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Biomedical subjects

A Shino

Publications and source records attributed to A Shino.

At least 37 records · Page 2Linked to original sources
PubMed1991

Effect of thyrotropin-releasing hormone (TRH) in experimental spinal cord injury: a quantitative histopathologic study.

Spinal cord injuries in rats were experimentally produced by compressing the cord (T11 vertebra level) for 60 min with stainless steel screws. Morphometric analysis of the injured cord revealed that at 14 days post-injury, there were significant correlations between the neurologic score (NS) and all morphometric parameters, including total cross-sectional area (rs = 0.438), lesioned area (rs = -0.421) and area of the gray (rs = 0.377) and white matter (rs = 0.704). Although rats treated with thyrotropin-releasing hormone (TRH; 22.5 mg/kg, s.c., twice daily for 7 days starting 24 hr post-injury) showed significant improvement in NS 14 days post-injury, there were no significant differences in morphometric parameters between saline- and TRH-treated rats. In addition, no significant correlation was observed between NS and any of the morphometric parameters in TRH-treated rats, even though there was a significant correlation between the area of white matter and NS in saline-treated rats. These results suggest that neurologic recovery closely reflects the histopathological changes evident at the injury site in the present model, and that the improvement of neurologic status seen in rats with cord injury given TRH starting 24 hr post-injury is not due to protection against progression of neural damage at the injury site.

Animals↗
PubMed1990

Pathophysiological role of endothelin in acute renal failure.

In conscious rats, the i.v. injection of endothelin (ET) caused an increase in blood urea nitrogen (BUN), an index of renal dysfunction. In the model of acute renal failure which was induced by occlusion of the bilateral renal arteries of rats followed by reperfusion, ET-monoclonal antibody improved the renal function. In this model, ET-antibody also protected the kidneys from renal proximal tubular necrosis and suppressed Ca++-accumulation in necrotic tissues. Plasma ET level increased 5 min and 5 hr and renal ET content did 5 and 20 hr after reperfusion. BUN level increased 5 and 20 hr after reperfusion. These results strongly suggest that the endogenously increased ET may be one of the important deleterious mediators in the pathogenesis of ischemic acute renal failure.

Acute Kidney Injury↗
PubMed1990

Histological studies on the therapeutic effect of sustained-release microspheres of a potent LHRH agonist (leuprorelin acetate) in an experimental endometriosis model in rats.

The therapeutic effect of sustained-release microspheres of a potent LHRH agonist (leuprorelin acetate) on experimental endometriosis in female rats was examined histologically. Endometriosis was produced in rats by autotransplantation of endometrial tissue obtained from the left uterine horn into the renal subcapsular space. In the nontreated rats, the transplants were well established and had formed large cysts containing fluid. The walls of the cysts were composed of epithelium and stroma resembling that of normal endometrium. In the rats which received the microspheres of leuprorelin acetate, growth of the transplant was markedly suppressed as evidenced by the reduced size of the cystic cavity and the flattened and pyknotic epithelium. Also, the uterine and ovarian weight decreased significantly. In the ovariectomized rats, growth of the transplant was also markedly suppressed, and the uterine weight decreased. The present results clearly indicate that a single injection of the sustained-release microspheres of leuprorelin acetate markedly suppresses growth of the transplant and produces uterine and ovarian atrophy in the rats.

Animals↗
PubMed1989

Combination therapy of colon carcinoma 26 in mice with recombinant human interleukin-2 and interferon-alpha A/D: occurrence of large granular cells in the tumor.

The antitumor effects of recombinant human interleukin-2 (rIL-2), in combination with recombinant human interferon-alpha A/D hybrid (rIFN-alpha A/D) on colon carcinoma 26 (colon 26) in mice were examined histologically. Colon 26 was transplanted subcutaneously into female BALB/c mice on day 0. The mice bearing the tumor received intramuscular injections of rIL-2, rIFN-alpha A/D or the combination of rIL-2 and rIFN-alpha A/D for 2-10 consecutive days starting on day 7. Mice were killed on days 9, 13, 17 and 21. After day 13, growth of the tumor was significantly suppressed in the mice treated with rIL-2 or rIFN-alpha A/D alone and was stopped in the mice treated with rIL-2 in combination with rIFN-alpha A/D. Histologically, tumor necrosis developed in all treated groups, though the degree was the most severe in the group receiving combination treatment. Many large cells (about 15-30 microns in diameter) infiltrated into the tumor, and they had Thy-1 surface antigen and many periodic acid-Schiff-positive round granules in the cytoplasm. The incidence of these large granular cells was correlated well with the reduction in tumor weight. The ultrastructural features of the large granular cells were very similar to those of murine large granular lymphocyte-like cells maintained in vitro in an IL-2-containing medium. The present large granular cells appear to be a kind of activated lymphoid cells.

Animals↗
PubMed1989

Histomorphometric study of the parathyroid glands of the spontaneously hypercholesterolemic (SHC) rats with chronic renal failure.

Light and electron microscopic morphometry was performed on the parathyroid (PT) glands of the SHC rats with naturally occurring chronic renal failure. Macroscopically, the PT glands were distinctively hypertrophied in 24-week-old male SHC rats when compared with the corresponding controls, Sprague Dawley (SD) rats. Light microscopic morphometry on consecutive sections of the PT glands showed that the volume was about 3 times greater in the SHC rats, whereas there was no difference in the size of the chief cells. Mitoses were often found in the PT glands of the SHC rats. The total number of mitoses was about 8.5 times greater in the SHC rats, and was closely related to the volume of the PT glands. Ultrastructural morphometry of the chief cells revealed an increase in the cell surface area by the interdigitation of the plasma membrane and increases in the volume of mitochondria and Golgi complex. Secretory granules sometimes existed close to the cell surface in the SHC rats, but not in the SD rats. These results suggest that the PT glands of the SHC rats are hyperplastic mainly because of the proliferation of the chief cells. Concurrently, an increase in volume of the cell organelles suggests enhanced secretion activity in the chief cells.

Animals↗
PubMed1988

Suppressive effect of ipriflavone on bone depletion in the experimental diabetic rat: dose response of ipriflavone.

The dose dependent effect of ipriflavone (7-isopropoxy-isoflavone) on the femoral bone in streptozotocin-induced diabetic rats was studied by microdensitometric analysis. Diabetic rats showed severe hyperglycemia, glucosuria, hypoinsulinemia, associated with increased urinary calcium and hydroxyproline. Microdensitometric analysis revealed decreases in femoral length, bone width, and bone density. The dietary administration of ipriflavone (about 270 mg/kg/day) to the diabetic rats for 6 weeks prevented reduction of the cortical thickness index in the diaphysis and depletion of bone density in the distal metaphysis, and also reduced the inner diameter of the diaphysis; diabetic state was not improved. A simple correlation and linear regression analysis revealed that ipriflavone also significantly reduced the inner diameter in the diaphysis at a dose of 90 mg/kg/day, but not at one of 25 mg/kg/day. These results suggest that ipriflavone suppresses the depletion of the femoral bone through inhibition of bone resorption in a dose dependent fashion; its minimum effective dose is 90 mg/kg/day in experimental diabetes.

Animals↗
PubMed1987

Histopathologic observations on the senescence-accelerated mice (SAM) reared under specific pathogen free conditions.

Five to 12 months old senescence-accelerated mice reared under specific pathogen free conditions (SPF SAM) were subjected to histopathologic examination. Senescence-prone SAM-P/1/Ta, P/3/Ta, and P/8/Ta exhibited marked depletion in thymic cortical lymphocytes which were associated with lymph follicle formation in the medulla, and marked infiltration of lymphocytes in the submaxillary gland, kidney, and other peripheral tissues. Morphometrical analysis of the adrenal gland revealed cortical atrophy and medullary hyperplasia in male SAM-P/8/Ta at 5 months of age. Other characteristic changes were marked vacuolation of the renal proximal tubules in male P/3/Ta and P/8/Ta mice, and degeneration of vascular wall in the testis of P/3/Ta mice. The pathogenesis of these changes appeared to be related to the adrenal lesions. Systemic amyloid deposition, one of the characteristic features of SAM housed in conventional facilities was not observed under the SPF condition. Acceleration of senescence in SPF SAM may arise from disorders of the thymus and adrenal.

Adrenal Glands↗
PubMed1987

A lethal role of platelet activating factor in anaphylactic shock in mice.

The lethal role of platelet activating factor (PAF) in anaphylactic shock was examined in mice, using the specific PAF antagonist, CV-3988. CV-3988 (0.3-3 mg/kg i.v.), given 5 min before PAF, protected mice from death (ED50, 0.9 mg/kg). CV-3988 (3 mg/kg i.v.), given 1 min after PAF was injected, was also effective, but no so effective when given 5 min later. Dexamethasone (2 mg/kg i.v. 3 hr before the PAF-injection), naloxone (1 and 10 mg/kg i.v. 5 min before), FPL-55712 (10 mg/kg i.v. 5 min before) and BW-755c (300 mg/kg p.o. 1 hr before) also improved the survival rate, but aspirin (100 mg/kg p.o. 1 hr before) did not. In anaphylactic shock, CV-3988 (0.3-3 mg/kg i.v.), given 5 min before and 5 min after rechallenge with antigen protected the sensitized mice from death (ED50, 1.2 and 0.48 mg/kg, respectively). Dexamethasone and naloxone protected mice from anaphylactic shock, but BW-755c and FPL-55712 had no protective effects. In contrast to CV-3988, dexamethasone and naloxone were ineffective when given 5 min after the rechallenge. Congestion of the lung, kidney and heart and infiltration of neutrophils in the lung were marked in mice with PAF-induced and anaphylactic shock. The related histology showed an improvement with CV-3988. These results strongly suggest that PAF may play a lethal role in anaphylactic shock and that CV-3988 may be an effective preventing agent.

4,5-Dihydro-1-(3-(trifluoromethyl)phenyl)-1H-pyraz↗
PubMed1986

Effect of ipriflavone on glucocorticoid-induced osteoporosis in rats.

Ipriflavone, 7-isopropoxy-3-phenyl-4H-1-benzopyran-4-one, was administered orally for 12 weeks to male rats with prednisolone-induced osteoporosis. Microdensitometric analysis of a roentgenograph of the femurs revealed that ipriflavone increased the density of the distal metaphysis dose-dependently and tended to increase the density of the diaphysis. It also inhibited dose-dependently the decrease in the mechanical strength of the tibia, breaking strain and breaking energy, and the fractional content of ash in femurs. These results indicate that ipriflavone markedly suppresses bone resorption at the metaphysis where the content of trabecular bone with a rapid turnover rate is high, and possibly inhibits bone reduction at the diaphysis.

Animals↗
PubMed1986

[Effects of ipriflavone (TC-80, an anti-osteoporotic drug) on acute and chronic pain].

The effects of TC-80 on acute and chronic pain in rats and mice were examined. Single oral administration of TC-80 at 50-300 mg/kg was not analgesic in the phenylquinone writhing, acetic acid writhing, and hot plate tests in mice or the tail flick test in rats. Three-weeks administration of TC-80 in a dose of 100 mg/kg/day, p.o., to rats had no analgesic action in the acetic acid writhing and tail flick tests. When TC-80 was given orally in a dose of 100 mg/kg/day for 3 weeks to rats with adjuvant arthritic chronic pain, analgesic effects were observed 2 weeks after the start of administration in males and in ovariectomized estrone-supplemented females; the effect seen in the females was statistically significant. Changes in the bones of the hind paws were examined radiologically, and synovitis, periosteal new bone formation and bone destruction were examined histopathologically in the females. These variables were improved by treatment with TC-80 for 3 weeks. It is concluded that TC-80 has no analgesic effect, but may inhibit chronic pain by anti-osteoporotic action on bone disease.

Administration, Oral↗
PubMed1984

Inhibitory effect of idebenone (CV-2619), a novel compound, on vascular lesions in hypertensive rats.

The effects of a novel compound, 6-(10-hydroxydecyl)-2,3-dimethoxy-5-methyl-1,4-benzoquinone (idebenone, CV-2619), on cerebral and renal vascular changes were examined in stroke-prone spontaneously hypertensive rats (SHRSP) and in rats with experimentally induced hypertension. CV-2619 (35 mg/kg/day, p.o.) significantly inhibited the onset of cerebrovascular lesions (stroke) and the elevation of blood pressure in SHRSP with mild hypertension. A higher dose (2 X 50 mg/kg/day, p.o.) clearly delayed the onset of both stroke and proteinuria without any effect on the blood pressure in SHRSP with severe hypertension. In DOCA-salt hypertensive rats, CV-2619 (2 X 5 or 2 X 25 mg/kg/day, p.o.) dose-dependently inhibited decreases in body weight and water balance and the development of cerebral and renal vascular changes. These results suggest that CV-2619 inhibits the development of stroke and renal vascular lesions in hypertensive rats.

Animals↗
PubMed1983

Preventive effect of a quinonyl derivative of N-acetylmuramyl dipeptide, QMDP-66, against adriamycin-induced ECG abnormalities in rats.

The effects on adriamycin cardiotoxicity of an immunoadjuvant, 2-[2-acetamido-2-deoxy-6-0-[10-(2,3-dimethoxy-5-methyl-1, 4-benzo-quinon-6-yl) decanoyl]-D-glucopyranos-3-0-yl]-D-propionyl-L-valyl D-isoglutamine methyl ester (QMDP-66), and a reference compound, ubiquinone-10, were studied in Wistar Kyoto (WKY) rats. Adriamycin, 1 mg/kg/day intra-peritoneally (i.p.) for 23 days, elicited cardiotoxicity, as judged by widening of the QRS complexes in ECGs. Electron microscopic examination of myocytes from the treated rats revealed many cytoplasmic vacuoles possibly originating from deranged endoplasmic reticula or mitochondria. In addition, the treatment significantly inhibited body weight gain, and decreased ventricular weight. QMDP-66 alone, 1 mg/kg/day i.p. for 23 days, had no effect on the parameters described above. When QMDP-66 (1 mg/kg/day, i.p.) or ubiquinone-10 (3 mg/kg/day, i.p.) was administered together with adriamycin, the widening of the QRS complexes was significantly depressed, and cytoplasmic vacuoles in myocytes were rarely observed. The QMDP-66 or ubiquinone-10 treatment, however, did not alleviate the decrease in body weight gain or ventricular weight due to adriamycin. Heart rate was not significantly changed by any of the treatments. These findings suggest that QMDP-66 is an effective antidote against adriamycin cardiotoxicity.

Acetylmuramyl-Alanyl-Isoglutamine↗
PubMed1983

Cardiovascular responses to cerebral ischemia following bilateral carotid artery occlusion in SHRSP, SHRSR and WKY rats.

Systemic arterial pressure was markedly increased in the early phase of cerebral ischemia induced by bilateral carotid artery occlusion (BCAO) in stroke-prone spontaneously hypertensive rats (SHRSP). The elevated level of arterial pressure was gradually returned to the initial level, and hypotension followed in the late phase. Severe neurological symptoms such as "ischemic seizure", dyspnea and coma were developed in the late phase. All SHRSP died within 6 hr after BCAO. The heart rate continued to increase during the brain ischemia. Cardiac arrhythmias, significant increases in plasma levels of creatine phosphokinase (CPK) and CPK-MB isozyme and disruption of myofibrils were observed after BCAO, particularly after the development of ischemic seizure. In contrast, in stroke-resistant SHR (SHRSR) and Wistar-Kyoto rats (WKY), ischemic seizure did not develop, yet all died within 8 hr after BCAO. Arterial pressures were moderately increased and never decreased to below the initial levels during the observation periods. Increases in CPK-MB isozyme activities in plasma from SHRSR and WKY were not detected. Pretreatments with propranolol and reserpine inhibited the increases in heart rate, reduced the frequency of arrhythmias and prolonged the survival time following BCAO in SHRSP. Our results indicate that cardiac dysfunction, which is a consequence of the cerebral ischemia, may be one of the causes of death following BCAO in SHRSP.

Animals↗
PubMed1981

A new genetically obese-hyperglycemic rat (Wistar fatty).

The fa-gene was transferred from the Zucker rat (13 M strain) to the Wistar Kyoto (WKY) rat. The survey, performed at the 10th generation of backcrossing, showed that Wistar fatty rats (fa/fa), a congenic strain of WKY, developed obesity and obesity-related features, such as hyperinsulinemia and hyperlipemia, in the same manner as Zucker fatty rats. Males, but not females, showed hyperglycemia, glucosuria, and polyuria as early as 8 wk of age. Tolerance and insulin response to oral glucose were decreased with advancing age in males. The diabetic changes appeared to be caused by an interaction between predisposition to develop diabetes in the WKY rat and fa-induced obesity. This is because WKY rats were found to be less sensitive to insulin than Zucker rats by both the glucose tolerance test and the steady-state blood glucose method which estimates overall insulin sensitivity.

Animals↗
PubMed1980

Implication of renal perfusion pressure in stroke of spontaneously hypertensive rats.

To elucidate the significance of hypertension associated with cerebrovascular lesions (CVL), renal perfusion pressure (RPP) was controlled by aortic clips of two different sizes in stroke-prone spontaneously hypertensive rats kept under normal or salt-loaded conditions. Tail and femoral arterial pressures (RPPs) in the mildly and severely clamped animals were reduced in proportion to the severity of the clamping. In contrast, carotid pressures in both clamped groups were significantly higher than that in the controls. Proteinuria and hyperreninemia accompanied by arteriolar changes in the renal cortex were observed in the controls prior to the onset of CVL. The renal changes were inhibited by both types of clamping. The onset of CVL was delayed by the mild clamping in salt-loaded animals, but accelerated by the severe clamping in both the normal and salt-loaded animals. Renal cortical blood flow was decreased only by the severe clamping. The results suggest that reduction in RPP and/or renal ischemia, which seems to be due to the hypertensive arteriolar changes in the renal cortex, may be related to the pathogenesis of CVL in the stroke-prone rats with or without hyperreninemia.

Animals↗