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Biomedical subjects

M Suematsu

Publications and source records attributed to M Suematsu.

154 records · Page 9Linked to original sources

The role of parasympathetic nerve activity in the pathogenesis of coronary vasospasm.

To evaluate the role of the autonomic nervous system, especially the parasympathetic nervous system, in the initiation mechanism of vasospastic angina pectoris (AP), the coefficient of R-R interval variation (CV) on the electrocardiogram (ECG) and plasma catecholamine concentration were measured in 25 patients with vasospastic AP, 10 patients with effort AP and 12 control subjects. CV which has been recognized as reflecting parasympathetic nervous system activity was calculated from 100 consecutive heart beats on the ECG and represented as the percentage of standard deviation of the R-R interval per mean R-R interval. Repeated measurements of plasma catecholamine concentration revealed higher values at any sampling point throughout a day in patients with vasospastic AP than those in control subjects. A distinctly higher CV was observed at night in the vasospastic AP group. This elevated CV was abolished by atropine sulfate (1.5 mg/day per os). Pilocarpine injection (1.3 mg/10 kg B.W. subcutaneously) induced a marked increase in CV that preceded the occurrence of chest pain and/or ischemic ECG changes in 5 patients with vasospastic AP. The increment in CV at 10 min after pilocarpine administration was greater in vasospastic AP than in control subjects (p less than 0.05). It is concluded that enhanced parasympathetic activity may play a role in the initiation of coronary vasospasm associated with sympathetic hyperactivity.

Angina Pectoris, Variant↗

Sulfasalazine and its metabolites attenuate respiratory burst of leukocytes--a possible mechanism of anti-inflammatory effects.

The effects of sulfasalazine and its metabolites, 5-amino salicylic acid and sulfapyridine on respiratory burst of polymorphonuclear leukocytes were investigated by determining not only luminol-dependent chemiluminescence for the detection of myeloperoxidase-mediated active oxidants, but also lucigenin-dependent chemiluminescence for the detection of superoxide anion. The present study showed that sulfasalazine, 5-amino salicylic acid and sulfapyridine attenuated active oxygen species from polymorphonuclear leukocytes at the concentrations comparable to clinical doses. Therefore, it was concluded that anti-inflammatory effects of sulfasalazine can be explained by the ability of sulfasalazine and its degraded compounds to scavenge active oxidants from polymorphonuclear leukocytes.

Aminosalicylic Acids↗

Increased respiratory burst of leukocytes in inflammatory bowel diseases--the analysis of free radical generation by using chemiluminescence probe.

Respiratory burst of leukocytes was determined in Crohn's disease, intestinal Behçet's disease and ulcerative colitis by using chemiluminescence assay. Oxygen-derived free radicals of monocytes in Crohn's disease and those of polymorphonuclear leukocytes in intestinal Behçet's disease were significantly raised as compared with those of controls. In ulcerative colitis, respiratory burst activities of both polymorphonuclear leukocytes and monocytes were found to be highly associated with the disease activities. These results suggest that active oxygen species from leukocytes may participate in the formation of intestinal mucosal lesions in inflammatory bowel diseases via auto-oxidative process.

Adult↗

Activation of macrophage function by intraperitoneal administration of the streptococcal antitumor agent OK-432.

Motility, adhesiveness, IL1 production, and inhibition of tumor cell growth in vitro were examined in murine peritoneal macrophages obtained after intraperitoneal injection of a streptococcal preparation OK-432, heat-inactivated OK-432 (HI-OK-432), and thioglycollate medium (TG). By varying the interval between intraperitoneal injection of OK-432 and the harvest of peritoneal macrophages, it was found that OK-432 induced a time-dependent multi-step alteration of these properties: step I increased motility on day 1: step II increased adhesiveness on day 2; and step II increased inhibition of tumor cell growth and IL1 production. During step III, the peritoneal macrophage population, including Ia-bearing cells, increased dramatically in the peritoneal cavities of OK-432-treated mice. In contrast, injection of either HI-OK-432 or TG, which lack antitumor activity in vivo, initiated steps I and II, but not step III. The Ia-bearing macrophages induced by OK-432 showed high ability of IL1 production, but low growth inhibitory activity against tumor cells. Based on these results, OK-432 seems to be performing a dual function: eliciting a new population of macrophages to the site of injection (heat stable function), and inducing two different populations of antitumor macrophages and Ia-bearing macrophages (heat unstable function).

Animals↗

Fluorographic study on the oxidative stress in the process of gastric mucosal injury: attenuating effect of vitamin E.

In vivo oxidative change was visualized in the gastric mucosa of rats and the alteration was analysed by using a fluorescence microscope equipped with a digital imaging processor during the development of mucosal damage. Dichlorofluorescein (DCF)-associated fluorescence increased after the repeated electrical stimulation on the gastric artery (irritation), suggesting the occurrence of lipid peroxidation. The increase was enhanced in the mid-zone of two adjacent collecting venules. Allopurinol attenuated the oxidative stress in mucosa, showing the involvement of xanthine oxidase. Luminol-dependent chemiluminescence value in the blood taken from gastric vein was elevated by the irritation, suggesting that leucocyte-generated oxygen radicals also participate in this oxidative process. alpha-Tocopherol attenuated both the DCF activation and the increase in chemiluminescence value and prevented gastric mucosal injury. The present results suggest that alpha-tocopherol may be useful for the prevention of oxidative alteration in gastric mucosa.

Allopurinol↗

Bile acid-induced depolarization of mitochondrial membrane potential preceding cell injury in cultured gastric mucosal cells.

Changes in energy metabolism elicited by sodium taurocholate and their relation to cell viability were determined in gastric mucosal cells. Cultured mucosal cells were labelled with rhodamine-123, a mitochondrial energization-sensitive fluorescence probe, or by propidium iodide, a fluorochrome which labels the nuclei of non-viable cells. The cells were observed under a fluorescence microscope with a laser scanning confocal imaging system. After the addition of sodium taurocholate at concentrations > 5 mol/L, mucosal cells showed a rapid and significant decrease in rhodamine-123 fluorescence. A decrease to 40% of the pretreated values at 30 min was seen with a concentration of sodium taurocholate of 7.5mmol/L. A marked increase in the percentage of propidium iodide-positive cells was noted when the concentration of sodium taurocholate exceeded 5mmol/L. However, the extent of the decrease in rhodamine-123 fluorescence was always greater than the increase in the percentage of propidium iodide-positive cells, suggesting that most of these gastric mucosal cells remained viable. It is therefore suggested that the decrease in rhodamine-123 fluorescence is largely due to the disturbed oxidative phosphorylation of mitochondria. Pretreatment of gastric mucosal cells with low concentrations of ethanol resulted in a significant cytoprotective effect against sodium taurocholate injury with significant prevention of a decrease in rhodamine-123 fluorescence. It is concluded that sodium taurocholate induces a depolarization of the mitochondrial membrane potential preceding cell injury and that the cytoprotective effect of ethanol relates to its attenuation of the uncoupling effect.

Animals↗