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Biomedical subjects

J Amano

Publications and source records attributed to J Amano.

At least 199 records · Page 11Linked to original sources
PubMed1987

Effects of myocardial ischemia on regional function and stiffness in conscious dogs.

The extent to which cardiac nerves influence responses of regional ventricular function to acute myocardial ischemia was investigated in conscious dogs with intact cardiac innervation (N) and dogs with chronic cardiac denervation (D). Following coronary artery occlusion (CAO) left ventricular (LV) end-diastolic pressure increased more (P less than 0.01) in D (18 +/- 3.2 mmHg) than in N dogs (3.4 +/- 0.7 mmHg), whereas heart rate increased more in N (32 +/- 4.8 beats/min) than in D dogs (16 +/- 3.0 beats/min). In nonischemic zones of D dogs there were greater increases, P less than 0.05, in end-diastolic segment length, systolic segment shortening, and velocity of shortening than in N dogs. In ischemic zones, significantly greater increases in end-diastolic segment length were also observed in the D group, but similar reductions in segmental shortening occurred in both N (-116 +/- 2.8%) and D (-108 +/- 5.2%) dogs. The time constant of isovolumic relaxation was not different in the two groups. However, in ischemic zones of N dogs myocardial stiffness constant (k) increased by 109 +/- 24 from 33 +/- 4.9 and end-diastolic stiffness (Eed) rose by 1527 +/- 310 from 253 +/- 34 mmHg, whereas k increased significantly less (P less than 0.05) in D dogs. Eed of ischemic zones also rose significantly less (P less than 0.05) in D dogs.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Structure identification of the complex-type, asparagine-linked sugar chains of beta-D-galactosyl-transferase purified from human milk.

The asparagine-linked sugar chains of human milk galactosyltransferase were quantitatively released as oligosaccharides from the polypeptide backbone by hydrazinolysis. They were converted into radioactive oligosaccharides by sodium borotritiate reduction after N-acetylation, and fractionated by paper electrophoresis and by Bio-Gel P-4 column chromatography after sialidase treatment. Structural studies of each oligosaccharides by sequential exoglycosidase digestion and methylation analysis indicated that the galactosyltransferase contains bi, tri-, and probably tetra-antennary, complex-type oligosaccharides having alpha-D-Manp-(1----3)-[alpha-D-Manp-(1----6)]-beta-D-Manp -(1----4)-beta-D- GlcpNac-(1----4)-alpha-L-[Fucp-(1----6)]-D-GlcNAc as their common core. Variation is produced by the different locations and numbers of the five different outer chains: beta-D-Galp-(1----4)-D-GlcNAc, alpha-L-Fucp-(1----3)-[beta-D-Galp-(1----4)]-D-GlcNAc, alpha-NeuAc-(2----6)-beta-D-Galp-(1----4)-D-GlcNAc, alpha-L-Fucp-(1----3)-[beta-D-Galp-(1----4)]-beta-D-GlcpNAc-(1---- 3)-beta- D-Galp-(1----4)-[alpha-L-Fucp-(1----3)]-D-GlcNAc, and alpha-NeuAc-(2----6)-beta-D-Galp-(1----4)-beta-D-GlcpNAc-(1----3)-beta-D - Galp-(1----4)-[alpha-L-Fucp-(1----3)]-beta-D-GlcNAc.

Asparagine↗
PubMed1986

Purification and characterization of a novel alpha-mannosidase from Aspergillus saitoi.

An alpha-mannosidase differing from 1,2-alpha-mannosidase was found to occur in Aspergillus saitoi. By a series of column chromatographies the enzyme was purified up to 1,000-fold, and its properties were studied in detail. The enzyme preparation, which was practically free from other exoglycosidases, showed a pH optimum of 5.0. In contrast to 1,2-alpha-mannosidase, the enzyme was strongly activated by Ca2+ ions. p-Nitrophenyl alpha-mannopyranoside was not hydrolyzed by the enzyme. Accordingly, the substrate specificity of the new alpha-mannosidase was studied by using a variety of tritium-labeled oligosaccharides. Studies with linear oligosaccharides revealed that the enzyme cleaves the Man alpha 1----3Man linkage more than 10 times faster than the Man alpha 1----6Man and the Man alpha 1----2Man linkages. Furthermore, it cleaves the Man alpha 1----6Man linkage of the Man alpha 1----6(Man alpha 1----3)Man beta 1----4GlcNAc beta 1----4GlcNAcOT only after its Man alpha 1----3 residue is removed. Because of this specificity, the enzyme can be used as an effective reagent to discriminate R----Man alpha 1----6(Man alpha 1----3)Man beta 1----4GlcNAc beta 1----4(+/- Fuc alpha 1----6)GlcNAcOT from its isomeric counterparts, Man alpha 1----6(R----Man alpha 1----3)Man beta 1----4GlcNAc beta 1----4(+/- Fuc alpha 1----6)GlcNAcOT, in which R represents sugars.

Aspergillus↗
PubMed1986

Augmented catecholamine uptake by the heart during hemorrhage in the conscious dog.

Changes in arterial and coronary sinus concentrations of norepinephrine (NE) and epinephrine (E) in response to hemorrhage were examined in conscious dogs. Hemorrhage (45 +/- 3.2 ml/kg) decreased mean arterial pressure by 47 +/- 6%, left ventricular (LV) dP/dt by 38 +/- 6%, and mean left circumflex coronary blood flow by 47 +/- 6%, while heart rate increased by 44 +/- 13%. Increases in concentrations of arterial NE (5,050 +/- 1,080 from 190 +/- 20 pg/ml) and E (12,700 +/- 3,280 from 110 +/- 20 pg/ml) were far greater than increases in coronary sinus NE (1,700 +/- 780 from 270 +/- 50 pg/ml) and E (4,300 +/- 2,590 from 90 +/- 10 pg/ml). Net release of NE from the heart at rest was converted to a fractional extraction of 66 +/- 9% after hemorrhage. Fractional extraction of E increased from 16 +/- 6% at rest to 73 +/- 8% after hemorrhage. In cardiac-denervated dogs, hemorrhage (46 +/- 2.8 ml/kg) decreased mean arterial pressure by 39 +/- 15%, LV dP/dt by 36 +/- 10%, and mean left circumflex coronary blood flow by 36 +/- 13%, while heart rate increased by 24 +/- 10%. Hemorrhage increased arterial NE (1,740 +/- 150 from 210 +/- 30 pg/ml) and E (3,050 +/- 880 from 140 +/- 20 pg/ml) more than it increased coronary sinus NE (460 +/- 50 from 150 +/- 30 pg/ml) and E (660 +/- 160 from 90 +/- 20 pg/ml) but significantly less (P less than 0.05) than observed in intact dogs. These experiments indicate that hemorrhage, unlike exercise and sympathetic nerve stimulation, does not induce net overflow of NE from the heart.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

Effects of catecholamines on myocardial viability in early reperfusion following hypothermic global ischemia in dogs--comparison between epinephrine and dobutamine.

Attempts were made to define the effects of epinephrine and dobutamine on the myocardium during early reperfusion for 60 minutes following hypothermic global ischemia at a myocardial temperature of 28 degrees C for 60 minutes under cardiopulmonary bypass. Ischemia was induced by cross-clamping the dog aorta. Epinephrine (0.1 microgram/kg/min) and dobutamine (5 micrograms/kg/min) were given throughout the reperfusion period by intravenous drip infusion, a control group was treated with saline infusion. Comparison of hemodynamic parameters was made before cardiopulmonary bypass, and at 30 and 60 minutes of reperfusion. Epinephrine and dobutamine significantly increased stroke volume index, left ventricular stroke work index and tissue calcium content compared with saline, however, myocardial water content was only slightly higher in the group given saline, compared with the other two groups. Myocardial mitochondrial membranes and cristae were slightly damaged and creatine phosphate content was reduced. Ultrastructural integrity was related to myocardial tissue calcium content, with a significant negative correlation. These results suggest that epinephrine (0.1 microgram/kg/min) will improve stroke volume index and left ventricular stroke work index, as does dobutamine (5 micrograms/kg/min), however, both agents had a minimal effect on reducing myocardial morphological and biochemical integrity, although catecholamines have detrimental effects on the myocardium in early reperfusion following ischemia.

Animals↗
PubMed1985

Creatine kinase release not associated with myocardial necrosis after short periods of coronary artery occlusion in conscious baboons.

The effects of 15 minute periods of coronary artery occlusion on plasma creatine kinase (CK) and CK-MB isoenzyme activity, regional myocardial function and subsequent myocardial necrosis were studied in six conscious baboons 2 to 3 weeks after recovery from instrumentation. Mid left anterior descending coronary artery occlusion induced complete loss of systolic wall thickening (ultrasound transit time technique) and decreases in epicardial (-93%) and endocardial (-96%) blood flows (microsphere technique). Reperfusion after 15 minutes resulted in complete recovery of regional function 24 hours later. Serial plasma enzyme activity revealed a significant increase in total CK from 71 +/- 11 to 976 +/- 158 U/liter and in CK-MB from levels that were too low to measure to 21.4 +/- 2.9 U/liter. At autopsy, neither gross pathologic evidence (triphenyltetrazolium chloride staining technique) nor histologic evidence of myocardial necrosis was observed. Thus, in the conscious baboon short episodes of myocardial ischemia are associated with a significant appearance of CK and CK-MB in the blood in the absence of cellular necrosis.

Animals↗
PubMed1985

Effects of coronary artery reperfusion on regional myocardial blood flow and function in conscious baboons.

The effects of coronary artery reperfusion initiated 1 hr and 3 hr after coronary artery occlusion were evaluated on measurements of overall and regional left ventricular function and on regional myocardial blood flow. These experiments were conducted in conscious baboons 2 to 3 weeks after recovery from instrumentation with a solid state left ventricular pressure gauge, aortic and left atrial catheters, a hydraulic occluder around the mid left anterior descending coronary artery, and pairs of ultrasonic transducers implanted in the endocardium of the left ventricular free wall or across the free wall to measure endocardial segment shortening and wall thickening, respectively. Coronary artery occlusion induced similar effects in both groups. At 1 hr after occlusion, the ischemic zone was characterized by severe and equal reductions in both endocardial (-97 +/- 1%) and epicardial (-95 +/- 4%) blood flows and complete loss of regional systolic function, which was replaced by paradoxical wall motion. Reperfusion initiated after 1 hr of ischemia was associated with a marked transient increase in endocardial (+386 +/- 51%) and epicardial (+544 +/- 79%) blood flows. During the subsequent 4 weeks, segment shortening and wall thickening tended to improve. However, at 4 weeks after reperfusion, segment shortening was still depressed by 45 +/- 12% and wall thickening by 58 +/- 14%. In contrast, reperfusion initiated after 3 hr of ischemia was not associated with a significant hyperemic response, and systolic segment shortening and wall thickening did not recover during the subsequent 4 week period.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

Mechanisms of supersensitivity to sympathomimetic amines in the chronically denervated heart of the conscious dog.

Mechanisms of denervation supersensitivity to sympathomimetic amines were studied in conscious animals. Norepinephrine, 0.1 micrograms/kg, increased left ventricular dP/dt significantly more (4208 +/- 828 mm Hg/sec) in dogs with cardiac denervation than in intact dogs (1029 +/- 280 mm Hg/sec), P less than 0.01, whereas responses to isoproterenol were similar in both groups. Denervation supersensitivity to isoproterenol could be demonstrated only after opposing reflex effects were blocked. After ganglionic blockade, norepinephrine still induced 2- to 3-fold greater increases in left ventricular dP/dt and 3- to 7-fold greater increases in heart rate in cardiac-denervated dogs, whereas isoproterenol and prenalterol, not taken up by presynaptic nerve endings, elicited only 40%-50% greater increases in left ventricular dP/dt and heart rate in dogs with cardiac denervation. The density of beta-adrenergic receptors [( 3H]dihydroalprenolol) was elevated (P less than 0.01) in denervated left ventricles (105 +/- 6.9 fmol/mg protein, n = 8) compared to normal left ventricles (70 +/- 6.3 fmol/mg protein, n = 12). This was accompanied by enhanced isoproterenol-mediated adenylate cyclase activity. However, muscarinic cholinergic receptor density, [( 3H]quinuclidinyl benzilate), decreased from control levels of 251 +/- 11 fmol/mg protein (n = 7) to 193 +/- 14 fmol/mg protein (n = 6). Thus, chronic cardiac denervation results in upregulation of the beta-adrenergic receptor and down-regulation of the muscarinic receptor. The increased beta-adrenergic receptor density and adenylate cyclase stimulation correlated well with the amount of denervation supersensitivity to isoproterenol and prenalterol, but accounted for only a minor fraction of denervation supersensitivity to norepinephrine. The major mechanism of denervation supersensitivity to norepinephrine appears to involve lack of the norepinephrine reuptake.

Adenylyl Cyclases↗
PubMed1985

Adverse effects of chronic cardiac denervation in conscious dogs with myocardial ischemia.

The extent to which total chronic cardiac denervation protects the ischemic myocardium was investigated in conscious dogs. The major hemodynamic difference after coronary artery occlusion was that left ventricular end-diastolic pressure rose significantly more, P less than 0.01, in the denervated group (12 +/- 1.5 mm Hg) than in the normal group (4.4 +/- 1.4 mm Hg). Blood flow (radioactive microspheres) in the ischemic endo- and epicardium fell to similar levels at 3-5 minutes after coronary occlusion, but was significantly less (P less than 0.01) in denervated dogs at 3 hours after occlusion in the endo- (0.05 +/- 0.01) and epicardium (0.30 +/- 0.02 ml/min per g), than in the endo- (0.13 +/- 0.03) and epicardium (0.42 +/- 0.05 ml/min per g) in the normal group. A subgroup of normal dogs was also studied, with left ventricular end-diastolic pressure increased by volume loading to levels similar to those observed in the denervated group after coronary occlusion; in these dogs, blood flow was similar to that in the other two groups 3-5 minutes after coronary artery occlusion, but, at 3 hours, was significantly more depressed (P less than 0.01) than that observed in normal dogs without volume loading in both endo- (0.03 +/- 0.01) and epicardial (0.25 +/- 0.03 ml/min per g) layers. Infarct size, as a fraction of the area at risk, was significantly greater (P less than 0.05) in the denervated group (60 +/- 4.3%) and in the subgroup of normal dogs with elevated left ventricular end-diastolic pressure (73 +/- 5.8%), compared with the normal group without volume loading (37 +/- 8.1%). Thus, in conscious dogs, total chronic cardiac denervation exerts an adverse effect on infarct size which may be related to the sustained elevation in left ventricular end-diastolic pressure and consequent impairment of collateral perfusion.

Animals↗
PubMed1984

Combined treatment of coenzyme Q10 and aprotinin with intraaortic balloon pumping following aorto-coronary bypass surgery.

The effect of combined treatment of coenzyme Q10 (CoQ10) and aprotinin with intra-aortic balloon pumping (IABP) was evaluated in patients who underwent aorto-coronary bypass surgery. Forty-one patients were divided into two groups. Group A (27) were treated by IABP only and Group B (14) were treated by the concomitant use of CoQ10 and aprotinin with IABP. Both groups were subdivided into two groups with regard to the ability to be weaned from IABP (Group A-I, Group B-I) or the inability (Group A-II, Group B-II). CoQ10 was administrated intravenously at doses of 5-10 mg/kg/day and aprotinin was infused at doses 5,000-10,000 KU/kg/day. The percentile incidence of ability to be weaned from IABP was 93 per cent (13/14) in Group B was higher than that of 74 per cent (20/27) in Group A. There were no significant differences among Group A-I, Group A-II, and Group B-I with regard to preoperative and intraoperative factors. Serum GOT and CPK levels on the first postoperative day were significantly higher in Group A-II and Group B-I than those in Group A-I but there was no significant difference between GOT or CPK levels in Group A-II and Group B-I. These results suggest that concomitant treatment of CoQ10 and aprotinin with IABP leads to an improvement in postoperative low cardiac output syndrome.

Aprotinin↗
PubMed1984

New evidence of the substrate specificity of endo-beta-N-acetylglucosaminidase D.

The susceptibility of a variety of oligosaccharides to endo-beta-N-acetylglucosaminidase D was investigated. The oligosaccharides having the structures of Man alpha 1----6 (GlcNAc beta 1----4Man alpha 1----3)Man beta 1----4GlcNAc beta 1----4(+/- Fuc alpha 1----6)GlcNAcOT, derived from complex type triantennary sugar chains, released +/- Fuc alpha 1----6GlcNAcOT upon incubation with the enzyme at almost the same rate as Man alpha 1----6(Man alpha 1----3)Man beta 1----4GlcNAc beta 1----4GlcNAcOT. When the reaction products were reduced with NaB3H4 and analyzed by Bio-Gel P-4 column chromatography, a new radioactive peak was detected in both cases. This new radioactive oligosaccharide was confirmed to be Man alpha 1----6(GlcNAc beta 1----4Man alpha 1----3)Man beta 1----4GlcNAcOT in the former case and Man alpha 1----6(Man alpha 1----3)Man beta 1----4GlcNAcOT in the latter. These results indicated that endo-beta-N-acetylglucosaminidase D does not require the presence of a free hydroxyl group at the C-4 position of the alpha-mannosyl residue of the trisaccharide glycon: Man alpha 1----3Man beta 1----4GlcNAc beta 1----.

Acetylglucosaminidase↗
PubMed1983

Correlation among water content, left ventricular function, coronary blood flow, and myocardial metabolism after hypothermic ischemic cardiac arrest.

Subendocardial ischemia is a common cause of death following ischemic cardiac arrest. We studied relationships among myocardial water content (WC), left ventricular function, coronary blood flow, and myocardial metabolism following ischemic cardiac arrest. Under cardiopulmonary bypass with hypothermia, 120 min of aortic occlusion was employed, and myocardial temperature was kept around 20 degrees C in 10 mongrel dogs. Left ventricular function (peak LVP, max dp/dt, LVEDP, LVSWI), coronary blood flow, myocardial enzymes (m-GOT, total CPK, MB-CPK), myocardial ATP and creatine phosphate (CP), and WC of the subendocardium of the left ventricle were measured. Data were obtained in the control state and immediately and 30 and 60 min after aortic unclamping. Significant negative correlations were obtained between WC and max dp/dt (r = -0.8384), coronary blood flow (r = -0.9928), ATP (r = -0.7038), and CP (r = -0.7835). Significant positive correlations were obtained between WC and LVEDP (r = 0.7525), m-GOT (r = 0.7638), and total CPK (r = 0.7079). These data suggest that myocardial edema results in depression of left ventricular function and metabolism.

Adenosine Triphosphate↗