sound in hypertrophic obstructive cardiomyopathy (HOCM) has been well known for more than 20 years. This was phonoechocardiographically regarded as the sound coincident with the abrupt halt of the systolic anterior movement (SAM) of the mitral valve echo, and it has been termed the SAM sound. A 58-year-old man with HOCM was admitted with right hemiplegia. He was found to have a SAM sound which waxed and waned in intensity, and at times moved earlier into systole. He was studied by cardiac catheterization, M-mode and two-dimensional Doppler echocardiography (pulsed, continuous wave and color flow Doppler methods). Asymmetric septal hypertrophy (interventricular septal thickness = 25 mm, left ventricular posterior wall thickness = 14 mm), as well as SAM and midsystolic aortic valve closure were demonstrated. The presence and intensity of the sound was not related to rhythm (normal sinus rhythm vs atrial flutter), heart rate, respiration, position, or inhalation of amyl nitrite. Two-dimensional Doppler echocardiography revealed the following: 1. In the left ventricular outflow tract just below the aortic valve, a systolic turbulent flow was always present. 2. In the left ventricular chamber near the apex, a systolic laminar flow was interrupted in those cycles where the SAM sound was present. Otherwise, in cycles lacking the SAM sound, laminar flow in this locality continued throughout systole (even shorter duration than normal). 3. In the left ventricular inflow tract, diastolic flow was unaffected by the presence of the sound. 4. No mitral regurgitation was observed using color flow Doppler echocardiography. In summary, a SAM sound appeared to be associated with sudden deceleration of blood flow from the apex to the mid left ventricle.

Cardiomyopathy, Hypertrophic↗
PubMed1984

[Studies on the nephrotoxicity of aminoglycoside antibiotics and protection from these effects. (1). Nephrotoxicity of gentamicin and mercuric chloride].

The present study was designed to find useful markers for detection of renal damage due to gentamicin (GM). Following the administration of 80 mg/kg GM, there were significant increases in urinary protein contents and alkaline phosphatase, N-acetyl-beta-glucosaminidase, lactate dehydrogenase, gamma-glutamyl transpeptidase and lysozyme activities. Alterations of these parameters had a peak at the 7th or 10th day and values restored to near normal levels by the 15th day. Light microscopic observations of the kidney on the 10th day showed mainly the necrosis of proximal tubular epithelial cells in the renal outer cortex, and there was regeneration of epithelial cells on the 15th day. In addition, when 1 mg/kg HgCl2 was given to rats, there were increases in urinary enzyme activities and protein contents, and BUN. The kidney of rats that received HgCl2 showed the necrosis of tubular epithelial cells in the renal inner cortex. It is considered from these results that determination of the activities of various urinary enzymes may be useful markers to detect tubular damage induced by GM.

Acute Kidney Injury↗
PubMed1984

[Studies on the nephrotoxicity of aminoglycoside antibiotics and protection from these effects. (2). Protective effect of latamoxef against gentamicin nephrotoxicity].

Effects of gentamicin (GM) alone and in combination with latamoxef (LMOX), an oxacefem antibiotic, were studied in rat kidney in order to determine the effect of combinations of nephrotoxic drugs. Groups of 7 male Sprague-Dawley rats, weighing approx. 230 g, were given daily s.c. doses of GM (80 mg/kg) or 80 mg/kg GM plus LMOX (500, 1000 or 2000 mg/kg) for 15 days. Treatment with GM alone resulted in marked increases in urinary lactate dehydrogenase, N-acetyl-beta-glucosaminidase and lysozyme activities, urinary protein contents and blood urea nitrogen contents, which peaked on the 10th day. The combination of GM plus LMOX significantly suppressed the increases in these biochemical parameters with GM alone. In this case, the suppressions were roughly dependent on the dose of LMOX. Although GM alone caused pronounced histological changes in proximal tubules between the 7th and 15th days, the combination with LMOX apparently protected against these changes. These results indicate that the combination with LMOX obviously protects the kidney from the nephrotoxicity of GM.

Acetylglucosaminidase↗