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Biomedical subjects

M Katori

Publications and source records attributed to M Katori.

At least 145 records · Page 8Linked to original sources
PubMed1986

Roles of leukotrienes in two rat allergic inflammatory models; IgE-mediated and IgG-antigen complex-induced pleurisies.

Rat IgE pleurisy was induced by the injection of di-nitrophenol-conjugated bovine serum albumin (DNP-BSA) 48 hours after the intrapleural injection of rat anti-DNP-IgE serum. IgG-BSA complex pleurisy was also induced by the intrapleural injection of IgG-BSA complexes produced at the optimum ratio in vitro. Plasma exudation was markedly increased in the first 20 minutes, but not observed thereafter, in IgE pleurisy, whereas marked plasma exudation in the first 20 minutes was followed by weak exudation at three and five hours in IgG-BSA complex pleurisy. Leukotrienes (LTs) E4 (100 ng/rat), D4 (32) and B4 (16) were detected on HPLC in the pleural exudate in the first 20 minutes of IgG-BSA complex pleurisy, but less (9 ng/rat) LTE4 alone was detected in the five-hour exudate. The first 20-minute pleural exudate contained 13 ng/rat of LTE4 in IgE pleurisy. The plasma was completely inhibited by simultaneous treatment of rats with pyrilamine (2.5 mg/kg, i.p.) and methysergide (3 mg/kg, i.p.), as it was in compound 48/80-induced pleurisy. In IgG-BSA complex pleurisy, 90% of the pleural exudate for the first 20 minutes was inhibited by the same treatment, and the rest was completely suppressed by simultaneous treatment with an intrapleural injection of AA-1777, a selective 5-lipoxygenase inhibitor. AA-1777 alone did not reduce the plasma exudation significantly. The 5-lipoxygenase inhibitor was also very effective in reducing the migrating numbers of polymorphonuclear and mononuclear leukocytes to half, without affecting the eosinophils of mast cells.

Animals↗
PubMed1986

Microcirculatory changes during skin allograft rejection and prolongation of survival time by antiplatelet agents.

The process of rejection of skin first-set-allograft transplantation was pursued by observing the microcirculation of living mice, in comparison with that of the isograft transplantation (BALB/C vs. BALB/C). The vascular connection of the skin allograft between the host (BALB/C) and graft (R III) was established on day 8, in just the same pattern as in isograft skin, but the blood flow slowed down on day 9, and the formation of microthrombi was observed in the arterioles and later in the venules and capillaries at the sites slightly inside the graft from the margin on day 10. Thereafter each small vessel of the host formed a loop and the blood flow from the host did not enter the graft. The thrombus formation was confirmed by light and electron microscopy. The importance of the thrombus formation in the rejection process was further strengthened by prolongation of the cessation of the blood flow at the boundary from day 10 to days 14-15, after daily administration from days 2 to 9 of OKY-1581 (0.4 mg/g i.p.), a selective thromboxane synthetase inhibitor, or ticlopidine (0.3 mg/10 g p.o.), an inhibitor of platelet aggregation, in combination with a subthreshold dose (0.4 mg/10 g i.p.) of azathioprine. None of these drugs alone significantly prolonged the survival time.

Acrylates↗
PubMed1984

Microdetermination of prostaglandins and thromboxane B2 by capillary gas chromatography and negative ion chemical ionization mass spectrometry.

Application of dimethyl-n- propylsilyl ( DMnPS ) ether derivatives of prostaglandins (PGs) and thromboxane (TX) B2 pentafluorobenzul ( PFB ) esters of negative ion chemical ionization mass spectrometry ( NICIMS ) was investigated. These derivatives were separated completely within 10 min by the use of a fused-silica capillary column coated with methyl silicone. In NICIMS , all of the DMnPS ether derivatives of PGs and TXB2 PFB esters yielded the characteristic negative ion [M - 181]- which was produced by elimination of PFB from the molecule. The detection limit of the DMnPS ether derivative of PGF2 alpha PFB ester was found to be 200 fg with a signal-to-noise ratio of 5 when monitoring the ion of m/z 653 ([M - 181]-) in the high-resolution mode (R = 2500) using ammonia as a reagent gas. The method was applied to the quantitation of PGE2 and PGF2 alpha in an extract obtained from the plasma of a lung-heart preparation from a dog.

Animals↗
PubMed1984

Enhanced prostacyclin generation by phenolic compounds acting as a tryptophan-like cofactor of PG hydroperoxidase.

Isolated rat aortae were incubated at 22 degrees C in tris-buffered saline (pH 7.4). The incubation medium was changed every 10 min, and the amounts of prostacyclin (PGI2) in the medium were immediately bioassayed as an inhibitory activity against rabbit platelet aggregation induced by ADP. The addition of arachidonic acid to the medium increased the generation of PGI2 but this was followed by a gradual decrease even in the presence of the same amount of arachidonic acid. The decrease of PGI2 generation from exogenous arachidonic acid was prevented by tryptophan, which is required by PG hydroperoxidase with heme compound as cofactors. MK-447 and its analogues, which are phenolic compounds and exerted tryptophan-like action on the PG endoperoxide biosynthesis by bovine seminal vesicle microsomes, also prevented the decrease of PGI2 generation in isolated rat aortae. The phenolic compounds enhanced PGI2 generation from endogenous arachidonic acid. These results indicate that the phenolic compounds enhanced PGI2 generation in vascular tissue, acting as a tryptophan-like cofactor of PG hydroperoxidase.

Animals↗
PubMed1983

Activation of plasma kallikrein-kinin system and its significant role in pleural fluid accumulation of rat carrageenin-induced pleurisy.

Rat pleurisy was induced by intrapleural injection of lambda-carrageenin. The pleural exudate began to be accumulated 1-3 h after carrageenin administration and showed a peak at 19 h. The levels of prekallikrein and high-molecular-weight (HMW), but not low-molecular-weight (LMW), kininogen in the pleural fluid were markedly decreased when compared with those in plasma. Prekallikrein in rat plasma was activated by incubation with carrageenin in vitro. Captopril increased the plasma exudation significantly at 1-5 h. Depletion of prekallikrein and HMW kininogen in rat plasma by preadministration of bromelain caused marked inhibition of the plasma exudation at 1-24 h. The rest of the plasma exudation after bromelain was further decreased by simultaneous pretreatment of rats with both bromelain and aspirin. These results clearly indicate that plasma prekallikrein was activated in the pleural cavity and bradykinin released was responsible for plasma exudation during the entire course of this pleurisy.

Animals↗
PubMed1983

The anti-inflammatory mechanism of MK-447 in rat carrageenin-induced pleurisy.

Intrapleural injection of 2% lambda-carrageenin caused the accumulation of exudate up to 19 hr. The rate of plasma exudation, measured by the exuded dye amounts for 20 min in the pleural cavity after intravenous injection of pontamine sky blue, showed a peak at 5 hr. Aspirin (100 mg/kg, i. p.) suppressed the dye exudation up to 5 hr, but did not at 7 hr. This inhibition coincided with the decrease of the PG and TXB2 levels, which were measured by gas chromatography-mass spectrometry, in the pleural exudate. In in vitro experiments, MK-447, a phenolic compound, stimulates PG endoperoxide biosynthesis at lower doses and inhibits it at higher doses, acting as a tryptophan-like cofactor required by PG endoperoxide synthetase. This drug (0.3, 1.0 and 3.0 mg/kg, i. p.) suppressed the dye exudation dose-dependently up to 5 hr, but did not at 7 hr even at a higher dose, in combination with the dose-dependent decrease of the pleural level of PGE2, which was reported to be a major PG among PGs and TXB2 in the exudate in inducing the plasma exudation (Harada et al; Prostaglandins, 23: 881, 1982). Thus, the anti-inflammatory action of MK-447 can be explained by inhibition of PGE2 generation, giving no consideration to the role of oxygen-derived free radicals as a prime mediator in inflammation.

Animals↗
PubMed1983

Detection of leukotriene C4 and D4 in the exudate of rat carrageenin-induced pleurisy.

Rat carrageenin-induced pleurisy was used as an acute exudative inflammatory model. The crude ethanol extract of the pleural fluid at 5 hr after carrageenin injection caused the very slow contraction of guinea-pig ileum, which was antagonized by FPL 55712 (1 microgram/ml). The ethanol extract was cleaned by LH-20 and was rendered for separation of LTC4 and LTD4 by reversed-phase high-performance liquid chromatography (HPLC). Two peaks which showed the same retention time on HPLC as those of LTC4 and LTD4 had the contractile activity of guinea-pig ileum and the ratios of the contractile activity to the height on HPLC agreed with those of synthetic LTC4 and LTD4. Two peaks of delta 6-trans-LTB4, 5S, 12R-(E, E, E, Z)-diHETE and 5S, 12S-(E, E, E, Z)-diHETE, were detected, but the appreciable amount of LTB4 was smaller than that of each delta 6-trans-LTB4 in the pleural fluid at 5 hr.

Animals↗
PubMed1982

Possible involvement of thromboxane in bronchoconstrictive and hypertensive effects of LTC4 and LTD4 in guinea pigs.

The actions of leukotriene (LT) C4 and D4 on the systemic arterial pressure and the insufflation pressure in guinea pigs and rabbits were examined. In guinea pigs, 0.3 - 3 nmole/kg of LTC4 and 0.1 - 1.0 nmole/kg of LTD4 administrated from left jugular vein caused dose-dependent increase of the airway resistance measured by the Konzett-Rössler method and a triphasic blood pressure response; an initial hypotension, a secondary hypertension and a third long-lasting hypotension. All of the hypertensive phase and 100 - 150% of the increase of the airway resistance by LTC4 and LTD4 were inhibited by a selective thromboxane synthetase inhibitor, OKY-1581 (10 mg/kg, i.v.) and only the hypotension was observed. Indomethacin (10 mg/kg, i.p.) also inhibited not only the airway resistance increase, but also the prolonged hypotension by LTC4 and shortened the duration of the hypotension by LTD4. It is suggested that thromboxane might be involved in bronchoconstriction and hypertensive effects by LTC4 and LTD4 and that hypotensive prostaglandin might be involved in the hypotensive phase after LTC4 and LTD4. In rabbits, the increase of the airway resistance by LTC4 and LTD4 (upto 100 nmole/kg, i.v.) was negligible and only the hypotension was observed.

Airway Resistance↗