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Biomedical subjects

M Katori

Publications and source records attributed to M Katori.

At least 199 records · Page 11Linked to original sources
PubMed1975

Potentiation of bradykinin-induced vascular permeability increase by prostaglandin E2 and arachidonic acid in rabbit skin.

The activity of prostaglandins (PG) in producing vascular permeability was quantitated by dye extraction method in skin of anaesthetized rabbits. PGE1 and PGE2 (0.01-10 mug) produced increase in vascular permeability. Activity was approximately equal to that of histamine (Hist) and 1/20 of that of bradykinin (BK) on a weight basis. The activity of PGF1alpha and PGF2alpha was only 1/20 of that of PGE1 or PGE2. In spite of the relatively low potency of PGE1 and PGE2 in the rabbit, near threshold doses (0.1 or 1 mug) of PGE2 could potentiate permeability responses to bradykinin (0.1 mug) by 10 or 100-fold, respectively. Equivalent doses (0.1 or 1 mug) of histamine could not potentiate the bradykinin responses. Arachidonic acid (AA) at 1 mug, produced a 10-fold potentiation in the permeability response to bradykinin (0.1 mug). Pretreatment of the rabbits with indomethacin (20 mg/kg, i.p.) reduced the responses of BK (0.1 mug) + AA (1 mug) down to a similar magnitude of those seen with bradykinin alone. However, indomethacin did not block responses to either, BK alone, BK + PGE2, or BK + Hist. Various doses (1, 10, 100 and 300 mug) of arachidonic acid alone also produced increase in cutaneous vascular permeability, although its potency was only 1/3-1/8 of that of PGE2. This activity of arachidonic acid was attributed in part to its bioconversion to PGE2, since its activity was significantly reduced by the prostaglandin antagonist, diphloretin phosphate (DPP) (60 mg/kg, i.v.) and by indomethacin (20 mg/kg, i.p.), which blocks conversion of arachidonic acid to prostaglandins. Arachidonic acid may owe some of its permeability increasing effects to histamine release, since its effects were also reduced by the anti-histamine, pyrilamine (2.5 mg/kg, i.v.).

Animals↗
PubMed1975

Inhibition of kinin formation by a kallikrein inhibitor during extracorporeal circulation in open-heart surgery.

Involvement of the kinin system was studied in 58 patients during extracorporeal circulation in open heart surgery. At the onset of extracorporeal circulation, there was no increase of free kinin in blood and no reduction of plasma kininogen, when the latter was expressed as mug bradykinin/mg plasma protein. With the lapse of time, kinin in the blood increased significantly, and decrease of kininogen was also significant. The longer the circulation time, the greater the consumption of kininogen. The site of the kinin formation was presumed to be the heart-lung machine since the level of kinin increased slightly and kininogen decreased gradually in the blood leaving the machine, compared with those levels entering the machine. The difference in kininogen was significantly different from zero at termination of extracorporeal circulation. Administration of a kallikrein-trypsin inhibitor, trasylol (A. G. Bayer), infused into the heart-lung machine, prevented the decrease of kininogen. Reduction of the total peripheral resistance during this circulation was also prevented. The hemoconcentration, presumably the result of vascular permeability increase caused by increased kinin, was prevented by trasylol in cases in which extracorporeal circulation lasted over 60 minutes. Trasylol applied thus appears to be an effective counteragent for circulatory disturbances which occur during extracorporeal circulation.

Adolescent↗