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Biomedical subjects

M Katori

Publications and source records attributed to M Katori.

At least 109 records · Page 6Linked to original sources
PubMed1992

Increase in the kinin levels in the bronchial washings after intravenous injection of leukotriene C4 in guinea pigs.

In guinea pig plasma, bradykinin (BK) was degraded mainly to des-Arg1-BK by an aminopeptidase-like enzyme, which was inhibited by 2-mercaptoethanol. Besides this degradation, BK was also hydrolyzed by kininase I and kininase II from C-terminal end to des-Arg9-BK, des-Phe8-Arg9-BK and Arg-Pro-Pro-Gly-Phe ([1-5] BK). The formation of des-9-BK was strongly blocked by DL-2-mercaptomethyl-3-guanidinoethylthiopropanoic acid (MGPA) and that of des-8,9-BK and [1-5] BK was inhibited by captopril. When guinea pigs were pretreated with a cocktail of 2-mercaptoethanol, MGPA and captopril, intravenous administration of leukotriene (LT) C4 (10 nmol/kg) caused an increase in the levels of free kinin in the bronchial washings of guinea pigs. This increase was accompanied with the increase in glandular-kallikrein activity, which could be inhibited by aprotinin. As BK is reported to induce both bronchoconstriction and bronchial secretion, the increased free BK induced by LTC4 might enhance the effect of LTC4.

3-Mercaptopropionic Acid↗
PubMed1992

[11-Dehydro-TXB2 and 2,3-dinor-TXB2 as new parameters of TXA2 generation].

Artifactual formation of thromboxane (TX) B2 during blood collection falsifies real value of TXB2 in plasma. A part (29.3%) of TXB2 is metabolized to 11-dehydro (DH)-TXB2 in several organs. 11-DH-TXB2 was not generated during blood collection or during serum formation. The peak amount of 11-DH-TXB2 after intravenous injection of TXB2 to rabbits was lower than that of TXB2, but the level of 11-DH-TXB2 was kept 2-3 times higher than that of TXB2 even after more than 5 min. A half life of 11-DH-TXB2 is 45-60 min in the human. Large species differences were found. In human urine, 11-DH-TXB2 was excreted 1.5-5.8 times more than 2,3-dinor-TXB2. Patients with ARDS and DIC, who received platelet transfusion, excreted increased amounts of 2,3-dinor-TXB2 and 11-DH-TXB2 in urine. 11-DH-TXB2 may be a useful parameter of TXA2 formation in pathological states.

Animals↗
PubMed1991

Interference in the radioimmunoassay of gastric prostaglandins by cimetidine, a histamine H2 blocker.

The present study was undertaken to assess whether cimetidine alters the levels of endogenous prostaglandin (PG) E2 and 6-keto-PGF1 alpha in the rat stomach. When cimetidine was mixed in vitro with a suspension of dextran-coated charcoal, to which [3H]-PGE2 had been adsorbed, levels of free [3H]-PGE2 were increased by cimetidine at concentrations above 1.0 mM, because of preferable adsorption of this blocker to the charcoal. Dextran-coated charcoal is used for the separation of antibody-bound [3H]-PGs from the free labelled compounds in the radioimmunoassay of PGs. Addition of cimetidine to standard solutions of PGE2 shifted the PGE2 calibration curve upward. Thus, when PGs in cimetidine-containing samples were quantitated by reference to the normal calibration curve, the assessed levels of PG were lower than the actual levels. Removal of cimetidine from the assay samples was successfully achieved by use of SEP-PAK C18 columns. Rats were injected intraperitoneally with 100 mg/kg of cimetidine only once or with 20 mg/kg twice daily for 7 days. Using this cleaning method, we found that both the basal levels of PGE2 and 6-keto-PGF1 alpha and those levels increased by intragastric administration of 1.0 M NaCl solution did not differ between rats treated with cimetidine and those treated with vehicle. It can be, therefore, concluded that cimetidine does not affect the gastric PG production.

6-Ketoprostaglandin F1 alpha↗
PubMed1991

Suppression of rat deoxycorticosterone-salt hypertension by kallikrein-kinin system.

Brown Norway kininogen-deficient rats had very low levels of plasma kininogens and lower levels of plasma prekallikrein, compared with those of normal rats of the same strain. Systolic blood pressure, determined by the tail-cuff method, of 5-week-old kininogen-deficient rats (106 +/- 0.4 mm Hg, n = 7) and the rate of systolic blood pressure increase with age were not different from those in normal rats. Weekly injections of deoxycorticosterone acetate (5 mg/kg s.c.) with 1% sodium chloride solution in drinking water after uninephrectomy at 7 weeks of age caused a gradual increase in the blood pressure of normal rats, reaching a plateau at 18 weeks of age, whereas that of deficient rats rose rapidly to 158 +/- 6 mm Hg 2 weeks after the start of treatment and continued to increase slightly, becoming significantly higher than normal rats at 8, 9, 10, 11, and 12 weeks of age (p less than 0.05 or 0.01). The levels of urinary prokallikrein and active kallikrein were slightly higher in deficient rats before deoxycorticosterone acetate-salt treatment but were not significantly increased after this treatment, whereas these levels in normal rats were increased 3.6- and 4.7-fold by this treatment. Urinary free kinin, collected from the ureter in untreated deficient rats, was below the detection limit. The plasma level of low molecular weight kininogen, the substrate of glandular kallikrein, was decreased in normal rats during the treatment. Continuous subcutaneous injection of aprotinin by an osmotic pump to normal rats induced significant increase in blood pressure. These results indicate that glandular kallikrein may play a suppressive role in deoxycorticosterone acetate-salt hypertension.

Animals↗
PubMed1991

Enhancement of endogenous prostaglandin I2 (prostacyclin) generation in vivo by a phenolic anti-inflammatory agent in the rabbit.

Angiotensin II (i.v.) increased the plasma level of 6-keto-PGF1 alpha from 241 +/- 60 pg/ml (n = 8) to 612 +/- 108 pg/ml (n = 8) in anesthetized rabbits, which was further significantly increased by pretreatment with a phenolic anti-inflammatory agent, MK-447, to 1007 +/- 218 pg/ml (n = 8). MK-447 alone did not affect the level. The level of thromboxane B2 was not affected by these treatments. These results suggest that MK-447 may selectively enhance the PGI2 level by acting as a tryptophan-like cofactor of PG endoperoxide synthase.

6-Ketoprostaglandin F1 alpha↗
PubMed1990

A site of action of dexamethasone on leukocyte extravasation in microcirculation.

When leukotriene (LT) B4 (15 pmol/50 microliters) was applied topically over the microvasculature of the hamster cheek pouch, polymorphonuclear (PMN) leukocytes started rolling and adhering on the inner wall of the venule. Over 90% of the PMN leukocytes adhered disappeared from the vascular lumen, taking 7.3 +/- 0.6 min for disappearance. Then, the PMN leukocytes stayed in the space between the endothelial cells and the pericyte basement membrane, as ascertained by electron micrographs. The number, which could be counted in the space, increased to 2.7, 12.2 and 19.2 cells on the TV screen for 30, 60 and 90 min, respectively. Administration of dexamethasone (0.1 or 0.3 mg/kg, i.p.) two hours before the LTB4 application did not cause the reduction of the numbers of adhered leukocytes nor the rate of disappearance, but reduced the numbers of leukocytes present in the interstitial space. Thus, dexamethasone inhibited the step of the penetration of the pericyte basement membrane.

Animals↗
PubMed1990

Possible role of endogenous prostaglandins against ethanol injury in rat stomach.

Exposure of the gastric mucosa for 3 min to 30% intragastric ethanol induced mucosal injury that appeared dark red in anesthetized rats. Microscopic observation of the microvasculature in the injured area after exsanguination of rats and in living rats confirmed that there was congestion of the blood flow in the collecting venules and capillaries. Hemorrhage was observed about 30 min after application of ethanol. Monastral blue dye was deposited along the postcapillary venules only at the border of the congestion area. A selective 5-lipoxygenase inhibitor, AA-861, inhibited the gastric lesion, and immunoreactive leukotriene C4 (LTC4) was detected in the gastric wall. Previous exposure of the gastric mucosa to 1.0 M NaCl solution inhibited the ethanol-induced mucosal injury markedly. NaCl solutions (0.5-1.0 M) also suppressed the electrical activity of smooth muscle and the suppression was released by indomethacin. Having observed that PGE2 generation in the stomach was induced dose-dependently by intragastric NaCl solutions (0.5-1.0 M), we propose the hypothesis that peptide LTs released by intragastric ethanol constrict the collecting venules or lamina muscularis mucosae and induce congestion of these venules, whereas the PGE2 released by intragastric NaCl solution releases the congestion of the collecting venules directly or through suppression of contraction of the lamina muscularis.

Animals↗
PubMed1990

Prostaglandin levels in the rat resting gastric wall and enhancement of prostaglandin E2 generation after administration of mild hyperosmotic saline solution into the gastric lumen.

The PGE2 level in the rat resting stomach, dropped into liquid nitrogen after removal, was 44.6 +/- 8.3 ng/stomach, when determined by radioimmunoassay, but cutting of the greater curvature with scissors after removal caused an approximately sixfold increase in the PGE2 level. Compression of the stomach in situ with metal tongs refrigerated in liquid nitrogen markedly reduced the PG levels, and further purification by reversed-phase high performance liquid chromatography reduced the PGE2 and 6-keto-PGF1 alpha levels to 4.7 +/- 0.6 and 4.8 +/- 0.8 ng/stomach, respectively. Pretreatment of the rats with indomethacin (10 mg/kg, i.v.) did not decrease the PGE2 level, but the 6-keto-PGF1 alpha level was reduced slightly. The lowest level of PGE2 in the resting state was significantly increased after administration of 1.0 M NaCl solution into the gastric lumen. The peak value was 70.0 +/- 21.8 ng/stomach at 30 min, after which the level decreased gradually. The level of 6-keto-PGF1 alpha was not significantly increased during the administration of 1.0 M NaCl solution.

Animals↗
PubMed1989

Evidence for the involvement of a plasma kallikrein-kinin system in the immediate hypotension produced by endotoxin in anaesthetized rats.

1. In vitro incubation of normal rat plasma with endotoxin from E. coli (3-10 mg ml-1) in the incubation mixture) caused a dose-dependent increase in levels of free kinin and plasma kallikrein in the presence of o-phenanthroline, together with a mirror-image, dose-dependent decrease in the residual levels of the precursors, plasma prekallikrein and high-molecular-weight kininogen. Low-molecular-weight kininogen levels were not modified. 2. Intravenous injection of endotoxin (3-30 mg kg-1) into the femoral vein of anaesthetized rats resulted in dose-dependent hypotension. In blood collected up to 15 min after injection, the levels of prekallikrein and high-molecular-weight kininogen in plasma were decreased while levels of the active forms, plasma kallikrein and free kinin, showed a transient increase in the blood 1 min after administration of endotoxin. 3. A degradation product of bradykinin, des-Phe8-Arg9-bradykinin, as measured by a newly developed enzyme immunoassay, was detectable up to 5 min after administration of endotoxin. 4. Intravenous infusion of soybean trypsin inhibitor inhibited both the formation of bradykinin and des-Phe8-Arg9-bradykinin and the initial hypotension. 5. It can be concluded from our results that plasma prekallikrein is activated in the blood immediately after administration of endotoxin to rats and that bradykinin is a major cause of the immediate hypotension.

Anesthesia↗
PubMed1989

Modulation of plasma exudation by PGE2 and that of leukocyte migration by LTB4 in inflammatory models.

Des-Phe8-Arg9-BK could be detected in the entire course of rat carrageenin pleurisy up to 24 h, together with a reduction of the residual levels of high molecular weight kininogen and prekallikrein. On the basis of this continuous release of bradikinin, prostaglandin E2 was released up to 5 h in the pleural exudate and enhanced the plasma leakage. In rat cardiac infarction, the initial increase in the number of polymorphonuclear leukocytes in the cardiac tissue was accompanied by leukotriene B4 in the tissue and this was followed by the second increase and activation of the complement system.

Animals↗