Retrograde infusion studies on urea accumulation in renal medulla of rabbits.
Explore the source record for details and available documents.
Animals↗
Biomedical subjects
Y Orita
Publications and source records attributed to Y Orita.
Echocardiographic features of persistent right sinus venosus valve in adult.
Explore the source record for details and available documents.
Cardiac Catheterization↗
Serum and urinary boron levels in rats after single administration of sodium tetraborate.
The pharmacokinetics of boron was studied in rats by administering a 1 ml oral dose of sodium tetraborate solution to several groups of rats (n=20) at eleven different dose levels ranging from 0 to 0.4 mg/100 g body weight as boron. Twenty-four-hour urine samples were collected after boron administration. After 24 h the average urinary recovery rate for this element was 99.6+/-7.9. The relationship between boron dose and excretion was linear (r=0.999) with a regression coefficient of 0.954. This result suggests that the oral bioavailability (F) of boron was complete. Another group of rats (n=10) was given a single oral injection of 2 ml of sodium tetraborate solution containing 0.4 mg of boron/100 g body wt. The serum decay of boron was followed and found to be monophasic. The data were interpreted according to a one-compartment open model. The appropriate pharmacokinetic parameters were estimated as follows: absorption half-life, t1/2a=0.608+/-0.432 h; elimination half-life, t1/2=4.64+/-1.19 h; volume of distribution, Vd = 142.0+/-30.2 ml/100 g body wt.; total clearance, Ctot=0.359+/-0.0285 ml/min per 100 g body wt. The maximum boron concentration in serum after administration (Cmax) was 2.13+/-0.270 mg/l, and the time needed to reach this maximum concentration (Tmax) was 1.76+/-0.887 h. Our results suggest that orally administered boric acid is rapidly and completely absorbed from the gastrointestinal tract into the blood stream. Boric acid in the intravascular space does not have a strong affinity to serum proteins, and rapidly diffuses to the extravascular space in proportion to blood flow without massive accumulation or binding in tissues. The main route of boron excretion from the body is via glomerular filtration. It may be inferred that there is partial tubular resorption at low plasma levels. The animal model is proposed as a useful tool to approach the problem of environmental or industrial exposure to boron or in cases of accidental acute boron intoxication.
Animals↗
An inner ear anomaly in golden hamsters.
A new mutation of the inner ear was discovered in golden hamsters raised in our laboratories. Although scanning electron microscopy showed a normal arrangement of individual stereocilia on the first row of outer hair cells, the entire bundle of stereocilia were irregular in orientation and scattered in several directions. Seventy per cent to 85% of the stereociliary bundles were found to be abnormal throughout the cochlea, with no apparent difference between the right and left sides. Transmission electron microscopy showed that the cuticles of the first row of the outer hair cells were dislocated, but no dislocation due to this mutation was apparent in the lower portions. This mutation of the inner ear was already present in the basal turn four days after birth. The kinocilium was located outside of the stereocilia in the first row of outer hair cells, but sensory hairs were scattered in every direction, as in the adult animals. A comparison of auditory brainstem response tests revealed no difference between the abnormal and normal hamsters.
Animals↗
Programmed cell death in the mouse cochleovestibular ganglion during development.
Programmed cell death (PCD) is as essential to development as is cell proliferation. Our objective was to elucidate the spatiotemporal occurrence of PCD during the development of the cochleovestibular ganglion. We performed a time-sequence study on the distribution of in situ PCD, apoptosis, during the development of the mouse cochleovestibular ganglion by using the TUNEL method to detect apoptosis histochemically. Apoptosis in the cochleovestibular ganglion was observed from the 11.5th gestational day (GD) to the 18. 5th GD. Apoptosis was seen most extensively in the vestibular ganglion cells at the 13.5th GD, while in the spiral ganglion cells apoptosis was maximal between the 15.5th and 16.5th GD. Because these times of peak apoptotic activity almost exactly corresponded to the events of innervation and terminal mitosis of the cochleovestibular ganglion cells, we infer that PCD is involved in the innervation and modulates the number of cochleovestibular ganglion cells overproduced by terminal mitosis.
Animals↗
Quantitation of myocardial dyssynergy in closed-chest dogs by two-dimensional echocardiography.
Myocardial infarction was produced in 29 anaesthetized mongrel dogs by a closed-chest coronary occlusion technique. A two-dimensional echocardiographic examination (2-D echo) was carried out just before occlusion and again 48 h after occlusion. Many cross-sectional images were recorded by a video-tape recorder. The applied site of the probe was fixed in an intercostal space and the direction of the ultrasonic beam was tilted stepwise from the basis to the apex. The animals were sacrificed at 49 hours after occlusion. The hearts were removed, quick frozen, sliced into radiating sections and stained with nitroblue tetrazolium (NBT). The outline of dyssynergy, including dyskinesis, akinesis or extreme hypokinesis, was traced with a tablet digitizer by two specialists. The three-dimensional image of dyssynergy in the left ventricular wall was reconstructed by a computer in spherical co-ordinates and assumed to be made of numerous triangular pyramids. The volume of dyssynergy was calculated quantitatively as the sum of volumes of these numerous triangular pyramids. The volume of dyssynergy seen in 2-D echo correlated well over a wide range with the volume of infarction determined by NBT staining.
Animals↗
Effect of hypertonic stress on amino acid levels and system A activity in rat peritoneal mesothelial cells.
OBJECTIVE: Peritoneal mesothelial cells (PMC) are exposed to a hypertonic environment during peritoneal dialysis. When exposed to a hypertonic medium, many types of cells accumulate small osmotically active organic solutes, which are called osmolytes, to match the higher external osmolality. However, no information has been available concerning the osmolytes in PMC. To investigate osmoregulation in rat PMC, the levels of amino acids in the cells and the activity of system A, a major neutral amino acid transport, were measured after switching to a medium made hypertonic by the addition of NaCl. System A was measured by Na+-dependent [14C]-2-methylamino-isobutyric acid (MeAIB) uptake. RESULTS: Total amount of 20 amino acids increased from 306 to 757 nmol/mg protein after 12 hours of hypertonicity. The amount of neutral amino acids accounted for 81% of the increase in total amino acids. Glutamine, alanine, glycine, threonine, and serine were the major neutral amino acids that accumulated in the hypertonic mesothelial cells. The amount of neutral amino acids increased 2.9-fold after 12 hr of hypertonicity, and decreased thereafter. MeAIB uptake increased 36-fold relative to the uptake in isotonic cells after 4-8 hr of hypertonicity. When the culture medium was made hypertonic by adding raffinose or glucose, the activity of system A was also stimulated (raffinose > glucose > NaCl). System A was located on both the apical and basal sides of isotonic PMC, and extracellular hypertonicity stimulated the MeAIB uptake on both sides. CONCLUSIONS: These data indicate that neutral amino acids and system A transport play an important role in early-phase osmoregulation in rat peritoneal mesothelial cells.
Amino Acids↗
Mechanism of induction of prostaglandin E2 production by endothelin 1 in cultured rat mesangial cells.
The phospholipase A2 inhibitors mepacrine, ONO-RS-082, and AACOCF3 completely inhibited prostaglandin E2 production induced by endothelin 1 in cultured rat mesangial cells, suggesting that phospholipase A2 is a critical enzyme in this process. TMB-8, an inhibitor of calcium mobilization from intracellular stores, abolished its production, while neither nicardipine nor chelation of extracellular calcium by EGTA did. The protein kinase C inhibitors, H-7 and staurosporine, and downregulation of protein kinase C could not inhibit prostaglandin E2 production, while W-7, a calmodulin inhibitor, abolished it. Pertussis toxin never influenced its production. Thus, endothelin 1 evokes prostaglandin E2 production in mesangial cells mainly through the activation of phospholipase A2, dependent on intracellular calcium and calmodulin and independent of extracellular calcium, protein kinase C, and pertussis toxin sensitive guanosine 5'-triphosphate binding proteins.
1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗