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Biomedical subjects

Y Abiko

Publications and source records attributed to Y Abiko.

At least 181 records · Page 10Linked to original sources

Vacuoles and vesicles in the rat junctional epithelium: a study with serial ultrathin sections.

To investigate whether the electron-lucent structures resembling vesicles and vacuoles in the rat molar junctional epithelium (JE) are in fact intracellular or extracellular, a study using serial ultrathin sections was carried out. In one series of experiments, the animals were not treated before the tissues were conventionally fixed; in another, anesthetized animals were administered horseradish peroxidase 20 min before the tissues were fixed. A large number of electron-lucent structures resembling vesicles and vacuoles were detected in both the peripheral and central cytoplasm of the JE localized at enamel and connective tissue sites. These were 70 to 800 nm in diameter and had a lucency similar to that of the extracellular space in untreated specimens fixed with conventional fixative. Serial ultrathin sectioning revealed that the electron-lucent structures gradually became part of the extracellular space in the following sections. There were also found in the middle portion of the cytoplasm in specimens pretreated with horseradish peroxidase. Numerous vacuole-like structures containing peroxidase-positive materials were found to be contiguous with the extracellular space. A small number of vesicles, also containing peroxidase-positive materials, did not appear in the previous or following sections. These results indicate that almost all electron-lucent structures resembling vesicles and vacuoles in the JE are located at the end of a long infolding, and are still in contact with the extracellular space.

Animals↗

The effect of pimobendan on myocardial mechanical function and metabolism in dogs: comparison with dobutamine.

The effect of pimobendan, a newly developed cardiotonic agent, on myocardial mechanical function and energy metabolism has been examined in the dog heart, and compared with that of dobutamine. Either saline, vehicle for pimobendan, dobutamine (0.3 and 1 microgram kg-1), or pimobendan (0.3 and 1 mg kg-1) was injected intravenously. Dobutamine and pimobendan both increased the first derivative of left ventricular pressure and percent segment shortening, indicating their positive inotropic action. After 2 min of dobutamine injection, or after 20 min of pimobendan injection, the myocardium was removed, and used for determination of the tissue levels of metabolites of energy and carbohydrate metabolism. In general, all metabolic parameters measured were not changed by either dobutamine or pimobendan injection. In animals with aortic constriction for 10 months, dobutamine and pimobendan injections did not alter the myocardial energy and carbohydrate metabolism. Although dobutamine and pimobendan increased the cardiac mechanical function, they did not disturb the myocardial energy and carbohydrate metabolism.

Adenine Nucleotides↗

Effects of human superoxide dismutase on ischemic and reperfused myocardium in isolated perfused rat heart.

The effect of human superoxide dismutase (h-SOD) on the ischemic heart was studied in the isolated perfused working rat heart. Myocardial mechanical function expressed as pressure-rate product decreased and completely stopped within 5 min after the onset of global ischemia, and never recovered after reperfusion following 20 min of ischemia. In the ischemic myocardium, the levels of ATP, ADP, and creatine phosphate decreased, and those of AMP and lactate increased. Reperfusion of the ischemic heart did not restore the level of ATP completely. When the heart was treated with h-SOD, the perfusion medium was switched from the buffer containing no h-SOD to that containing h-SOD at either 100, 300 or 1,000 units/ml 5 min before the onset of ischemia. The pressure-rate products of the heart treated with 100, 300, and 1,000 units/ml of h-SOD were restored by reperfusion to 22%, 59%, and 51% of the preischemic level, respectively. The levels of ATP and creatine phosphate in the reperfused heart with 300 and 1,000 units/ml of h-SOD were significantly higher than those without h-SOD. However, a dose-response relationship was not observed when h-SOD was used in concentrations greater than 300 units/ml. These results indicate that a certain amount of h-SOD has some beneficial effects on the ischemic myocardium.

Adenine Nucleotides↗

An ultrastructural study of the pocket epithelium in rats.

The purpose of the present study was to elucidate the biological characteristics of pocket epithelium in experimental periodontitis. Elastic rubber was inserted between the first and second molars of the left maxilla in rats. The rubber was removed after one week, and the animals were sacrificed one week after the removal, i.e., two weeks after the insertion. Sections of the teeth and surrounding tissues were examined by electron microscopy. Periodontal pockets were evident between the tooth surface and epithelial cell layer in the coronal portion. A large number of bacteria surrounded by neutrophils were observed on the cementum surface in the pocket; however, no bacterial invasion could be seen in the epithelium. The epithelial cells were spilt in the central portion by invasion of neutrophils, so that one or two layers of surviving epithelial cells were present on the cementum surface. Numerous fenestrations of capillaries were found in the connective tissue immediately below the epithelium. These results suggest that the pocket epithelium is formed by an intercellular split of the epithelium, not between cementum surface and epithelium.

Animals↗

Beneficial effect of magnesium on the isolated perfused rat heart during reperfusion after ischaemia: comparison between pre-ischaemic and post-ischaemic administration of magnesium.

The effect of high concentration of magnesium on both mechanical dysfunction and metabolic damage after ischaemia-reperfusion was studied in isolated rat hearts. The heart was perfused by the Langendorff's technique at a constant flow (10 ml/min) with modified Krebs-Henseleit solution and driven at 300 beats/min. The heart was made ischaemic by reducing the flow to 0 ml/min for 25 min, and then reperfused at the constant flow for 15 min. MgSO4 was added to the perfusate for 5 min before the onset of ischaemia, or after the end of ischaemia (after the onset of reperfusion). Ischaemia-reperfusion produced both mechanical dysfunction (as evidenced by an increase in the left ventricular end diastolic pressure and a decrease in the left ventricular developed pressure) and metabolic damage [as evidenced by a decrease in the myocardial adenosine triphosphate (ATP)]. When 15 mmol/l MgSO4 was given before ischaemia, there was no appreciable recovery of mechanical function, whereas when given after ischaemia (during reperfusion), there was a marked recovery of mechanical function. Lower concentrations (10 or 5 mmol/l) of MgSO4 given after ischaemia recovered the mechanical function concentration-dependently. The beneficial effect of 15 mmol/l MgSO4 was minimized by the coexistence of 4.5 mmol/l CaCl2 in the reperfusion solution. The decrease in the myocardial level of ATP induced by ischaemia-reperfusion was attenuated by 15 mmol/l MgSO4 given in the reperfusion solution. These results suggest that high Mg2+ is effective in attenuating both functional and metabolic damage of the post-ischaemic heart, provided it is given after ischaemia.

Adenosine Triphosphate↗

Effect of diltiazem on the oxymyoglobin level of myocardial cells in the isolated, perfused rat heart during hypoxia.

The effect of diltiazem on the oxymyoglobin level was studied in the isolated rat heart during hypoxia. The heart was perfused with Krebs-Henseleit solution equilibrated with a gas mixture containing 95% O2 + 5% CO2 (normoxic perfusion solution) at a constant flow rate (9 ml/min) according to Langendorff's method. All the hearts were paced at 300 beats/min. The myocardial oxymyoglobin level (i.e., intracellular oxygen level) of the left ventricular surface was continuously measured by means of an optical technique. Diltiazem (infused into the aortic cannula for 10 minutes at concentrations of 0.72, 2.41, or 4.82 microM, expressed as the final concentration in the solution) decreased the left ventricular pressure (LVP) and perfusion pressure (PP) dose dependently, and did not change the oxymyoglobin (MbO2) level during normoxic perfusion. Hypoxic perfusion (using a gas mixture containing 30% O2 + 5% CO2 + 65% N2) decreased the MbO2, LVP, and PP. Diltiazem (infused 5 minutes after the hypoxic perfusion) at a concentration of 2.41 or 4.82 microM increased the MbO2 level and further decreased the LVP, without affecting the PP. The low concentration of 2.41 or 4.82 microM increased the MbO2 level and further decreased the LVP, without affecting the PP. The low concentration (0.72 microM) of diltiazem, however, had practically no effect on these parameters. In summary, diltiazem in high concentrations decreased the LVP and increased the intracellular oxygen level of the myocardial cells during hypoxia, but not during normoxia.

Animals↗

Changes in myocardial nonesterified fatty acids during ischemia and reperfusion in isolated, perfused, working rat hearts.

The time course of changes in the myocardial levels of nonesterified fatty acids (NEFA), adenosine triphosphate (ATP), creatine phosphate (CrP) and lactate, and those in the cardiac mechanical function during ischemia and reperfusion was investigated in the isolated, perfused, working rat heart. Ischemia was produced by lowering the afterload pressure from 60 to 0 mm Hg, and reperfusion resulted from raising the afterload pressure to 60 mm Hg. Ischemia stopped the heart beat, and increased the myocardial levels of unsaturated NEFA (such as arachidonic, palmitoleic, and linoleic acids) as a function of the ischemic period; it decreased the myocardial levels of ATP and CrP, and increased the myocardial level of lactate. The level of arachidonic acid increased when the myocardial level of ATP fell below 5 mumol/g dry weight. Reperfusion after ischemia started the heart beat, and restored the mechanical function which depended on the preceding ischemic period. Reperfusion also increased the levels of ATP and CrP and decreased the level of lactate, whereas it further increased the levels of the NEFA that had been elevated by ischemia. The recovery of mechanical function was inversely correlated with the myocardial level of arachidonic acid during ischemia and reperfusion. We concluded that changes in the myocardial levels of NEFA during ischemia and reperfusion are different from those of ATP, CrP, and lactate, and suggest that the myocardial level of arachidonic acid during ischemia and reperfusion can be a sensitive and suitable marker for the recovery of mechanical function during reperfusion.

Adenosine Triphosphate↗

Cloning of a Bacteroides gingivalis outer membrane protein gene in Escherichia coli.

Gene banks of chromosomal DNA from Bacteroides gingivalis 381 were constructed using the bacteriophage replacement vector lambda L47.1. A clone encoding an outer membrane protein from B. gingivalis was identified by Western blot screening with antiserum raised against the outer membrane fraction of B. gingivalis 381 cells. The DNA insert contained within this phage was cloned into the plasmid vector pACYC184 to create the recombinant plasmid pMD123. An Escherichia coli transformant, MD123, containing pMD123 produced a protein having an apparent molecular weight of 40 kDa. The recombinant protein was purified, and amino acid analysis revealed the recombinant protein to have a relatively high content of hydrophobic amino acids (43.6%). Antiserum against the purified recombinant 40 kDa protein reacted with a polypeptide of similar size in the outer membrane fraction and vesicles of B. gingivalis.

Amino Acids↗

Studies on cholesterol accumulation in radicular cyst fluid--origin of heat-stable cholesterol-binding protein.

1. The amount of apolipoprotein B (apo B) was measured using slit-immunoblotting in 20 specimens of radicular cyst fluids. Apo B was detected in all the cyst fluids with varying amounts. 2. Relationship between the amounts of apo B and free cholesterol or activity of heat-stable cholesterol-binding protein (HCBP) were examined. The amount of apo B was correlated well with the activity of HCBP (n = 20, r = 0.72, P less than 0.01) and with the amount of free cholesterol (n = 20, r = 0.45, P less than 0.05). 3. Anti-human apo B antibody inhibited cholesterol-binding activity in radicular cyst fluid. 4. When human-serum was chromatographed on a HPLC ion-exchange column, both cholesterol-binding activity and apo B had exactly the same retention time. 5. These results suggest that HCBP originates from beta-lipoprotein, and beta-lipoprotein may have an important role in cholesterol accumulation on radicular cysts.

Apolipoproteins B↗

Effect of nipradilol on myocardial energy metabolism in the dog ischaemic heart.

The effect of nipradilol, a newly developed beta-adrenoceptor blocking agent with a vasodilatory action, on myocardial energy metabolism has been examined in the dog ischaemic heart, and compared with that of propranolol. Ischaemia was induced by ligating the left anterior descending coronary artery. Either saline, nipradilol (0.3 mg kg-1), or propranolol (1 mg kg-1) was injected intravenously 5 min before coronary ligation. After 3 or 30 min of coronary ligation, the ischaemic region of the myocardium was removed, and the endocardial portion used to determine the levels of adenosine triphosphate (ATP), adenosine diphosphate (ADP), adenosine monophosphate (AMP), creatine phosphate (CrP) and lactate. Ischaemia decreased the levels of ATP and CrP, and increased the levels of ADP, AMP and lactate. Immediately after the injection of nipradilol, rapid falls in blood pressure and heart rate were observed. Pretreatment with nipradilol lessened the decreases in the levels of ATP and CrP and the increases in the levels of AMP and lactate, caused by 3 min of ischaemia, to the same extent as propranolol. However, after 30 min of ischaemia, nipradilol had no effect on myocardial metabolism unlike propranolol. These results indicate that nipradilol can reduce ischaemic influences on myocardial metabolism as well as propranolol, but only in the early stages of ischaemia.

Adenine Nucleotides↗

Myocardial non-esterified fatty acids during normoxia and ischemia in Langendorff and working rat hearts.

In isolated perfused rat hearts, the tissue levels of non-esterified fatty acids (NEFA) decreased during normoxic perfusion for 60 min in the working heart but not in the Langendorff heart. The levels of both saturated and unsaturated NEFA increased during ischemia for 20 min in the working heart but not in the Langendorff heart, although unsaturated NEFA increased in the Langendorff heart when the ischemic period was 40 min. Arachidonic and linoleic acids were the NEFA that accumulated most prominently.

Animals↗

Effects of bunazosin, a selective alpha 1-adrenergic blocking agent, on myocardial energy metabolism in ischemic dog heart.

Effects of a selective alpha 1-adrenergic blocking agent, bunazosin, on myocardial energy metabolism in the ischemic heart were studied. Ischemia was induced by ligating the left anterior descending coronary artery of the dog heart. Bunazosin was injected intravenously either 5 or 20 min before coronary artery ligation. Hearts were removed 3 min after coronary ligation and used for determination of the levels of cardiac tissue metabolites. Ischemia decreased the levels of ATP, creatine phosphate, glycogen and glucose, and increased the levels of ADP, AMP, hexose monophosphates and lactate. The energy charge potential (ECP) calculated was decreased by ischemia. Pretreatment with bunazosin inhibited the decrease in ATP and the increase in AMP caused by ischemia, resulting in the high value of ECP in the ischemic myocardium. Bunazosin also prevented the changes in carbohydrate metabolism caused by ischemia. It is concluded that bunazosin may reduce the influence of ischemia on the myocardium.

Adenine Nucleotides↗

Immunohistochemical study of basal cell adenoma in the parotid gland.

Basal cell adenoma of the parotid gland was studied with immunohistochemical methods. We observed cells in the tumor with positive reaction to polyclonal keratin, prekeratin, monoclonal PKK-1, polyclonal S-100 protein, monoclonal S-100 protein (alpha), secretory component, actin and laminin. However, no cells which stained positively with monoclonal KL-1, amylase, carcinoembryonic antigen, or epithelial membrane antigen were recognized. From these immunohistochemical results and our ultrastructural observations reported previously, we conclude that the cells constituting the basal cell adenoma are ductal, myoepithelial, and squamous cells but not secretory ones. It is also suggested that the origins of basal cell ademona as well as those of pleomorphic and clear cell adenoma are undifferentiated cells of intercalated duct.

Adenoma↗

[Change of beta-actin gene expression during culture on osteoblast-like cell line, MC3T3-E1].

Multiple forms of actin (alpha, beta, and gamma-actin) have been found in a variety of mammalian cell lines and tissues by the use of high resolution, two-dimensional gel electrophoresis. alpha-Actin is found only in differentiated muscle cells, and its synthesis is induced during myogenesis in culture, beta- and gamma-actin isotypes are the principal components of microfilaments, structures believed to be involved in cellular morphogenesis, motility, and mitosis. Recent studies have shown that mammalian actin mRNA levels are modulated in response to changes in cell shape and during cell differentiation in vitro. On the other hand, Kodama et al. isolated clone MC3T3-E1 cells from newborn mouse calvaria, which have retained the ability to produce and mineralize a bone-like ground substance after many serial passages. Thus clone is useful for studying osteoblast differentiation as well as the mechanism of calcification. It is demonstrated that bone cells assume a stellate morphology after some hormone treatment and these changes were clearly associated with altered reorganization of the microfillaments which resulted in an enhanced osteoblast phenotype. We have now examined the effect of culture day on expression of beta-actin gene in MC3T3-E1 cells and found that expression of beta-actin gene reduced with culture days. These alternative on the expression of actin gene suggest that beta-actin may be involved in bone remodeling in vivo.

Actins↗

Both d-cis- and l-cis-diltiazem have anti-ischemic action in the isolated, perfused working rat heart.

The effect of diltiazem (d-cis-diltiazem) on the ischemic myocardium was compared with that of l-cis-diltiazem, an optical isomer having less potent calcium channel-blocking action, in the isolated, perfused working rat heart. Ischemia decreased mechanical function and tissue levels of ATP and creatine phosphate, and increased tissue levels of nonesterified fatty acids (NEFA), AMP and lactate. Reperfusion did not restore mechanical function, but restored incompletely the levels of metabolites (except NEFA) that had been altered by ischemia. The ischemia-induced changes in NEFA were prevented by d-cis-diltiazem completely and by l-cis-diltiazem incompletely. Other metabolic changes induced by ischemia were attenuated by d-cis-diltiazem but not by l-cis-diltiazem. In heart pretreated with d-cis- or l-cis-diltiazem, both the mechanical function and the levels of metabolites recovered during reperfusion, the degree of recovery with both drugs being similar. These results indicate that not only d-cis-diltiazem but also l-cis-diltiazem has an anti-ischemic action probably due to inhibition of the tissue NEFA accumulation. These results also suggest that the mechanism of the protective effect of d-cis-diltiazem on the ischemic myocardium is not entirely due to the calcium channel-blocking action. Treatment with low Ca2+ (1.0 mM CaCl2) also attenuated the ischemia-induced changes. The interval between reoxygenation and start of function in the reperfused heart that had been treated with low Ca2+ was significantly longer than that with d-cis- or l-cis-diltiazem. The effect of these isomers to shorten this interval may contribute to their common anti-ischemic action.

Adenosine Triphosphate↗

Effect of lidocaine on the accumulation of non-esterified fatty acids in the ischemic perfused rat heart.

The effect of lidocaine on the accumulation of non-esterified fatty acids (NEFA) was investigated in the isolated, perfused working rat heart. Ischemia was induced by lowering the afterload pressure to 0 mm Hg for 20 min, and reperfusion was induced by raising the pressure to the pre-ischemic value (60 mm Hg) for 20 min. The heart was frozen for biochemical studies immediately after ischemia or reperfusion. Ischemia decreased the mechanical function, increased the levels of palmitoleic, arachidonic and linoleic acids, left unchanged the levels of oleic, lauric, myristic, palmitic and stearic acids, decreased the levels of adenosine triphosphate (ATP), creatine phosphate (CrP), decreased the energy charge potential (ECP) and increased the level of lactate. Lidocaine (10(-5) or 3 x 10(-5) M) improved the mechanical function and attenuated the changes in NEFA, ATP, CrP, and ECP caused by ischemia. These findings suggest that lidocaine attenuates the ischemia- and reperfusion-induced metabolic changes in the myocardium.

Adenosine Triphosphate↗

Effect of flunarizine on ischemic myocardial metabolism in dogs.

The effect of flunarizine, a calcium entry-blocker, on the ischemic myocardial metabolism of the open-chest dog heart was examined and compared to that of diltiazem. During ischemia, initiated by ligating the left anterior descending coronary artery, the metabolism of the myocardium switched from aerobic to anaerobic; the levels of glycogen, fructose-1,6-diphosphate (FDP), adenosinetriphosphate and creatinephosphate decreased, and the levels of glucose-6-phosphate (G6P), fructose-6-phosphate (F6P), lactate, adenosine diphosphate and adenosine monophosphate increased during 3 min of ischemia. The calculated energy charge potential decreased, and the [( G6P] + [F6P]/[FDP] ratio and the lactate/pyruvate ratio were increased by ischemia. Flunarizine (0.3 or 1 mg/kg) or diltiazem (0.1 mg/kg) was injected i.v. 5 min before the start of ischemia. Pretreatment with either flunarizine or diltiazem reduced the decrease in the energy charge potential and the increase in the [( G6P] + [F6P]/[FDP] ratio during ischemia. Flunarizine (1 mg/kg) and diltiazem (0.1 mg/kg) reduced the accumulation of lactate due to ischemia, leading to a decrease in the lactate/pyruvate ratio. Flunarizine and diltiazem may lessen the influence of ischemia on the myocardial tissue.

Adenine Nucleotides↗

Effect of propranolol on accumulation of NEFA in the ischemic perfused rat heart.

The effect of propranolol on the accumulation of non-esterified fatty acids (NEFA) in the isolated, perfused working rat heart was investigated. Ischemia was induced by lowering the afterload pressure to 0 mm Hg for 20 min and for reperfusion, the pressure was raised to the pre-ischemic pressure (60 mm Hg) for 20 min. The heart was frozen for biochemical studies immediately after ischemia or reperfusion. Ischemia decreased mechanical function, increased the levels of palmitoleic, arachidonic and linoleic acids, left oleic, lauric, myristic, palmitic and stearic acids unchanged, decreased the levels of adenosine triphosphate (ATP), creatine phosphate (CrP) and the energy charge potential (ECP), and increased the level of lactate. Propranolol (10(-5) or 3 x 10(-5) M) restored mechanical function and inhibited the changes in NEFA, ATP and ECP caused by ischemia. It is suggested that propranolol inhibits the decrease in mechanical function and high energy phosphates caused by ischemia, and thereby inhibits the accumulation of NEFA, especially of the unsaturated fatty acids such as arachidonic acid, during ischemia.

Animals↗