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Biomedical subjects

M Tada

Publications and source records attributed to M Tada.

At least 487 records · Page 27Linked to original sources
PubMed1987

Altered lipoxygenase metabolites and leukocyte involvement in an acute occlusion-reperfusion model of canine myocardial infarction.

We compared amounts of lipoxygenase products with the extent of leukocyte infiltration in the ischemic myocardium with an occlusion-reperfusion model of open-chest dog. Changes in peripheral leukocyte count and leukocyte function estimated by neutrophil aggregation induced by calcium ionophore A23187 were also examined. The ischemic tissue (120 +/- 40 ng/g, mean +/- SEM) showed a marked increase in 12-hydroxyeicosatetraenoic acid (HETE) production compared with the normal tissue (13 +/- 1 ng/g, p less than 0.01). The production of 5-HETE in the ischemic tissue was also augmented as well. When we examined the correlation between production of either 12-HETE or 5-HETE and leukocyte infiltration in the ischemic tissue, the former was augmented markedly in proportion to the extent of the latter. Leukocyte count in peripheral circulation was gradually increased after reperfusion. Similarly, neutrophil aggregation was significantly augmented during reperfusion. These results indicate that production of lipoxygenase metabolites associated with leukocyte infiltration in the reperfused ischemic tissue was increased during the course of myocardial infarction, which was accompanied by activation of leukocyte in peripheral circulation. Further studies should be done to clarify the importance of lipoxygenase metabolites in the evolution of reperfusion-induced myocardial injury.

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗
PubMed1987

Thromboxane A2 as an enhancing factor of coronary vasospasticity in variant angina.

To clarify the role of thromboxane A2 (TXA2) in evoking coronary spasm, we compared coronary arterial spasticity induced by ergonovine maleate (EM) with coronary sinus thromboxane B2 (TXB2: a stable catabolite of TXA2) in 34 patients with documented variant angina and 11 patients with chest pain syndrome (CPS). We also examined the effect of OKY-1581 (8 mg/kg, i.v.), a TXA2 synthetase inhibitor, on the coronary arterial spasticity of these patients. When blood samples were taken from coronary sinus just before EM test, all patients with variant angina exhibiting markedly augmented TXB2 levels (424 +/- 138 pg/ml), had positive EM test results, while CPS exhibiting lower TXB2 levels (223 +/- 38 pg/ml), had negative EM test. We found that the amounts of EM needed to induce coronary spasm were inversely correlated with TXB2 levels in coronary sinus. In 7 out of these 8 patients, OKY-1581 was found to attenuate the increased spasticity with reduction of coronary sinus TXB2 levels. In 3 patients, an EM rechallenge at symptomatically quiescent stage resulted in negative test with augmented TXB2 levels being markedly decreased. These findings indicate that increased TXA2 in circulating plasma is closely correlated with the hypersensitivity of coronary arteries to EM in patients with variant angina, suggesting a possible role of augmented TXA2 production in the enhancement of coronary vascular spasticity.

Adult↗
PubMed1987

The effect of dilazep on puromycin-induced rat renal mitochondrial dysfunction.

The effect of tetrahydro-1 H-1,4 (5H)-dipropanol bis(3,4,5-trimethoxybenzoate)hydrochloride monohydrate (dilazep, Comelian) on puromycin-induced rat renal damage was investigated. In vivo study: Rats were divided into 3 groups, the control group; untreated, the puromycin group; puromycin (150 mg/kg) was injected intraperitoneally once, the dilazep + puromycin group; puromycin (150 mg/kg) was injected 1 h after intraperitoneal dilazep injection (2 mg/kg), and dilazep (2 mg/kg) was injected every 12 h until the end of the experiment. In each group, 84 h after puromycin injection, kidneys were isolated and renal mitochondria were prepared. The endogenous phospholipase activity in kidney homogenate was determined by high performance liquid chromatography. The activities of three segments (NADH-cytochrome c reductase, succinate-cytochrome c reductase and cytochrome c oxidase) of the electron-transport chain in mitochondria were measured enzymatically. In the puromycin group, phospholipase activity was increased and activities of all of three segments of the electron-transport chain were decreased. In the dilazep + puromycin group, premedication with dilazep prevented activation of phospholipase and maintained mitochondrial electron-transport activity. In vitro study: Mitochondria prepared from intact rat kidney were incubated with phospholipase C. Activities of the mitochondrial electron-transport chain were deteriorated by phospholipase C. These results indicated that activation of endogenous phospholipase, which digests membrane phospholipids, essential components in maintaining mitochondrial electron-transport activity, is responsible for the puromycin-induced renal damage. Premedication with dilazep prevented the damage by inhibition of the activation of phospholipase.

Animals↗
PubMed1986

Formation of 8-hydroxyguanine residues in cellular DNA exposed to the carcinogen 4-nitroquinoline 1-oxide.

8-Hydroxyguanine (8-OH-Gua) residues were formed in DNA of Ehrlich ascites cells exposed to the carcinogen 4-nitroquinoline 1-oxide. Formation of 8-OH-Gua was confirmed by chemical treatment of calf thymus DNA with the proximate metabolite of this carcinogen, 4-hydroxyaminoquinoline 1-oxide, together with seryl-adenosine monophosphate. The ratio of the rates of formations of 8-OH-Gua and the quinoline-bound adducts was about 0.2-0.3. A conceivable mechanism of formation of 8-OH-Gua is proposed.

4-Hydroxyaminoquinoline-1-oxide↗
PubMed1986

Characterization of structural unit of phospholamban by amino acid sequencing and electrophoretic analysis.

The partial amino acid sequence of phospholamban from canine cardiac sarcoplasmic reticulum was determined by sequence analysis of the peptides obtained from the protein cleaved by cyanogen bromide and with TPCK-trypsin. The sequence determined initiated with N alpha-acetylated methionine followed by 44 amino acid residues intervening two unidentified residues. This polypeptide would represent a structural unit (protomer) of phospholamban. Analysis of temperature-dependent conversion of phospholamban from 26 kDa to lower molecular weight form (6 kDa) suggested that phospholamban holoprotein is composed of five identical protomers.

Amino Acid Sequence↗
PubMed1986

2-Deoxy-2-[18F]fluoro-D-galactose: a new tracer for the measurement of galactose metabolism in the liver by positron emission tomography.

We prepared 2-deoxy-2-[18F]fluoro-D-galactose as a potential radiopharmaceutical for liver imaging and for the assessment by positron emission tomography of regional metabolic function of the liver. In biodistribution studies of rats, the liver uptake of the compound was very high, almost reaching a plateau (6.33% dose/g) at 30 min and remaining constant until 120 min. This high uptake was reduced by simultaneous administration of D-galactose, but D-glucose had no effect. The compound was much less concentrated in the liver that had been damaged by CCl4 treatment. Positron imaging of a rabbit liver showed a remarkable uptake of the compound with a high liver-to-blood ratio. The high concentration in the liver was also reduced by the administration of D-galactose. These data suggest that the compound was trapped in the liver by a metabolic process and could be used for the measurement by positron emission tomography of galactose metabolism in the liver.

Animals↗
PubMed1986

A case of primary amyloidosis confined to the small intestine.

A 60 year-old man with primary amyloidosis confined to the small intestine was reported. Multiple polyps of the small intestine were found by an upper GI series and enteroscopic polypectomy revealed massive deposition of amyloid in the lamina propria and the submucosa. No predisposing disorder or other sites of deposition were found, and the diagnosis of primary amyloidosis of the small intestine was confirmed.

Amyloidosis↗