Biomedical subjects
Publications and source records attributed to Y Abiko.
The effect of indomethacin, which is a nonsteroidal anti-inflammatory drug, on Ca2+-stimulated adenosine triphosphatase (Ca2+-ATPase) activity in the microsomes of rat submandibular gland was investigated. The effect of aspirin on Ca2+-ATPase activity was also studied.
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The effect of pretreatment with verapamil (100 micrograms/kg i.v.) or nifedipine (10 micrograms/kg i.v.) on ischemic myocardial metabolism was studied in dogs anesthetized with pentobarbital. The results are summarized as follows: 1. Verapamil or nifedipine lowered both systolic and diastolic blood pressures markedly, and increased heart rate slightly. 2. Verapamil or nifedipine increased both endo- and epicardial phosphorylase activities significantly. 3. Coronary artery ligation increased the phosphorylase activity, and also increased the levels of glucose-6-phosphate, fructose-6-phosphate, and lactate, and decreased the levels of glycogen, fructose-1,6-diphosphate, and phosphocreatine in both endo- and epicardial layers, without affecting the level of the endo- and epicardial adenosine triphosphate. 4. In the presence of verapamil or nifedipine, coronary artery ligation did not increase but decreased the phosphorylase activity that had been increased by verapamil or nifedipine alone. 5. Changes in the levels of intermediates induced by coronary artery ligation were not markedly influenced by pretreatment of the dog with verapamil or nifedipine.
The effect of pretreatment with ouabain (40 microgram/kg, i.v.) on myocardial metabolic and contractile responses to regional ischemia induced by coronary artery ligation was studied in the canine left ventricle. In control dogs, ischemia increased activity of phosphorylase a and the levels of glucose-6-phosphate and lactate, and decreased the levels of glycogen and phosphocreatine, without affecting the levels of adenosine triphosphate, adenosine diphosphate, and adenosine monophosphate (AMP). Ouabain increased the activity of phosphorylase a. In ouabain-treated dogs, ischemia did not further increase the phosphorylase a activity but it increased the epicardial AMP level. Other metabolic responses to ischemia in ouabain-treated dogs were similar to those in control dogs. In control dogs, myocardial contractile force decreased by about 10% after ischemia, but blood pressure and heart rate remained unchanged. Ouabain increased contractile force by about 32%. In ouabain-treated dogs, ischemia decreased contractile force by about 54% without affecting blood pressure and heart rate. It is concluded that ouabain increases the activity of the myocardial phosphorylase a and that the inotropic action of ouabain can be nullified by coronary artery ligation.
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In control rats, the arsenic level in the spleen and blood cells was 1.59 and 10.79 microgram/g wet tissue, respectively. In the kidney, lung, heart, brain, and hair, the arsenic level was lower than 1.1 microgram/g wet tissue. In rats in which a pellet containing 2 mg of arsenic tsioxide was implanted subcutaneously, the arsenic level in the spleen and blood cells was markedly high for at least 2 months after implantation; after 67 days of implantation, the arsenic level in the spleen and blood cells was 16.79 and 66.34 microgram/g wet tissue, respectively. In the kidney, liver, lung, heart, brain, and hair, the increase in arsenic after implantation was smaller than that in the spleen. In the plasma, arsenic was not detected before and after arsenic implantation. It is concluded that arsenic implanted subcutaneously concentrates in the blood cells, possibly in the red cells, in rats.
The effect of coronary artery ligation on myocardial glyocogenolysis was studied in the endo- and epicardial layers of the left ventricle in dogs pretreated with saline or 1 mg/kg of propranolol. Coronary artery ligation was performed by ligating one of the small branches of the left anterior descending coronary artery. Even after coronary artery ligation, neither increase in phosphorylase activity nor breakdown of glycogen was observed in both layers of ischemic region of myocardium in propranolol-pretreated dogs. These results indicate that pretreatment with propranolol inhibits the increase in glycogenolysis being caused by coronary artery ligation. Propranolol howefer, did not inhibit completely the coronary artery ligation-induced increase in glucose 6-phosphate and lactate and decrease in phosphocreatine in the myocardium, especially in the endocardial layers.
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The subcellular distribution of calcium-stimulated adenosine triphosphatase in the albino rabbit dental pulp was studied. The purity of the microsomal fraction was examined by measuring the marker enzymes and by electron microscopic observation. Some properties of calcium-stimulated adenosine triphosphatase were investigated.
Effects of coronary artery ligation on myocardial glycogenolysis were studied in the endo- and epicardial layers of the left ventricular wall in dogs pretreated with 10 or 100 microgram/kg (i.v.) of carteolol, a potent beta-adrenergic blocking agent. Coronary artery ligation was performed by ligating one of the small branches of the left anterior descending coronary artery. In control (saline-pretreated) dogs, an increase in phosphorylase alpha activity and an increase in breakdown of glycogen were observed in both endo- and epicardial layers after coronary artery ligation. In the presence of 10 or 100 microgram/kg of carteolol, however, increases in phosphorylase alpha activity and increase in breakdown of glycogen were not observed in either the endo or epicardial layers. These results indicate that pretreatment of the dog with carteolol inhibits the increase in glycogenolysis caused by coronary artery ligation. Nevertheless, carteolol did not completely inhibit the coronary artery ligation-induced increase in glucose-6-phosphate and lactate levels, and the coronary artery ligation-induced decrease in phosphocreatine level, particularly in the endocardial layers.
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The effect of long-term ingestion of an anabolic steroid, furazabol, was studied on coagulo-fibrinolytic systems in the rat. During the administration of furazabol at the daily dose of 0.04, 0.2 or 1 mg/rat for 3 months, the most remarkable changes were increase in the plasminogen activator activity in blood and the lung tissue and decrease in plasma fibrinogen level as well as decrease in plasma cholesterol. It was a very important finding that in most of the rats the furazabol treatment was effective in reducing susceptibility to lactic acidosis-induced pulmonary thrombosis. No meaningful changes were observed in other parameters tested including ADP-induced platelet aggregability, plasma recalcification time, plasma plasminogen, plasma antiplasmin activity, plasminogen activator content of tissues other than the lungs and the release of vascular activator induced by venous occlusion. One month after cessation of the furazabol treatment, these altered parameters tended to return to normal. Independently on the furazabol treatment, highly significant positive correlation existed between the plasma activator activity and the pulmonary tissue activator content. This indicated that the major source of plasma activator in the rat was the lung tissue and that the furazabol treatment increased the circulating activator activity through enhancing activator content in the lungs.
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The respiratory effect of dog myocardial mitochondria was studied by measuring oxygen content in a reaction chamber using Garbani electrode. 1) In normal dog mitochondria, oxygen consumption rate (QO2) in state 3 and state 4, respiratory control ratio (RCR) and ADP/O ratio were not different between the inner and outer layers when glutamate or succinate was used as substrate. 2) Thirty min after the occlusion of one of the small branches of the anterior descending artery, there were no differences in the respiratory effects between the inner and outer layers when glutamate or succinate was used as substrate. HOowever, compared with the normal dog mitochondria, ADP/O ratio, QO2 in state 3 and state 4 were lower in the outer layer and QO2 in state 4 was lower in the inner layer when succinate was used as substrate. 3) When the anterior descending branch was narrowed to decrease the blood flow to about a half, the respiratory effects were not different between the inner and outer layers when succinate was used as substrate. However, ADP/O ratio in the outer layer was lower than that of the normal dog. 4) Nitroglycerin had no effect on the respiratory effects either in vitro (1.63 X 10(-6) M, succinate as substrate) or in vivo (20 mug/kg i.v., glutamate as substrate.) 5) Dipyridamole had no effect on the respiratory effects in vivo (250 mug/kg, i.v., glutamate as substrate) but, ADP/O ratio in the outer layer was diminished in vitro (7.34 X 10(-6) M, succinate as substrate).
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