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PubMed1982

[Mediators of allergic reaction (author's transl)].

It is by now well established that allergic and inflammatory reactions interact interdependently. The mediators of inflammation such as histamine, the neutrophil chemotactic factor, the leukotrienes and the platelet aggregating factor are responsible for the cellular infiltration which defines acute, subacute and chronic inflammatory reactions. Thus, new perspectives are opened up as to the pathophysiological disease process "bronchospasm-asthma".

Arachidonic Acid↗
PubMed1982

Regulation of colonic blood flow.

Intrinsic and extrinsic regulation of colonic blood flow is reviewed. The existence of intrinsic vascular control mechanisms is evidenced by pressure-flow (and oxygen uptake) autoregulation, reactive hyperemia, vascular responses to acute venous hypertension, and functional hyperemia in denervated colon preparations. Although myogenic factors have long been considered to be solely responsible for the intrinsic ability of the colon to regulate its blood flow, recent developments indicate that metabolic mechanisms may be of equal importance in this regard. Both parasympathetic and sympathetic nerves play an important role in regulating colonic blood flow. Although many hormones and circulating vasoactive substances alter colonic hemodynamics, their contribution toward the overall regulation of colonic blood flow remains uncertain.

Adrenergic Agonists↗
PubMed1982

Formation of leukotrienes C and D and Pharmacologic modulation of their synthesis.

Our attempts to find a physiologically relevant means for inducing leukotriene synthesis in rat peritoneal mononuclear cells have thus far been unsuccessful in addition to the IgE-anti-IgE challenge which we previously reported, we have now tried human C3a and C5a as well as crude and semipurified fractions of the prostaglandin-generating factor of anaphylaxis. In each case, it was possible to show that these substances activated the cells even though no leukotrienes were formed. A cell-free system in which LTC + LTD formation can be studied was developed as a modification of published methods. Arachidonic acid and LTA4 served as precursors in this system in the presence of added glutathione. Calcium was required for LTC and LTD synthesis from arachidonic acid but was not required for the glutathione S-transferase terminal step in the synthesis. Using inhibitor profiles, substrate specificity for chromogenic substrates, and inactivation by selective antibodies, we tried to identify the subtype of the glutathione S-transferase in RBL cells. Although antibody to type E of the enzyme was most effective in neutralizing the enzyme activity, neither the substrate specificity nor the inhibition profiles agreed with the conclusion that the E-type enzyme was the major form in these cells. The effect of known inhibitors of glutathione S-transferase on the conversion of arachidonate to LTC and LTD was examined. Bilirubin, an inhibitor which binds to the enzyme and is not a substrate, was much more active in inhibiting LTC + LTD formation than were steroid sulfates, which were markedly less active in inhibiting this reaction. The inhibitory activities of the other compounds were similar on all substrates tested.

Animals↗
PubMed1982

Modulation of leukotriene formation by various acetylenic acids.

A series of acetylenic acids varying in chain length as well as in number and position of triple bonds were tested for their effect on arachidonic acid metabolism via cyclo-oxygenase and 5-lipoxygenase in homogenates of RBL-l cells. A number of trends which differentiate 5-lipoxygenase from cyclo-oxygenase were observed: (a) In general, the potency of the acetylenic acids to inhibit 5-lipoxygenase increased with the carbon chain length up to carbons. (b) A minimum of three triple bonds is necessary for the inhibitory action. (c) With the 20-carbon delta 8 and delta 6 acetylenic acids, activity decreased when the number of triple bonds increased from three to four. These structure activity relationships were not observed with cyclo-oxygenase. The delta 4 acetylenic acids proved to be an interesting group of compounds. They did not inhibit cyclo-oxygenase or 5-lipoxygenase but were good inhibitors of SRS synthesis. The potency of the delta 4 acetylenic acids increased with chain length, and 21:4 (4a, 7a, 10a, 13a) was the most potent compound inhibiting SRS formation. The delta 4 acetylenic acids are therefore useful tools for investigating the function and action of LTC4 and LTD4.

Animals↗
PubMed1983

Synthesis of slow reacting substance-like activity in rabbit conjunctiva and anterior uvea.

The ability of rabbit conjunctiva and anterior uvea to synthesize lipoxygenase products was assessed. Using autoradiographic techniques, we demonstrate that rabbit anterior uvea synthesizes 5 and 12 lipoxygenase products such as 12-HETE, 5-HETE and 5,12-DiHETE and cyclooxygenase product HHT from 14C-arachidonic acid. Indomethacin pretreated conjunctiva and anterior uvea generated slow reacting substance (SRS)-like activity from arachidonic acid in the presence of reduced glutathione and A23187. This SRS-like activity contracted guinea pig ileum. Specific SRS-like activity antagonist FPL-55712 inhibited the contractions of guinea pig ileum induced by SRS-like substance generated by either conjunctiva or anterior uvea. The activity was still present in the sample following extraction with organic solvents. SRS-like activity was destroyed by arylsulfatase and its generation was prevented by either boiling or pretreatment with cyclooxygenase/lipoxygenase inhibitors, BW755 and nordihydroguaiacetic acid. These results indicate that following cyclooxygenase inhibition by indomethacin rabbit conjunctiva and anterior uvea generate SRS-like activity from arachidonic acid via lipoxygenase pathways.

4,5-Dihydro-1-(3-(trifluoromethyl)phenyl)-1H-pyraz↗