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Biomedical subjects

M Katori

Publications and source records attributed to M Katori.

At least 163 records · Page 9Linked to original sources
PubMed1982

Changes in the levels of prostaglandins and thromboxane and their roles in the accumulation of exudate in rat carrageenin-induced pleurisy--a profile analysis using gas chromatography-mass spectrometry.

Injection of lambda-carrageenin into the pleural cavity of rats caused the accumulation of the pleural exudate. When levels of prostaglandins (PGs) and thromboxane (TX) B2 were quantified by gas chromatography-mass spectrometry as their methyl ester (ME)-dimethylisopropylsilyl (DMiPS) ether or ME-methoxime-DMiPS ether derivatives, 6-keto-PGF1 alpha reached the maximum at 1 hr after carrageenin, then PGE2 and TXB2 showed peaks at 3 hr and waned off before 9 hr. The PGF/ alpha level was kept low, but PGD2, PGE1 and PGF1 alpha were not detected. Aspirin (100 mg/kg, i.p.) significantly decreased the PG and TXB2 levels and suppressed the rate of plasma exudation until 5 hr, but did not at 7 hr, when it was measured by the amount of exuded pontamine sky blue injected intravenously. OKY-025 (300 mg/kg, i.p.), a selective TXA synthetase inhibitor, and tranylcypromine (20 mg/kg, i.p.), a PGI synthetase inhibitor, could not extensively inhibit the accumulation of the exudate. These results suggest that the cyclooxygenase products of arachidonic acid, particularly PGE2, definitely play an important role in the exudation during the first 5 hr.

Animals↗
PubMed1982

Manipulation of thrombus formation in the hamster cheek pouch with drugs that interact with PGI2 in vitro.

A single platelet thrombus was formed in an arteriole of the hamster cheek pouch by electrical stimulation followed by topical application of ADP. The sizes of the thrombi were continuously recorded with a photocell placed on a TV monitor screen and quantified by areas on the record. Repeated application of small doses of ADP (5-15 nmole/10 microliters) resulted in very reproducible formation of the thrombi, and the size of the thrombi was reduced dose-dependently by topical application of PGI2. Three drugs were tested in this model. Cyclooxygenase inhibitor (indomethacin 10 mg/kg, i.p.) increased the formation of thrombi, while a smaller dose (3 mg/kg) did not have any significant effect. This could be explained by inhibition of the generation of endogenous PGI2, since aggregation of hamster platelets by ADP was not inhibited by indomethacin in vitro. EG-626 (phthalazinol, a phosphodiesterase inhibitor) (300 mg/kg, i.p.) decreased the size of thrombus. AI-122 (1.0 mg/kg, i.p.), which has been proven to enhance PGI2 biosynthesis from isolated rat aortae, also decreased the formation. Thus, drugs such as EG-626 or AI-122 are quite promising as anti-thrombotic drugs.

Adenosine Diphosphate↗
PubMed1981

Species difference in increased vascular permeability by synthetic leukotriene C4 and D4.

The activity of synthetic LTC4 was tested in guinea-pig ileum and was 200 times more potent than histamine in contraction of the ileum (3 x 10(-11) M- 3 x 10(-9) M). The activities of LTC4 and LTD4 in increased vascular permeability in guinea pigs, rats and rabbits were compared with those of histamine, bradykinin and prostaglandin (PG) E2. LTC4 was approximately equipotent to bradykinin on a molar basis in guinea pigs and rats and 5-100 times more potent than histamine. LTD4 was about 10 times more potent than LTC4 in guinea pigs and was equipotent to LTC4 in rats. On the contrary, in rabbits, neither LTC4 (up to 30 nmole/site) nor LTD4 (1 nmole/site) induced the dye exudation. These results show that species difference is present in activity of LTC4 and LTD4 in vascular permeability. Furthermore, in guinea pigs, the vascular permeability increased by LTC4 was not affected after pretreatment with pyrilamine (2.5 mg/kg, i.v.), and LTC4 and LTD4 did not potentiate the activity of bradykinin in vascular permeability.

Animals↗
PubMed1981

Abnormalities in the contact activation through factor XII in Fujiwara trait: a deficiency in both high and low molecular weight kininogens with low level of prekallikrein.

Fujiwara trait, the first case of kininogen deficiency in Japan previously reported which did not show any clinical symptom except the prolonged activated partial thromboplastin time was further examined. The activated partial thromboplastin time of the patient was corrected by addition of normal, Factor XII deficient or Fletcher plasma, but not corrected by Fitzgerald or Williams plasma. It was also corrected by addition of highly purified bovine or human high molecular weight (HMW) kininogen, but not by low molecular weight (LMW) kininogen. When total kininogen was measured as the amount of bradykinin released by trypsin, only a trace amount was detected in Fujiwara as well as Williams plasma. No immunoreactive protein against anti-human-HMW-kininogen nor anti-human-LMW-kininogen was found in Fujiwara plasma. Acetone-kaolin-activated plasma kallikrein was not generated by Fujiwara plasma. Substitution with normal plasma in various ratios showed the generation of various plasma kallikrein activities. Calculations with these activities of mixed plasma gave the prekallikrein content of Fujiwara trait plasma about 30% of the normal level. These results suggest that Fujiwara trait is very similar to Williams trait in that both plasmas were deficient in HMW and LMW kininogens with reduced content of prekallikrein.

Factor XII↗
PubMed1980

Potentiation of anti-aggregating activity of PGI2 by 7-ethoxycarbonyl-6,8-dimethyl-4-hydroxymethyl-1(2H)-phthalazinone (EG-626) in rabbit platelets in vitro.

Anti-aggregating activity of 7-ethoxycarbonyl-6,8-dimethyl-4-hydroxymethyl-1(2H)-phthalazinone (EG 626) was tested using rabbit platelets in vitro. EG-626 alone, when added before, prevented platelet aggregation induced by ADP, as did PGI2, papaverine and dipyridamole. Spontaneous disaggregation was also accelerated when EG-626 was added after the maximal aggregation induced by ADP. EG-626 alone also inhibited platelet aggregation induced by collagen and arachidonic acid. ID50s of these agents in ADP-induced aggregation were 7-9 nM for PGI2, 223 microM for EG-626, 266 microM for papaverine and 957 microM for dipyridamole. When EG-626 was used in combination with PGI2, a threshold dose (50 microM) of EG-626 potentiated the antiaggregation effect of subthreshold dose (3 nM) of PGI2 upto 100% inhibition in collagen-induced platelet aggregation. The marked potentiating effect of EG-626 was accompanied by an accumulation of cyclic AMP in the platelets. These effects might be due to inhibition of phosphodiesterase. Papaverine and dipyridamole, other phosphodiesterase inhibitors, also potentiated the anti-aggregating activity of PGI2. The activity of papaverine, however, was one eighth of EG-626 and that of dipyridamole was much less. The most effective combination of PGI2 and EG-626 to induce 50% inhibition was obtained with 20% of ID50 of each agent, whereas that of PGI2 and papaverine or dipyridamole was 39 or 41%, respectively.

Animals↗
PubMed1980

The first cases of Fitzgerald factor deficiency in the Orient: three cases in one family.

Asymptomatic, female, 56-year-old identical Japanese twins were found to have a severe abnormality in the surface-mediated intrinsic coagulation, fibrinolysis and esterolytic activity. These defects were thought to be due to the lack of Fitzgerald factor, because of the prolongations of kaolin-activated partial thromboplastin time and kaolin-activated euglobulin lysis time that were not corrected by the addition of Fitzgerald trait-plasma but were corrected to normal levels by the addition of isolated bovine high-molecular-weight kininogen, Fletcher trait-plasma or Hageman trait-plasma.

Animals↗
PubMed1980

Selective inhibitory effects of chlorpromazine and imipramine on platelet aggregation.

The effects of chlorpromazine (CPZ) and imipramine (IMP) on platelet aggregation in vitro were investigated. Both CPZ and IMP inhibited epinephrine-induced secondary aggregation in a dose-dependent fashion and changed adenosine diphosphate (ADP)-induced irreversible aggregation into a reversible response in human platelets. With rabbit platelets, CPZ (0.6-20 microM) and IMP (6-60 microM) showed a selective inhibitory effect on the aggregation by collagen, whereas, even at 200 microM, this effect was found neither in arachidonic acid (AA)-induced aggregation nor in ADP-induced one. CPZ and IMP also inhibited human platelet aggregations induced by collagen, but not by AA. The antiaggregating action of CPZ and IMP was thought to be due to their inhibitory effects on AA liberation from platelet membranes, suggesting that they might inhibit participating enzymes (phospholipase A2, C or lipase) or the process of the activation of the enzymes.

Acetophenones↗
PubMed1980

Dual effects of a basic anti-inflammatory agent, 2-aminomethyl-4-t-butyl-6-iodophenol hydrochloride (MK-447), on biosynthesis of prostaglandin endoperoxides.

Effects of MK-447 on prostaglandin (PG) endoperoxide formation from arachidonic acid by bovine seminal vesicle microsomes in the presence of cofactors (hemoglobin and tryptophan) were studied by cascade superfusion on rabbit aorta and mesenteric artery and rat stomach and colon. In the presence of hemoglobin (0.2 muM), MK-447 (up to 30 muM) accelerated PG endoperoxide formation, as tryptophan did, whereas higher concentrations of MK-447 lost the acceleration effect and finally inhibited the PG endoperoxide formation. Increased concentration of hemoglobin (2 muM) shifted the dose of MK-447 for peak generation from 30 to 100 muM. Thus, MK-447 shows dual action, acceleration and inhibition, on the PG endoperoxide formation.

Animals↗
PubMed1980

Negligible potency of acetylcholine in increasing vascular permeability.

As acetylcholine (ACh) is claimed to be a possible mediator of cholinergic urticaria, the potency of acetylcholine (ACh) in increasing vascular permeability was tested by skin perfusion technique in rats and by dye extraction method from the skin of rabbits. The potency of vascular permeability increase of ACh was much lower than that of histamine (Hist) and bradykinin (BK) in rats and rabbits. The higher dose of ACh (10 mg in 0.1 ml of saline), however, produced slight increase of vascular permeability in rabbits, which was inhibited by the antihistamine, pyrilamine maleate. Furthermore, ACh did not potentiate the responses to BK or Hist, when injected simultaneously. It seems unlikely that ACh did increase or potentiate vascular permeabilitay in physiological doses.

Acetylcholine↗
PubMed1979

Assay methods for prekallikrein and kininogens and their applications.

Prekallikrein activity in plasma was assayed using a synthetic peptidyl fluorogenic substrate (carbobenzoxy-L-phenylalanyl-L-arginine 4-methylcoumarinyl-7-amide), after activation of prekallikrein by acetone and kaolin. For total kininogen assay, the pretreatment of plasma at pH 2.0 was the best to eliminate bradykinin potentiators and kininase activity, before addition of trypsin to convert kininogen to bradykinin. Assay method of high molecular weight (HMW) kininogen was established by conversion of HMW-kininogen to bradykinin through activation of Hageman factor by glass powder and that of low molecular weight (LMW) kininogen was also by treatment of HMW-kininogen-depleted plasma in the same way as that for total kininogen. The marked reduction of prekallikrein and HMW-kininogen, not of LMW-kininogen, was found in pleural fluid of rat carrageenin pleurisy, and in plasma after i.v. injection of bromelain in rats. Members of the pedigree of hereditary angioneurotic edema patients also show low levels of prekallikrein and kininogens in plasma.

Animals↗