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Biomedical subjects

Y Abiko

Publications and source records attributed to Y Abiko.

At least 235 records · Page 13Linked to original sources
PubMed1987

Effects of nicorandil and other antianginal drugs on myocardial pH in the ischemic dog heart.

The effects of nicorandil and other antianginal drugs on the pH of ischemic myocardium were examined in dogs anesthetized with pentobarbital. The myocardial pH was measured with a micro glass pH electrode placed in the inner layers of the area of myocardium perfused by the left anterior descending coronary artery (LAD). The myocardium (LAD area) was made ischemic by partially occluding the LAD so that only about one-third of the normal blood flow was allowed to perfuse the tissue. The period of LAD occlusion was 90 min. By 30 min, the partial occlusion had produced a decrease in myocardial pH (about 0.5 U) which lasted until the end of occlusion. The acidosis in the myocardium induced by LAD partial occlusion was metabolic acidosis. The experimental drugs were injected intravenously 30 min after the LAD was occluded. Nicorandil (50 micrograms/kg), nitroglycerin (20 micrograms/kg), and diltiazem (100 micrograms/kg) moderately restored the myocardial H+ concentrations induced by LAD occlusion; propranolol (1 mg/kg) and sotalol (5 mg/kg) markedly restored these concentrations. It was concluded that all five experimental drugs improved ischemic myocardium; nicorandil, nitroglycerin, and diltiazem only moderately counteracted the increased myocardial H+ concentrations produced by LAD occlusion, whereas propranolol and sotalol markedly returned myocardial pH close to normal levels.

Acidosis↗
PubMed1987

Inhibition of ischemia-induced subcellular redistribution of lysosomal enzymes in the perfused rat heart by the calcium entry blocker, diltiazem.

Effect of diltiazem on subcellular distribution of lysosomal enzymes, high-energy phosphate metabolism and mechanical function in the ischemic heart was studied. Ischemia was induced by lowering the afterload pressure of the perfused working rat heart. The activities of cathepsin D, beta,N-acetylglucosaminidase and acid phosphatase were determined in the nonsedimentable and sedimentable fractions after centrifugation of the tissue extract to assess the subcellular distribution of lysosomal enzymes. After ischemia, decreases in the mechanical function and the tissue level of high-energy phosphates were observed. In addition, ischemia caused subcellular redistribution of lysosomal enzymes from the lysosomes to the cytoplasm. Reperfusion of the ischemic heart did not restore the mechanical function and the level of high-energy phosphates completely. Diltiazem (2.21 X 10(-6), 1.11 X 10(-5) and 2.21 X 10(-5) M) was provided for the heart 5 min before the onset of ischemia. Diltiazem preserved high-energy phosphates in the ischemic heart, and inhibited the subcellular redistribution of lysosomal enzymes being caused by ischemia, depending on its concentration. Reperfusion after ischemia with diltiazem recovered the mechanical function that had been decreased by ischemia. These results may indicate that diltiazem can protect the myocardium against ischemic damage.

Acetylglucosaminidase↗
PubMed1987

Effect of lidocaine on the myocardial acidosis induced by coronary artery occlusion in dogs.

The effect of lidocaine on ischemic myocardial acidosis was investigated in the dog heart, in which the left anterior descending coronary artery was occluded to reduce to about one-third (partial occlusion). Myocardial pH (MpH) was measured by means of a micro glass pH electrode. MpH before partial occlusion was 7.52 to 7.66. Partial occlusion decreased the left anterior descending coronary artery flow by 49 to 68%, MpH by 0.58 to 0.76 and myocardial contractile force by 26 to 43%, and increased ST segment (surface electrocardiogram) by 3.2 to 11.7 mV. Lidocaine (injected i.v. 30 min after partial occlusion) decreased heart rate, blood pressure and myocardial contractile force, and attenuated the decrease in MpH during ischemia. Lidocaine in doses of 2, 5 and 10 mg/kg restored the myocardial [H+], that had been increased by partial occlusion, by 23, 38 and 50%, respectively. Even in the paced heart, lidocaine (10 mg/kg) attenuated the myocardial acidosis, although the degree of attenuation was smaller (36%). Partial occlusion elevated the ST segment even in the presence of 5 or 10 mg/kg of lidocaine. In the nonischemic heart, however, lidocaine (2, 5 or 10 mg/kg) did not change in MpH. It is concluded that lidocaine attenuates the myocardial acidosis during ischemia, and the primarily important mechanism of pH attenuation is not a decrease in heart rate.

Acidosis↗
PubMed1986

Effect of sixth component of complement on the prostaglandin E1 stimulated adenyl cyclase activity in rat calvaria.

Human serum enhanced the PGE1 stimulated adenyl cyclase activity in membrane rich fraction of rat calvaria, but heated serum did not. Human C6 enhanced the PGE1 stimulated adenyl cyclase activity. C6 did not enhance the PTH stimulated adenyl cyclase activity. The enhancement of the PGE1 stimulated adenyl cyclase activity with C6 was due to increasing Vmax. The enhancement of the enzyme activity with C6 was significantly inhibited with anti-C6 antibody. Adenyl cyclase was not activated with C6 alone.

Adenylyl Cyclases↗
PubMed1986

Protective effect of diltiazem on ultrastructural alterations induced by coronary occlusion and reperfusion in dog hearts.

This study was designed to examine whether diltiazem, a calcium channel-blocker, inhibits the cardiac ultrastructural alterations induced by coronary occlusion with or without reperfusion, in dogs anesthetized with pentobarbital. The left anterior descending coronary artery (LAD) was completely occluded for 60 min with or without reperfusion (induced by release of occlusion) for 20 min. Coronary occlusion increased ST segment in the ischemic area, and also produced typical ultrastructural alterations including decreased glycogen granules, destruction of mitochondria, and margination of the nuclear chromatin, especially in the subendocardium. Reperfusion of the ischemic area resulted in more severe alterations of the myocardial ultrastructure, including many myofibrillar contraction bands. Diltiazem was injected intravenously at the dose of 200 micrograms/kg (bolus injection) 20 min before LAD occlusion, and was then infused intravenously at the rate of 80 micrograms/kg/min for 10 min starting at the beginning of LAD occlusion, the total dose being 1 mg/kg. Diltiazem decreased heart rate and diastolic blood pressure, inhibited the increase in ST segment, and also inhibited the ultrastructural alterations induced by coronary occlusion, regardless of reperfusion. A bolus injection of diltiazem alone (200 micrograms/kg), however, did not inhibit markedly the ultrastructural alterations induced by coronary occlusion, regardless of reperfusion. It is concluded that the large dose of diltiazem (1 mg/kg) protects the myocardium from ischemic injury.

Animals↗
PubMed1986

Attenuation by isosorbide dinitrate of coronary occlusion-induced acidosis in the dog myocardium.

In dogs anaesthetized with pentobarbitone, the thorax was opened and myocardial pH measured continuously by the use of a glass pH electrode inserted in the left ventricular wall. The left anterior descending coronary artery (LAD) was partially occluded so that the LAD flow could be reduced to a half or one-third of the original flow (partial occlusion). LAD partial occlusion was continued for 90 min, drug or saline being infused for the last 60 min of this period. LAD occlusion decreased myocardial pH significantly by 0.41 to 0.67 pH units, and increased ST segment of the surface electrocardiogram from 11.7 to 12.1 mV. In dogs with non-ischaemic normal hearts, isosorbide dinitrate (ISDN; 1 mg kg-1) did not change markedly either the LAD flow, myocardial pH or heart rate, whereas it decreased myocardial contractile force (determined by a strain gauge arch) slightly and both the systolic and diastolic blood pressure markedly. In dogs with partial LAD occlusion, ISDN (1 mg kg-1) increased myocardial pH significantly and decreased blood pressure, but did not change ST segment elevation in an epicardial lead. These results indicate that ISDN attenuates ischaemia-induced acidosis without attenuating ischaemia-induced ST elevation in the dog myocardium.

Acidosis↗
PubMed1986

Inhibitory effect of trimetazidine on utilization of myocardial glycogen during coronary ligation in dogs.

The left anterior descending coronary artery (LAD) of the dog was ligated completely for 1.5 min, and immediately after LAD ligation the heart was taken for determination of the glycogen phosphorylase and glycogen. Trimetazidine was injected intravenously 20 min before LAD ligation. LAD ligation increased the activity of glycogen phosphorylase and decreased the level of glycogen in both ischemic (LAD) and nonischemic (circumflex) areas. Trimetazidine at the dose of 0.3 or 1.0 mg/kg, being the dose that did not affect blood pressure and heart rate markedly, inhibited the ischemia-induced changes in glycogen phosphorylase and glycogen level. It is concluded that trimetazidine inhibits the ischemia-induced increase in the utilization of glycogen in the dog myocardium.

Animals↗
PubMed1986

Effect of xamoterol, a beta 1-adrenoceptor partial agonist, on myocardial pH decreased by coronary occlusion in dogs.

The effect of xamoterol on ischemic myocardial pH was examined in dogs. Partial occlusion of the left anterior descending coronary artery (LAD) decreased myocardial pH from 7.52-7.63 to 6.80-6.85. Xamoterol was injected intravenously 30 min after LAD occlusion that lasted for 90 min. Xamoterol (30 or 70 micrograms/kg) increased the myocardial pH that had been decreased by partial occlusion, the degree of pH increase being greater with 30 micrograms/kg than with 70 micrograms/kg, but at the dose of 200 micrograms/kg it did not increase. In the nonischemic normal heart, xamoterol (30 or 70 micrograms/kg, i.v.) had no marked effect on hemodynamic parameters, but the drug (200 micrograms/kg, i.v.) increased contractile force and heart rate with a transient decrease of myocardial pH. It is concluded that only the small dose (30 or 70 micrograms/kg) of xamoterol is effective in restoring the myocardial pH that has been decreased by partial occlusion of the LAD.

Adrenergic beta-Agonists↗
PubMed1986

Functional and metabolic responses to ischemia in the perfused heart isolated from normotensive and spontaneously hypertensive rats.

The difference between normotensive rats (WKY) and spontaneously hypertensive rats (SHR) in functional and metabolic responses to ischemia was studied. Systolic arterial blood pressure of SHR (171.2 +/- 2.9 mmHg) was significantly higher than that of WKY (135.3 +/- 1.2 mmHg), and the left ventricular mass of SHR was larger than that of WKY. Hearts isolated from either WKY or SHR were perfused by the working heart technique. Ischemia was induced by lowering the afterload pressure of the working heart. Ischemia produced cardiac arrest, and decreased the tissue levels of adenosine triphosphate and creatine phosphate in both WKY and SHR. Recovery of mechanical function of the heart during reperfusion following ischemia in SHR was better than that in WKY, while recovery of the high-energy phosphates level in SHR was less prominent than in WKY. It is postulated that hypertension has a deleterious effect on myocardial energy metabolism in ischemic heart, even when cardiac mechanical function is maintained.

Adenosine Triphosphate↗
PubMed1986

Mode of action of probucol in reducing serum cholesterol in mice.

The mode of action of probucol in reducing serum cholesterol was studied in normal and cholesterol-fed mice. Probucol did not affect intestinal absorption of radioactive cholesterol in normal and cholesterol-fed mice. In normal mice, probucol treatment resulted in inhibition of incorporation of [14C]-acetate into cholesterol in the liver, while it stimulated the incorporation in the small intestines. Incorporation of [14C]-mevalonate into cholesterol was not affected by the treatment. These results were consistent with the finding that the HMG-CoA reductase activity was decreased in the liver, but increased in the intestinal tissues of the treated mice. In cholesterol-fed mice, probucol treatment had no effect on cholesterol synthesis in the liver, while it increased the intestinal cholesterol synthesis. The over-all effect of this drug on cholesterol synthesis was not significant, although it tended to be inhibitory in normal mice and stimulatory in cholesterol-fed mice. On the other hand, probucol treatment resulted in acceleration of the clearance of [14C]-cholesterol-derived radioactivity from the circulation and resulted also in a significant increase in fecal excretion of the radioactivity, cholesterol and bile acids without changes in lipid composition of the bile. Cholesterol content in and radioactivity distribution among the tissues were not affected by probucol. Hepatic cholesterol 7 alpha-hydroxylase activity was increased by probucol. These findings indicate that probucol lowers serum cholesterol mainly by increasing catabolic excretion of cholesterol into bile.

Animals↗
PubMed1986

Myocardial ischemia stimulates catecholamine synthesis and catabolism in the dog adrenal medulla.

The effects of regional ischemia of the myocardium upon metabolism and catabolism of catecholamines were studied in the dog adrenal medulla. Regional ischemia was induced by ligating a small branch of the left anterior descending coronary artery for 1 or 24 hours. Sham-operated controls were run in parallel. Coronary ligation for 24 hours resulted in a decrease in the level of epinephrine and an increase in the level of dopamine in the adrenal medulla, and also resulted in an increase in the activities of the phenylethanolamine-N-methyltransferase (PNMT), monoamine oxidase, and catechol-O-methyltransferase. The results after coronary ligation for 1 hour were essentially the same as those after coronary ligation for 24 hours, except that the activity of PNMT decreased. These results suggest that both synthesis and catabolism of catecholamines in the adrenal medulla are accelerated during coronary ligation for a period of 1 to 24 hours.

Adrenal Medulla↗
PubMed1986

A method for evaluating antianginal drugs in experimental animals: assessment of myocardial ischemia by myocardial pH.

This paper describes a method by which antianginal drugs can be evaluated in the dog heart in situ. Myocardial pH was measured continuously by a micro glass pH electrode inserted in the left ventricular endocardial layers of the dog anesthetized with pentobarbital. Occlusion of the left anterior descending coronary artery (LAD) decreased myocardial pH, and release of the LAD restored the pH. The myocardial acidosis induced by ischemia was metabolic in nature and accompanied by a decrease in the levels of adenosine triphosphate and creatine phosphate and an increase in the levels of lactate in the myocardium. Drugs were injected intravenously 30 min after incomplete (partial) occlusion ot the LAD, lasting until 60 min after drug injection. Propranolol, atenolol, and sotalol markedly attenuated the myocardial pH that had been decreased by LAD occlusion. Nitroglycerin, diltiazem, and nicorandil also attenuated the pH, but these drugs were less active in attenuating myocardial acidosis. Dipyridamole, nifedipine, and beta-2 adrenoceptor antagonists were least active in this regard. It is concluded that myocardial pH can be used as an indicator of myocardial regional ischemia and utilized for evaluation of antianginal drugs.

Acidosis↗
PubMed1986

Nifedipine increases oxygen saturation level of myoglobin in the rat heart during hypoxia.

Rat hearts were perfused by means of the Langendorff's technique and paced at 150/min. Oxygen saturation level of myocardial myoglobin was measured continuously according to an optical method, by which the intracellular oxygen level in the myocardial cells can be monitored continuously. Krebs-Henseleit solution was bubbled with a gas mixture containing either 95% O2 + 5% CO2 (high oxygen solution) or 95% N2 + 5% CO2 (anoxic solution), or both (low oxygen solution). Hypoxia was produced by changing the perfusion fluid from high to low oxygen solution. After 10 min of hypoxia, drugs were infused into the inflow tube at a rate of 0.1 ml/min for 10 min. Hypoxia increased coronary flow by about 25%, decreased oxygen saturation level of myoglobin by 23.1-35.7%, without a marked change in left ventricular pressure. Nifedipine (1.0 microgram/ml) increased oxygen saturation level, which had been reduced by hypoxia, by 16-27%. Nifedipine at the concentration of 0.1 microgram/ml also increased the oxygen saturation level of myocardial myoglobin slightly, but at the concentration of 10 micrograms/ml it decreased. Nitroglycerin (100 micrograms/kg) increased the oxygen saturation level, which had been decreased by hypoxia, by 6-8%, whereas dipyridamole (100 micrograms/ml) did not. It is concluded that nifedipine as well as nitroglycerin can increase the oxygen saturation level of myocardial myoglobin during hypoxia, suggesting that both drugs may increase the intracellular oxygen tension in the hypoxic heart.

Animals↗
PubMed1986

Effect of nifedipine and niludipine on myocardial pH in the ischemic canine heart.

The effect of nifedipine and niludipine on ischemic myocardial pH was studied. To make the myocardium ischemic (60% reduction of coronary flow), the left anterior descending coronary artery (LAD) was partially occluded 30 min before either vehicle (1% ethanol solution) or drugs were injected intravenously. In the non-occlusion group, nifedipine (10 micrograms/kg) and niludipine (10 micrograms/kg) increased coronary flow, decreased blood pressure, and did not change myocardial pH appreciably. In the partial occlusion group, reduction of coronary flow decreased the myocardial pH, increased ST segment, and did not change heart rate and blood pressure. Vehicle was injected 30 min after the occlusion, but did not change any of the parameters. A small dose (1 microgram/kg) and a large dose (10 micrograms/kg) of nifedipine, and niludipine (10 micrograms/kg) did not exert any beneficial effect on the myocardial pH, coronary flow and the ST segment during coronary occlusion.

Animals↗