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Biomedical subjects

N Sakamoto

Publications and source records attributed to N Sakamoto.

At least 343 records · Page 19Linked to original sources
PubMed1988

Stimulatory action of ascorbic acid on methyl mercury-induced lipid peroxidation in rabbit kidney cortex slices.

Effects of ascorbic acid on the methylmercuric chloride (MMC)-induced lipid peroxidation and the accumulation of MMC in rabbit kidney cortical slices were studied. Ascorbic acid had a powerful stimulatory effect on the MMC-induced lipid peroxidation, while it produced only a small increase in the MMC accumulation. This results suggests that ascorbic acid increases slightly the accumulation of MMC, but that the stimulatory action of ascorbic acid on the MMC-induced lipid peroxidation cannot be explained simply by the increase in the MMC accumulation.

Animals↗
PubMed1987

Neurotensin immunoreactive neurons in the human infant diencephalon.

Neurotensin-like immunoreactive (NT-IR) neurons are present in discrete subregions of the anterior, medial and lateral thalamic nuclear groups of the human infant brain. The pulvinar is notably rich in such cells. Smaller numbers of cells are present in the ventral group, centromedian nucleus, reticular nuclei and intralaminar nuclei. Neurotensin immunoreactive axons accumulate dorsally in the thalamus and cross the deep white matter. The cerebral cortex contains a rich network of NT-IR axons. The subthalamic nucleus is rich in NT-IR neurons. Within the hypothalamus NT-IR perikarya are present in parts of the lateral and tuberal regions and in the lateral mammillary area. NT-IR axons are widespread being particularly prominent in parts of the tuberal region and the mammillary body.

Diencephalon↗
PubMed1987

Analyses on lipid-rich organelles of the rat liver after bile duct ligation.

A fraction of lipid-rich organelles of rat livers was analyzed to study the effect of bile duct ligation on lipid metabolism. The lipid fraction of the control rats consisted mainly of Golgi-derived dense bodies. Three days after the ligation, myelin-like figures and increased phospholipids and cholesterol were characteristic of the fraction. Two weeks ligation resulted in proliferation of lysosomal electron dense bodies. As their volume density expanded, phospholipids and cholesterol increased. Electrophoresis indicated a reduced rate of VLDL assembly after ligation. The Golgi-dominant phase is converted to the lysosomal phase in the heavy subfraction after the bile duct ligation. This subcellular change could be a consequence of secondary lipidosis: hepatocyte lysosomes have been exhausted in sorting accumulated lipids into secretory lipoproteins.

Animals↗
PubMed1987

Greater disturbance of water and ion homeostasis in the periphery of experimental focal cerebral ischemia.

Differences in disturbed water and ion homeostasis in the periphery and the center of focal cerebral ischemia were investigated. Focal cerebral ischemia was induced by occlusion of the right common carotid artery in gerbils. Water and electrolyte content were determined using punched-out samples. In 2 h of ischemia, water content of the cerebral cortex was 79.0 +/- 0.3, 82.0 +/- 0.4, and 80.7 +/- 0.4% (means +/- SE) for the nonischemic region, the periphery, and the center of the ischemic region, respectively (significantly different). Na+ content was increased and K+ content was decreased most prominently in the periphery of the ischemic region. K+ depletion and exogenous Ca2+ accumulation in the peripheral region were visualized by K+ staining and 45Ca autoradiography, respectively. Thus, water and electrolyte changes in the periphery of ischemia were different from those in the center. Brain edema was developed initially in the marginal region of the focal cerebral ischemia.

Adenosine Triphosphate↗
PubMed1987

A transfer-function representation for regulatory responses of a controlled metabolic pathway.

A transfer-function representation for the response of a controlled metabolic pathway to the changes in influx and efflux rates of metabolites is formulated to describe analytically and approximately the regulatory behavior of the pathway around a steady state. The pathway model analyzed is an open and homogeneous system which consists of two consecutive enzymatic reactions catalyzed by an allosteric enzyme of Monod-Wyman-Changeux (MWC) dimeric model and a Michaelis-Menten-type enzyme, respectively, and undergoes the feedback inhibition by the end product. The rate equation for the system (a system of ordinary differential equations) is linearized about a steady state, so that the responses of the reaction rates to the changes in influx rate of the substrate and efflux rate of the end product are expressed in a form of transfer function. The formulation leads to the transfer function for the response of production rate of the end product to the change in its efflux rate to clarify the regulatory response of feedback mechanism in controlled metabolic pathways. The relationship among the chemical species in the system at steady states also supports a reasonable assumption that the regulatory mechanisms in metabolic pathways are to control the production of end product against the change in its demand from the cellular environments.

Allosteric Regulation↗
PubMed1987

Substance P- and enkephalin-immunoreactive neurons in the hippocampus and related areas of the human infant brain.

Neurons strongly immunoreactive for substance P are present as subpopulations in the stratum oriens, pyramidal layer and polymorphic layer of the hippocampus of the human infant. Substance P immunoreactive terminals are numerous on other neuronal cell bodies in the polymorphic layer and over pyramidal cells of the subiculum and the CA1, 2 and 3 regions. There is a high density of substance P-immunoreactive axons in the granular layer. Enkephalin immunoreactive neurons are relatively few in number and are present in the polymorphic and pyramidal layers. The results indicate that substance P probably plays a major role in short range circuits in the human hippocampus and that intrinsic enkephalin neurons probably play a relatively minor role.

Brain Mapping↗
PubMed1987

Evaluation of the effect of metoprolol on energy metabolism in the ischaemic myocardium in relation to regional myocardial blood flow.

To evaluate the effect of beta blockade on energy metabolism in ischaemic myocardium metoprolol tartrate in doses of 0.2 or 0.5 mg.kg-1 or saline was injected into 24 anaesthetised dogs 20 min after coronary ligation. Regional myocardial blood flow was measured by the hydrogen gas clearance method, and the heart rate and aortic pressure were recorded. After 60 min coronary occlusion myocardial biopsy specimens were removed from five areas where myocardial blood flow had been recorded to determine their content of adenosine-5'-triphosphate (ATP). Respiratory function and acyl-coenzyme A contents of mitochondria isolated from ischaemic and non-ischaemic myocardium were also measured. In the control group the ATP content in severely ischaemic myocardium where myocardial blood flow was less than 20 ml.min-1.100 g-1 was decreased to 27.5% of that in the non-ischaemic area, whereas the administration of metoprolol 0.5 mg.kg-1 maintained ATP content at 46.3%. In ischaemic myocardium metoprolol inhibited the accumulation of long chain acyl-coenzyme A in mitochondria and significantly preserved their respiratory function. In contrast, metoprolol did not affect myocardial blood flow in myocardium where flow was less than 60 ml.min-1.100 g-1. Heart rate was decreased by metoprolol in proportion to the dose, whereas mean aortic pressure was not changed. These results suggest that beta blockade had beneficial effects on the energy metabolism of ischaemic myocardium and that such effects might be due not only to a reduction in cardiac work but also to a reduction in the vicious circle of fatty acid metabolism in ischaemic myocardium.

Acyl Coenzyme A↗
PubMed1987

Prostaglandins affect the central nervous system to produce hyperglycemia in rats.

The influence of prostaglandins (PG) on central nervous system regulation of blood sugar homeostasis was studied in rats. Substances were injected into the third cerebral ventricle of anesthetized rats while rectal temperature and hepatic venous plasma glucose concentration were recorded. Stereotaxic microinjection of PGD2, E1, E2, and F2 alpha produced hyperglycemia and hyperthermia. The relative order of potency in hyperglycemia, PGF2 alpha greater than D2 greater than E1 greater than E2, was not consistent with that of hyperthermia, PGE2 greater than F2 alpha greater than E1 greater than D2, which suggests that hyperglycemia was a primary, not secondary, response to hyperthermia. Injection of PGF2 alpha caused a dose dependent (5-200 micrograms) increase in the hepatic venous plasma glucose level. Neither the injection of PGF2 alpha (50 micrograms) into the cortex nor into the systemic vein caused hyperglycemia. The injection of PGF2 alpha into the ventricle resulted in the increase of not only glucose, but also glucagon, epinephrine, and norephinephrine in the hepatic venous plasma. However, constant infusion of somatostatin through the femoral vein completely prevented the increase of glucagon after administration of PGF2 alpha, although the increase of plasma glucose level was still observed. PGF2 alpha-induced hyperglycemia did not occur in adrenodemedullated rats. Intravenous injection of naloxone or propranolol did not affect the hyperglycemia, but phentolamine significantly prevented the hyperglycemic effect of PGF2 alpha. These results suggest that intraventricular PGF2 alpha affects the central nervous system to produce hyperglycemia by increasing epinephrine secretion from the adrenal medulla.

Alprostadil↗
PubMed1987

Effect of diltiazem on acute myocardial ischemia. Study of the relationship between regional myocardial blood flow and myocardial energy metabolism.

To examine the effects of diltiazem on myocardial ischemia, 200 micrograms/kg of diltiazem were injected intravenously into anesthetized open-chest mongrel dogs 10 min after coronary ligation. This was followed by a continuous infusion of diltiazem at 10 micrograms/kg/min for 50 min. Regional myocardial blood flow (MBF) was measured by the hydrogen gas clearance method. Sixty minutes after ligation, myocardial specimens were taken from the areas where MBF was measured, and the ATP and CP contents were determined by the bioluminescence method. Simultaneously, mitochondria were isolated from the ischemic and nonischemic areas, and both the respiratory control index (RCI) and the rate of oxygen consumption in state III (QO2 III) were calculated. The aortic systolic pressure and heart rate of diltiazem treated and untreated dogs were not significantly different, and diltiazem did not increase the MBF in the area with a MBF below 40 ml/min/100 g. When MBF was 10 to 30 ml/min/100 g, the ATP content in the diltiazem treated hearts was significantly higher than that in the untreated dogs, whereas the CP content was not significantly changed. Thus, diltiazem administered after ischemia preserved ATP content in the ischemic myocardium with a MBF of 10 to 30 ml/min/100 g without significantly affecting the hemodynamics or MBF. This suggests that diltiazem exerts a cardioprotective effect by acting directly on the ischemic myocardium if it has an MBF above a certain level, even when the drug is administered after the onset of ischemia.

Adenosine Triphosphate↗
PubMed1987

Inhibitory effects of heparin plus cortisone acetate on endothelial cell growth both in cultures and in tumor masses.

A combination of heparin and cortisone acetate significantly inhibited both embryonic angiogenesis and the tumor growth of Lewis lung carcinoma (3LL) transplanted into C57BL/6 mice, although each of these agents used alone affected neither angiogenesis nor tumor growth. On the other hand, this combination neither decreased the number of metastatic foci in the lung nor prolonged the survival time of mice with 3LL. All tumor-bearing mice died of hemothorax due to pulmonary metastases. Cortisone acetate by itself increased metastasis, and addition of heparin did not affect accelerated metastasis. Because an antiangiogenic activity appears independent of metastasis acceleration by cortisone acetate, the use of steroids other than cortisone acetate having no metastasis-promotion effect should be required for an antiangiogenic tumor therapy in the presence of heparin. Heparin plus cortisone acetate prevented the DNA synthesis of cultured vascular endothelial cells but not that of cultured 3LL cells. Additionally, oral administration of this combination decreased the [3H]thymidine labeling of endothelial cells of tumor blood vessels prior to the suppression of tumor growth. The specific inhibition of the growth of endothelial cells by heparin plus cortisone acetate was revealed in both the in vitro and the in vivo tests.

Animals↗
PubMed1987

Effect of angiostatic steroid with or without glucocorticoid activity on metastasis.

The effect of angiostatic steroids on pulmonary metastasis was investigated using mice treated with such a steroid before or after intravenous inoculation with Lewis lung carcinoma; cortisone acetate and tetrahydro S, of which the former possesses glucocorticoid activity, and the latter lacks it, were used as the angiostatic steroids. In the presence of heparin, both types of steroids prevented angiogenesis in chick embryo and also pulmonary metastasis in mice when the administration started after cell lodgement. On the other hand, one-shot cortisone treatment before cell inoculation increased the weight of lung colonies to twice that seen in the controls, while tetrahydro S pretreatment did not enhance metastasis. These results revealed that both angiostatic steroids with and without glucocorticoid activity in the presence of heparin inhibited tumor growth in the lungs, and further indicated that cortisone acetate affected the steps of metastasis after the invasion of tumor cells into the blood stream until angiogenesis in the secondary foci, and consequently promoted metastasis, whereas tetrahydro S (which has no glucocorticoid activity) did not affect the steps before angiogenesis. It was thus indicated that the inhibitory effect of angiostatic steroids against tumor growth due to an anti-angiogenic activity was not dependent at all on the metastasis promotion by these steroids having glucocorticoid activity.

Allantois↗
PubMed1987

Studies on glucose intolerance in chronic renal failure: estimation of insulin sensitivity before and after initiation of hemodialysis.

Using the euglycemic insulin clamp technique, we quantified insulin resistance in the genesis of the glucose intolerance observed in patients with CRF. Tissue sensitivity to insulin was evaluated in 11 patients with CRF (just before, and at one and four weeks after initiation of hemodialysis). The glucose infusion rate in patients with CRF (4.38 +/- 0.28 mg/kg/min) was significantly lower than in 28 controls (7.40 +/- 0.21 mg/kg/min) (p less than 0.001). The decreased glucose infusion rate in patients with CRF increased to 5.63 +/- 0.44 mg/kg/min (p less than 0.02) one week after starting hemodialysis and further improved to 7.46 +/- 0.90 mg/kg/min (p less than 0.02) after four weeks of hemodialysis. During the insulin clamp study, free fatty acid (FFA) decreased more rapidly in patients with CRF (both before and after initiation of hemodialysis) than in the controls (p less than 0.05-0.001). Glycerol decreased gradually in both groups, showing only a 50-60% reduction in 120 min. These results confirm that glucose intolerance in patients with CRF can be improved by the initiation of hemodialysis.

Adult↗
PubMed1987

Protective effects of indeloxazine hydrochloride on cerebral ischemia in animals.

Effects of indeloxazine hydrochloride [(+/-)-2-[(inden-7-yloxy)methyl]morpholine hydrochloride, YM-08054] on cerebral ischemia were investigated in animals. Indeloxazine prolonged the gasping duration dose-dependently in decapitated mice. Bilateral occlusion of the carotid artery for 5 min shortened the latency of step-through in passive avoidance task 4 days following ischemia in mongolian gerbils. The i.p. administration of indeloxazine was started just after the surgical operation and repeated twice a day for 4 days. Indeloxazine (2 mg/kg) significantly prolonged the latency of step-through in this amnesic model, indicating a reversal effect on the ischemia-induced amnesia. In biochemical studies, decreases in brain ATP and total adenine nucleotide levels were inhibited by indeloxazine (2 mg/kg i.p., once a day for 7 days) in four-vessel occluded rats. These findings indicate that indeloxazine possesses protective effects on cerebral ischemia presumably due, in part, to improvement of the cerebral energy metabolism.

Animals↗