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Biomedical subjects

N Yamazaki

Publications and source records attributed to N Yamazaki.

At least 235 records · Page 13Linked to original sources
PubMed1985

Antiarrhythmic and myocardial metabolic effects of verapamil during coronary artery reperfusion.

The accumulation of metabolic intermediates subsequent to impaired beta-oxidation of free fatty acids has been suggested to be a cause of cellular damage and ventricular arrhythmias in the ischemic heart. The effects of verapamil on ventricular arrhythmias and free fatty acids metabolism during coronary artery reperfusion in experimental dogs were evaluated over a period of 40 minutes and followed by reperfusion for 15 minutes. One tenth mg/kg/min of verapamil was administered for 5 minutes before occlusion and followed by an infusion of 0.01 mg/kg/min to the end of the experiment. Myocardial samples were obtained from both the non-ischemic and ischemic areas after coronary artery reperfusion and then ATP, free carnitine, long chain acyl carnitine and long chain acyl CoA were measured. In the control group, 3 dogs (27%) had ventricular fibrillation and 2 dogs (18%) had ventricular tachycardia during coronary occlusion. In addition, 2 dogs (25%) developed ventricular fibrillation after reperfusion. On the other hand, all 6 dogs treated with verapamil had neither ventricular fibrillation nor tachycardia during both coronary artery occlusion and reperfusion. ATP and free carnitine levels in the ischemic area were significantly higher in the verapamil group than in the control group (ATP: p less than 0.01, free carnitine: p less than 0.05), while long chain acyl carnitine levels in the ischemic area were significantly lower in the verapamil group than in the control group (p less than 0.01). However, there was no significant change in long chain acyl CoA levels between the control and verapamil groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Acyl Coenzyme A↗
PubMed1985

Effects of idebenone (CV-2619) on metabolism of monoamines, especially serotonin, in the brain of normal rats and rats with cerebral ischemia.

The effects of 6-(10-hydroxydecyl)-2,3-dimethoxy-5-methyl-1,4-benzoquinone (idebenone, CV-2619) on the contents, turnover, release and uptake of monoamines, especially serotonin (5-HT), in various brain regions of Wistar rats were studied in vivo and in vitro. In normal rats, an intraperitoneal (i.p.) dose of 100 mg/kg of CV-2619 had no significant effect on the levels of norepinephrine (NE), dopamine (DA) and their metabolites, and 5-HT in the brain regions examined, but it increased the levels of 5-hydroxyindole-3-acetic acid (5-HIAA), the main metabolite of 5-HT, in many brain regions. In rats with cerebral ischemia, a low dose (10 mg/kg, i.p.) of CV-2619 normalized the decreased levels of 5-HIAA in the cerebral cortex, hippocampus, diencephalon and brain stem. A 5-HT biosynthesis inhibitor, DL-p-chlorophenylalanine (PCPA, 150 mg/kg, i.p.), decreased the levels of 5-HT in all brain regions to one-third of the control levels 24 hr after administration in normal rats. CV-2619 (10, 30 or 100 mg/kg, i.p.), administered 24 hr after the treatment with PCPA, accelerated the PCPA-induced 5-HT decreases in the hippocampus, diencephalon and brain stem in a dose-dependent manner. In vitro CV-2619, like p-chloroamphetamine (PCA), stimulated 5-HT release from slices of the hippocampus and diencephalon. CV-2619 slightly inhibited and PCA markedly inhibited 5-HT uptake into hippocampal slices. The mechanism of the 5-HT releasing action of CV-2619 in hippocampal slices seems to be mediated through endogenous calcium. These results suggest that CV-2619 has an enhancing effect on the turnover of 5-HT in the hippocampus, diencephalon and brain stem of rats.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1985

Effect of nitroglycerin on left ventricular function in patients with ischemic heart disease.

To evaluate the effects of nitroglycerin on left ventricular function in 27 patients with ischemic heart disease, ejection fraction (EF) was measured every 1 to 5 min by a nuclear stethoscope after sublingual administration of nitroglycerin (0.3 mg). There was a good correlation between EF determined by the nuclear stethoscope and EF by left ventriculography (r = 0.80, p less than 0.001). EF showed a rise after sublingual nitroglycerin, which was most marked at 4 to 7 min and returned to the control level in 20 to 25 min. There were no significant differences in the maximum percent increase in EF among patients with 0, 1, 2 and 3 vessel disease. The maximum percent increases in EF were 34.0 +/- 10.0% in the normal contraction group, 24.0 +/- 8.5% in the hypokinesis group (p less than 0.05 vs the normal contraction group) and 15.2 +/- 8.5% in the akinesis group (p less than 0.01 vs the normal contraction group, p less than 0.05 vs the hypokinesis group). There was a weak correlation between the maximum percent increase in EF and the changes in heart rate (r = 0.49, p less than 0.05) and there was an inverse correlation between the maximum percent increase in EF and the changes in systolic blood pressure (r = -0.65, p less than 0.01). It was shown that the improvement in EF by sublingual nitroglycerin was greatest in the normal contraction group, somewhat less in the hypokinesis group and least in the akinesis group. The nuclear stethoscope is useful in monitoring changes in left ventricular function during intervention.

Adult↗
PubMed1985

Effects of pantethine on action potential of canine papillary muscle during hypoxic perfusion.

Pantethine, which is known to be converted to coenzyme A, has been reported to have antiarrhythmic action on experimental cardiac arrhythmias. Using standard microelectrode techniques, the electrophysiological effects of pantethine under hypoxic (95% N2 + 5% CO2) perfusion were studied. Hypoxia decreased resting membrane potential, action potential amplitude and maximum velocity of phase 0 and shortened action potential duration and effective refractory period. Application of pantethine 5 X 10(-3) Gm/ml under hypoxic perfusion prolonged action potential duration and effective refractory period significantly. Prolongation of action potential duration by pantethine might be caused by an increase in intracellular ATP. The findings in this study could be an explanation of the possible antiarrhythmic effects of pantethine.

Action Potentials↗
PubMed1985

Carnitine derivatives in hereditary cardiomyopathic animals.

BIO 14.6 Syrian hamsters and diabetic KK mice have been reported to develop hereditary cardiomyopathy spontaneously. In order to investigate the pathophysiological role of carnitine metabolism in hereditary cardiomyopathy, tissue levels of carnitine derivatives and the histology of the heart, liver and skeletal muscles from BIO 14.6 hamsters and KK mice were studied. Free carnitine levels in the heart of the BIO 14.6 hamsters (287.0 +/- 27.0 n mole/g wet tissue) were significantly lower than in the control group (348.8 +/- 83.8, p less than 0.05). Short chain acylcarnitine (197.0 +/- 56.0 n mole/g wet tissue) and total carnitine (667.6 +/- 136.4 n mole/g wet tissue) in the hearts of the BIO 14.6 hamsters were significantly lower than in the control group (short: 425.2 +/- 54.8, total: 1023.6 +/- 81.4, p less than 0.001). There was no significant difference in the levels of various carnitine derivatives of the liver and skeletal muscles from the BIO 14.6 hamsters and control hamsters. On the other hand, carnitine derivatives in KK mice did not change significantly compared with those in the heart, liver and skeletal muscles of the control mice. Histological findings showed that heart muscle degeneration and necrosis were found in both cardiomyopathic animals. Coagulative necrosis was found in both animals, whereas myocytolytic necrosis was found only in the BIO 14.6 hamsters. In KK mice, the right ventricle, especially tissue under the epicardium, was severely affected compared with the left ventricle. In the BIO 14.6 hamsters, however, lesions were scattered over both ventricles with a predilection for the left ventricle.

Animals↗
PubMed1985

[Effect of TRH and its analog DN-1417 on anoxia-induced amnesia in mice].

The effect of neuropeptides and their analogs on anoxia-induced amnesia was examined using one-trial passive avoidance task in mice. Anoxia, produced by the exposure to CO2 immediately after the acquisition of avoidance response, induced amnesia which is shown by a short latency to enter from the safety compartment into the shocked compartment in the retention test conducted 24 hr later. In these anoxia-treated animals, thyrotropin-releasing hormone (TRH: 10-20 mg/kg), its analog DN-1417 (10-20 mg/kg) and ACTH 4-10 (66 micrograms/body), which were given sc 15-60 min before the retention test, markedly prolonged the latency in a dose-dependent manner, indicating a reversal of the amnesia. Arginine- and lysine-vasopressin also reversed the amnesia at a dose of 100 micrograms/body. These results suggest that TRH and DN-1417, known to reverse the amnesia produced by the protein synthesis inhibitor cycloheximide, have ameliorating effects on the retrieval process of memory.

Adrenocorticotropic Hormone↗
PubMed1985

[Effect of idebenone on scopolamine-induced impairment of short-term memory in rats].

The effects of a novel compound, idebenone [6-(10-hydroxydecyl)-2, 3-dimethoxy-5-methyl-1, 4-benzoquinone] and cholinergic drug on short-term memory (STM) were studied in a delayed alternation task in rats. Rats were initially trained using a delayed alternation task in which a forced run to one arm of a T-maze was followed by a free-choice run. A correct free-choice response was defined as a turn toward the arm opposite to that in the forced run, and was rewarded with food pellets. When the time interval between the forced run and free-choice run was longer than 60 sec, the correct responses decreased by about 30% compared with that in no delay trials. After repeated training of the 60 sec-delayed alternation task, the effect of an anticholinergic drug scopolamine (0.1-0.5 mg/kg, ip) on the delayed alternation task was tested. The drug administered 20 min before the test significantly decreased the correct responses in a dose dependent manner. The effect of scopolamine (0.2 mg/kg, ip) was antagonized by the simultaneous administration of physostigmine (0.05-0.2 mg/kg, ip) in a dose dependent manner. Furthermore, physostigmine (0.1 and 0.2 mg/kg, ip) alone increased correct responses in the same task. Idebenone (3-30 mg/kg, ip), administered simultaneously with scopolamine, significantly improved the scopolamine-induced decrement of correct responses, with the highest efficacy at 10 mg/kg. The compound alone did not affect the number of correct responses. These results suggest that STM is closely related to the cholinergic system, and that idebenone may have an improving effect on the impairment of STM induced by a decreased cholinergic activity.

Animals↗
PubMed1985

[Serum and urinary tissue polypeptide antigen (TPA) in patients with urological cancer].

We measured the serum and urinary TPA in 64 patients with urological cancer, 55 patients with benign urological disease and 37 healthy volunteers. The serum TPA levels in patients with pre-treated cancer were significantly higher than those of healthy volunteers, but showed no significant difference compared to those in patients with a benign urological disease. The urinary TPA levels in patients with pre-treated cancer were significantly higher than those with a benign urological disease, but in some patients with urinary tract infection, very high urinary TPA concentrations were observed. Therefore, the determination of serum and urinary TPA may be useful in detecting urological cancer, but they were not specific tests. On the other hand, as lower serum and urinary TPA levels were observed after treatment of bladder and prostatic cancer, their determinations were considered to be useful in following up patients with these cancers.

Adolescent↗
PubMed1985

Anti-ulcer effect of 3-[p-(trans-4-aminomethylcyclohexylcarbonyl) phenyl] propionic acid hydrochloride (TEI-5103).

The anti-ulcer effects of the newly synthesized compound 3-[p-(trans-4-aminomethylcyclohexylcarbonyl)-phenyl]propionic acid hydrochloride (TEI-5103) on experimentally induced ulcers in rats were studied. TEI-5103 at doses of 25 to 400 mg/kg p.o. prevented formation of ulcers induced by serotonin, indomethacin, acetylsalicylic acid or stress (acute ulcer models), its effect being greater against gastric ulcers induced by serotonin. On acetic acid ulcer (chronic ulcer model), TEI-5103 at a daily dose of 200 mg/kg p.o. accelerated the healing of ulcers. TEI-5103 at doses of 100 to 400 mg/kg i.d. did not inhibit gastric acid secretion in pylorus-ligated rats. It markedly increased gastric blood flow in anesthetized rats (at 10-20 mg/kg i.v., measured by the aminopyrine clearance method), and also increased gastric blood flow in anesthetized dogs (at 2.5-10 mg/kg i.v., measured by the cross thermocouple method). These results indicate that TEI-5103 is effective as an anti-ulcer agent increasing gastric mucosal blood flow and possibly promoting the healing process of peptic ulcers.

Acetates↗
PubMed1984

Effect of clenbuterol, a new beta 2 selective adrenoceptor stimulant, on the release of histamine and SRS-A from passively sensitized guinea-pig chopped lungs.

Effect of clenbuterol on the release of histamine and SRS-A from passively sensitized guinea-pig lungs was studied in a superfused-cascade bioassay system, and compared with isoproterenol and salbutamol. One-week-old guinea-pig lungs were used, since histamine and SRS-A were released more in these than in 6- or 12-week old lungs during anaphylaxis. Clenbuterol, isoproterenol and salbutamol (10(-8) - 10(-7) M) were found to inhibit the releases of histamine and SRS-A. These actions were inhibited by propranolol. These results suggest that clenbuterol inhibits the releases of histamine and SRS-A via the beta-adrenoceptor.

Aging↗
PubMed1984

Effects of l-carnitine on action potential of canine papillary muscle during hypoxic perfusion.

Under hypoxic (95% N2 + 5% CO2) perfusion, electrophysiological effects of L-carnitine on canine papillary muscles were studied using standard microelectrode techniques. During hypoxic perfusion for 60 min, resting membrane potential (RMP), action potential amplitude (APA) and maximum upstroke velocity of phase 0 were decreased, and action potential duration (APD) and effective refractory period (ERP) were shortened. Application of L-carnitine 25 mM under hypoxic perfusion increased RMP and APA and prolonged APD and ERP significantly. As effects of L-carnitine during hypoxic perfusion might be that of hypertonicity, effects of sucrose of the same tonicity as L-carnitine were studied under hypoxia. Sucrose did not cause significant changes on various parameters of action potential compared with hypoxic perfusion. It was suggested that the increase in RMP, and the prolongation of APD and ERP might be caused by an increase in intracellular ATP content. The findings in this study could be an explanation of possible antiarrhythmic effects of L-carnitine.

Action Potentials↗
PubMed1984

Effect of palmitoyl carnitine on Na+, K+-ATPase and adenylate cyclase activity of canine myocardial sarcolemma.

The accumulation of long chain of acyl carnitine, which is thought to exaggerate myocardial ischemic damage, has been demonstrated in ischemic myocardium. The purpose of this study was to determine the effect of palmitoyl carnitine on the Na+, K+-ATPase and adenylate cyclase activity of myocardial sarcolemma in vitro. Controversial views exist at present regarding the effect of palmitoyl carnitine on Na+, K+-ATPase. Wood et al. [23] observed that palmitoyl carnitine inhibited the activity of Na+, K+-ATPase but this inhibition was not observed by Owens et al. [17]. We did observe an inhibition of Na+, K+-ATPase by palmitoyl carnitine. The 50% inhibition of the maximum activity was observed at a palmitoyl carnitine concentration of 110 microM and complete inhibition at 160 microM. Adenylate cyclase activity was inhibited by palmitoyl carnitine irrespective of the assay conditions. The (isoproterenol + GTP)-stimulated activity, fluoride-stimulated activity and basal activity with Mg-ATP or Mn-ATP as a substrate were all inhibited though to varying degrees. The 50% inhibition of adenylate cyclase activity was observed at 84 microM, 94 microM, 200 microM and 105 microM of palmitoyl carnitine in the above mentioned order. The inhibition curve showed a shoulder or even a peak at about 75 microM of palmitoyl carnitine. It is suggested that elevated levels of palmitoyl carnitine in ischemic myocardium may play a role in inhibiting sarcolemmal function.

Adenylyl Cyclase Inhibitors↗
PubMed1984

Effects of glucose-insulin-potassium solution on free fatty acid metabolism in ischemic myocardium.

The accumulation of intermediates subsequent to impaired oxidation of free fatty acids has been suggested as a cause of cellular damage in ischemic myocardium. Many reviews have supported the theory that glucose-insulin-potassium (GIK) solution has a beneficial effect on the ischemic myocardium. We evaluated the effects of GIK solution on intermediates of free fatty acid metabolism in ischemic myocardium. The left coronary artery was occluded for 40 minutes in twelve dogs. In six dogs, 10 minutes before coronary artery occlusion, GIK solution (50 percent of glucose, 50 units/liter of regular insulin, 50 mEq/liter of potassium) was given at the rate of 0.1 ml/kg per minute until the time of excision of the heart. In the ischemic area, adenosine triphosphate (ATP) level in the GIK group (3.80 +/- 1.34 mumole/g) was significantly higher than that in the control group (2.04 +/- 0.68, p less than 0.05). The free carnitine level was significantly increased was GIK in both ischemic and nonischemic areas (p less than 0.05). In the control group, the long chain acyl coenzyme A (CoA) level in the ischemic area (23.0 +/- 7.0 nmole/g) was significantly higher than that in the nonischemic area (17.1 +/- 3.5, p, less than 0.05). On the other hand, GIK prevented the increase in the long chain acyl CoA in the ischemic area (17.8 +/- 5.6). This study suggests that GIK has a protective effect on ischemic myocardium, probably by preventing the accumulation of long chain acyl CoA by improving free fatty acid metabolism.

Acyl Coenzyme A↗
PubMed1984

[Physiological and biochemical study of temporary cerebral ischemic rats produced by bilateral vertebral and carotid artery occlusion].

We investigated the changes of behavioral, electrophysiological and biochemical parameters during and after global cerebral ischemia in rats. Global cerebral ischemia was produced by the temporary occlusion of both common carotid arteries 24 hr after the permanent electrocauterization of bilateral vertebral arteries. Just before recirculation following 10 or 30 min of cerebral ischemia, loss of righting reflex, flattenning of cortical EEG activity, and detrimental decrease of ATP content and marked increase of lactate content in the cerebrum were observed. The alterations of all parameters completely recovered within 60 min after recirculation in 10-min cerebral ischemic rats. However, the 30-min cerebral ischemic rats showed almost no recovery after recirculation, suggesting that some irreversible damages are produced in the cerebrum of the 30-min ischemic rat. On the other hand, it was found that the auditory brain stem evoked response (ABER) and ATP content in the pons plus medulla were only slightly affected by the ischemic procedure, which indicates that the ischemic damages do not ensue in the lower part of the brain stem.

Animals↗