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Biomedical subjects

N Yamazaki

Publications and source records attributed to N Yamazaki.

At least 289 records · Page 16Linked to original sources
PubMed1981

Bacteriocin-like substance (melaninocin) from oral Bacteroides melaninogenicus.

A bacteriocin-like substance, designated melaninocin, was extracted from a strain of Bacteroides melaninogenicus by ultrasonic treatment and purified. Melaninocin was heat labile and was destroyed by digestion by several proteolytic enzymes. Among the oral indigenous microorganisms, Bacteroides, Actinomyces, and streptococci were found to be sensitive to melaninocin.

Amino Acids↗
PubMed1981

Effects of L-carnitine on ventricular arrhythmias in dogs with acute myocardial ischemia and a supplement of excess free fatty acids.

The effects of L-carnitine on ventricular arrhythmias were evaluated in dogs with acute myocardial ischemia and a supplement of excess free fatty acids (FFA). Acute myocardial ischemia was induced by ligation of left anterior descending coronary artery. After 80 minutes of coronary occlusion, high plasma FFA was induced by intravenous injection of heparin 200 mu/kg and Intralipid 5 ml/kg as a bolus. After additional 60 minutes, beating hearts were removed from animals and tissue levels of free carnitine, short and long chain acyl carnitine, FFA and adenosine triphosphate (ATP) were determined. L-carnitine 100 mg/kg was administered intravenously 5 minutes before coronary artery ligation. Electrocardiograms were recorded continuously by a Holter electrocardiographic recorder during the experiment and ventricular arrhythmias were quantified by an arbitrary scoring system. In ischemic and excess FFA supplemented myocardium, free carnitine and ATP decreased, whereas long chain acyl carnitine and FFA increased. And these metabolic changes tended to be reduced by L-carnitine. Pretreatment of L-carnitine also reduced the grade of ventricular arrhythmias induced both by acute myocardial ischemia and by supplemented of excess FFA. These results suggest that the administration of L-carnitine may be beneficial to prevent serious arrhythmias in ischemic heart disease, presumably by restoring the imparied FFA oxidation.

Adenosine Triphosphate↗
PubMed1981

Effect of L-carnitine on cardiac hemodynamics.

The effect of L-carnitine on cardiac hemodynamics was evaluated in normal closed chest dogs. Extracorporeal circulation was produced to measure coronary blood flow in closed chest dogs. Coronary venous blood was introduced to the extracorporeal circuit through a polyethylene catheter wedged into the coronary sinus under fluoroscopic control and was returned to the animal through the jugular vein. L-carnitine was infused intravenously at a constant rate of 80 mg/Kg/min for 8 min. Hemodynamic responses appeared within 1 to 3 min of carnitine infusion and peak effects were observed nearly after 5 min. Peak effects on cardiac hemodynamics after 5 to 8 min of carnitine infusion were as follows. Heart rate decreased by 17% from control (p less than 0.05). Aortic and left ventricular pressure increased by 20% (p less than 0.05 and p less than 0.01 respectively) and peak positive left ventricular dp/dt increased by 35% (p less than 0.01), the mean rate pressure product as the index of myocardial oxygen consumption remained unchanged. Coronary blood flow increased by 60% (p less than 0.01) and coronary vascular resistance decreased by 25% (p less than 0.01). As the infusion of carnitine was discontinued, the effects promptly disappeared. These data suggest that L-carnitine has direct vasodilating and positive inotropic effects on cardiovascular system.

Acetyl Coenzyme A↗
PubMed1981

Carnitine distribution in subepicardial and subendocardial regions in normal and ischemic dog hearts.

In order to evaluate the role of carnitine on fatty acid metabolism in subepicardial (Epi) and subendocardial (Endo) regions in ischemic heart, tissue levels of carnitine, free fatty acids (FFA), and adenosine triphosphate (ATP) were determined in ischemic, non-ischemic and border areas in dog hearts with acute regional ischemia. Acute regional ischemia was induced by ligation of the left anterior descending coronary artery for 15 min. In normal hearts, tissue carnitine levels were lower in Endo than in Epi. On the other hand, FFA levels were higher in Endo than in Epi. In ATP levels, no significant differences were observed between Endo and Epi. In acute regional ischemia, tissue carnitine levels decreased not only in ischemic and border areas but also in nonischemic area. And the levels were lower in Endo than in Epi in all areas. Tissue ATP levels were also lower in endo than in Epi in all areas. From nonischemic area toward the center of ischemic area, the difference in ATP levels between Endo and Epi became more prominent. Tissue FFA levels increased in ischemic and border areas, while no significant differences were observed between Endo and Epi. These results confirmed that Endo as metabolically more anaerobic than Epi even in normal heart and it became more prominent in the heart with acute regional ischemia.

Adenosine Triphosphate↗
PubMed1981

Effect of nitroglycerin on the free radical formation of myocardial mitochondria impaired by ethanol. Studies by electron spin resonance (ESR) spectrometry.

In order to investigate the direct metabolic effect of nitroglycerin on myocardium, its effect on mitochondrial free radical formation was studied in vitro, using the dog heart mitochondria impaired by ethanol. Free radical concentrations in state 4 respiration or the ratio of free radical concentrations in state 4 to state 1 was used as an index of mitochondrial function. Free radical concentrations were represented as ESR intensity. In normal control, ESR intensity increased from 0.115 +/- 0.030 (mean +/- SD) per mg protein in state 1 to 0.178 +/- 0.017 in state 4 (p less than 0.001). When mitochondria were treated with 10(-4) M ethanol, on the other hand, ESR intensity decreased from 0.163 +/- 0.34 in state 1 to 0.137 +/- 0.019 in state 4 (p less than 0.05). When mitochondria were treated with 10(-6) M nitroglycerin, in spite of the presence of 10(-4) M ethanol, ESR intensity increased from 0.124 +/- 0.23 in state 1 to 0.153 +/- 0.024 in state 4 (p less than 0.05). ESR intensity in state 1 was increased by the treatment of ethanol (p less than 0.05), whereas ESR intensity in state 4 was decreased (p less than 0.001), and these effects were prevented by nitroglycerin (p less than 0.05). The ratio of ESR intensity in state 4 to state 1 demonstrated more remarkably the effects of ethanol and nitroglycerin. Ethanol reduced the ratio from 1.65 +/- 0.47 in the control to 0.86 +/- 0.13 (p less than 0.001) and the reduction was prevented by nitroglycerin to 1.25 +/- 0.23 (p less than 0.01). It is concluded that nitroglycerin prevented the impairment of free radical formation of the mitochondria induced by ethanol, presumably by a mitochondrial membrane-stabilizing action.

Animals↗
PubMed1981

Effect of high plasma free fatty acids on the free radical formation of myocardial mitochondria isolated from ischemic dog hearts.

Effects of high plasma free fatty acids (FFA) on the free radical formation of myocardial mitochondria, isolated from normal and ischemic dog hearts, were studied by electron spin resonance (ESR) spectrometry. Free radical concentrations in state 4 respiration were used for the evaluation of the function in the mitochondria in this study. High plasma FFA levels were induced either by intravenous injection of Intralipid and heparin, or by infusion of norepinephrine. Ischemic hearts were induced by inserting a Cournand's 7F catheter into the left coronary artery under fluoroscopic control. Exogenous high plasma FFA induced by Intralipid and heparin caused the decrease of free radicals in state 4 respiration in the mitochondria isolated from normal and ischemic dog hearts. Endogenous high FFA induced by continuous infusion of norepinephrine also caused the decrease of free radicals. On the other hand, nicotinic acid prevented the decrease of free radicals as well as the rise of plasma FFA by the norepinephrine infusion. These results suggest that high plasma FFA itself, whether it may be exogenous or endogenous, may impair the oxidative phosphorylation of the mitochondria isolated from normal and ischemic hearts.

Animals↗
PubMed1981

Comparative coronary vasodilatory effects of nifedipine and niludipine.

Comparative coronary vasodilatory effects of nifedipine and niludipine were studied in normal anesthetized dogs. Nifedipine increased the coronary blood outflow by 142% at 2 min after administration of 10 micrograms/kg and the duration of the effect was over 30 min. On the other hand, niludipine increased the coronary blood outflow by 200% at 2 min after the injection of 25 micrograms/kg and the duration of the effect was over 60 min. Niludipine is a potent calcium antagonistic coronary vasodilator with less cardiodepressant effect than nifedipine. Both drugs are clinically useful as coronary vasodilators and hypotensive agents.

Animals↗
PubMed1980

Changes of cyclic AMP concentration to isoproterenol after abrupt cessation of propranolol in rats.

Because the mechanism of adverse reactions to abrupt cessation of propranolol in patients with coronary heart disease was an enigma, we studied the effect of cessation of propranolol on beta-adrenergic receptor reactivity to catecholamine stimulation. The cyclic AMP concentrations in plasma and left ventricular muscle after the administration of isoproterenol (5 mg/Kg) were measured in rats before, during, 2 days after, and 4 days after of the administration of propranolol (5 mg/Kg). Two days after withdrawal from propranolol, the cyclic AMP concentrations in plasma and left ventricular muscle were significantly increased (p less than 0.005, p less than 0.01). Four days after withdrawal from propranolol, the cyclic AMP concentration in plasma was significantly increased (p less than 0.001). On the other hand, that of left ventricular muscle showed a tendency to have higher value, although, this was statistically not significant. From these results, this study suports that there is a hypersensitivity to adrenergic stimultion after abrupt cessation of long-term propranolol treatment. The explanation of propranolol withdrawal phenomenon most likely lies in lthe nature of beta adrenergic receptors that become activated during long-term blockade.

Animals↗
PubMed1980

The effects of dilazep and SG 75 on cyclic nucleotides in the coronary artery.

We examined the effects of new long acting coronary vasodilators (dilazep and SG 75) on cyclic nucleotides in the coronary artery and the myocardium at the maximum coronary blood flow. The cyclic AMP concentrations in the anterior descending coronary artery after the injection of saline (control), SG 75 (0.2 mg/Kg), and dilazep (0.1 mg/Kg) were 229 +/- 20 pmole/Gm, 249 +/- 21 pmole/Gm, and 320 +/- 21 pmol/Gm, respectively. A significant increase above control values was found in the dilazep treated group (p less than 0.02). The cyclic GMP concentrations in the coronary artery after the injection of saline, SG 75, and dilazep were 35.6 +/- 4.4 pmole/Gm, 40.4 +/- 3.3 pmole/Gm, 35.3 +/- 3.2 pmole/Gm, respectively. There were no significant differences between them. The cyclic AMP and cyclic GMP concentrations in the left ventricular muscle did not significantly increase after the administration of dilazep and SG 75. Our findings showed that the mechanism of coronary vasodilating action of dilazep might be associated with an increased cyclic AMP in the coronary artery.

Adenosine↗
PubMed1980

Studies on myocardial mitochondria in ischemic dog hearts by electron spin resonance (ESR) spectrometry.

The free radical concentration of myocardial mitochondria from ischemic dog heart was studied by means of electron spin resonance (ESR) spectrometry, and the effects of acute free fatty acid (FFA) mobilization on the process of electron transport and oxidative phosphorylation of ischemic dog heart mitochondria were studied using free radical concentration in the state IV respiration of the myocardial mitochondria as the indicators. 1. The intensity of the ESR signal of mitochondria (g = 2.003) from intact dog heart was significantly increased in state IV compared to state I (state IV/state I = 2.01 +/- 0.18). On the other hand, in state III, the ESR intensity was markedly decreased compared to state IV (state III/state IV = 0.33 +/- 0.06). 2. The ESR intensity ratio of state IV/state I of the mitochondria from the ischemic area of 1-hr ischemic dog heart decreased remarkably compared to normal group. 3. The ESR intensity ratio of state IV/state I of the mitochondria isolated from the ischemic area of 2-hr ischemic dog heart was significantly lower than in the control. The ESR intensity ratio of state IV/state III of this group was significantly higher than in the control. 4. In ischemic heart with high plasma FFA, the free radical concentration in state IV respiration of the myocardial mitochondria was significantly decreased as compared to ischemic heart without high plasma FFA. These results suggest that the free radical concentration of myocardial mitochondria in respective respiratory states may be useful for evaluation of functional disturbance of oxidative phosphorylation and the electron transfer system in myocardial mitochondria in ischemic heart. Sudden and abnormal rise of plasma FFA seems to further facilitate the uncoupling of oxidative phosphorylation in the mitochondria of the ischemic portion of the heart.

Animals↗