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Biomedical subjects

J A Lindgren

Publications and source records attributed to J A Lindgren.

At least 91 records · Page 5Linked to original sources
PubMed1981

Leukotrienes promote plasma leakage and leukocyte adhesion in postcapillary venules: in vivo effects with relevance to the acute inflammatory response.

Leukotrienes B4, C4, and D4, members of a recently discovered family of substances biosynthesized from arachidonic acid, were found to have potent microvascular actions in the hamster cheek pouch. When applied topically to the vascular network, leukotrienes C4 and D4 caused an intense constriction of arterioles, being similar to angiotensin in potency in this respect. The vasoconstriction induced by leukotrienes C4 and D4 was short-lived, and it was consistently followed by a marked and dose-dependent extravasation of macromolecules from postcapillary venules. Histamine did not constrict arterioles, but it elicited leakage of plasma, although on a molar basis it was no more than 1/1000th as potent as the leukotrienes. When used in the same concentration range as leukotrienes C4 and D4, leukotriene B4 did not evoke vasoconstriction or promote plasma leakage. On the other hand, leukotriene B4 caused a conspicuous and reversible adhesion of leukocytes to the endothelium in postcapillary venules. Our findings that leukotrienes induce microcirculatory alterations in vivo, closely resembling the early events in the acute inflammatory response, imply that leukotrienes, formed in several blood-borne and tissue-bound cells, may mediate important microcirculatory adjustments to noxious stimuli.

Animals↗
PubMed1980

Endogenous synthesis of prostaglandins E1 and I2 in 3T3 fibroblasts transformed by polyoma virus. Effects on adenosine 3':5'-monophosphate production.

Prostaglandins (PG)E1, E2 and I2 were produced by polyoma virus transformed (py) 3T3 fibroblasts. The levels of PGE1, PGE2 and 6-keto-PGF1 alpha (degradation product of PGI2) were 22.7, 225 and 33.2 ng/ml medium, respectively, 72 h after medium change. The stimulatory potencies of exogenous PGE1, PGE2 and PGI2 on adenosine 3':5'-monophosphate (cyclic AMP) formation were similar. Therefore, the prostaglandin mediated increase in cyclic AMP levels observed during growth of these cells (Claesson, H.-E., Lindgren, J.A. and Hammarström, S. (1977) Eur. J. Biochem. 74, 13) is largely (greater than 80%) mediated by PGE2 and to lesser extents by PGE1 and PGI2.

8,11,14-Eicosatrienoic Acid↗
PubMed1980

Prostaglandins and thromboxanes in amniotic fluid during rivanol-induced abortion and labour.

Abortion or delivery were induced by extra-amniotic instillation of Rivanol during the second trimester in twelve patients and during the third trimester in two patients with fetal death and one patient with fetal acrania. Serial sampling of amniotic fluid was performed through a transabdominal catheter and the levels of free arachidonic acid (AA), prostaglandin F2 alpha (PGF2 alpha), prostaglandin E2 (PGE2), 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) and thromboxane B2 (TXB2) were determined. The levels of AA, PGF2 alpha, PGE2, 6-keto-PGF1 alpha and TXB2 in amniotic fluid increased significantly during induction with the exception of AA in fetal death which was high and remained constant during induction. Furthermore, PGF2 alpha, 6-keto-PGF1 alpha and TXB2 were all significantly correlated to AA. These observations suggested that free AA is released during Rivanol-induction of abortion and labour giving an increased synthesis of PGF2 alpha, PGE2 prostacyclin and thromboxane A2 in the fetal membranes and the decidua but not in the fetus. This increase might be relevant for the initiation and progress of abortion and labour in these patients.

Abortion, Induced↗
PubMed1980

On the mechanism of elevated prostaglandin E2 production in 3T3 fibroblasts transformed by polyoma virus.

Polyoma-virus-transformed 3T3 fibroblasts (py 3T3 cells) produce considerably more prostaglandin E2 than regular 3T3 cells during growth in cell culture. Incubations with exogenous arachidonic acid showed no increase in prostaglandin-producing capacity in the transformed cells. The rates of degradation of prostaglandin E2 were similar in the two lines. After labeling of cells with [1-14C]arachidonic acid, py 3T3 cultures continuously released radioactivity while the release by regular 3T3 cells was almost completed after 3 h. Prostaglandin E2 production during short incubations in buffer at various times after medium change was constantly higher in the transformed cells. Furthermore, hydrocortisone completely inhibited prostaglandin synthesis by the transformed cells. These results suggest that the increased formation of prostaglandin by py 3T3 cells is due to continuously elevated activity of phospholipase A2 or another acyl hydrolase.

Animals↗
PubMed1977

Prostaglandin E2 production in 3T3 cells transformed by polyoma virus raises the intracellular adenosine 3':5'-monophosphate levels.

High cellular adenosine 3':5'-monophosphate (cyclic AMP) were found in a polyoma-virus-transformed 3T3 fibroblast line, which produces comparatively high prostaglandin E2 concentrations. Prostaglandin E2 and cyclic AMP increased with time during 6 days of growth. Both effects were prevented by three different cyclo-oxygenase inhibitors. Addition of prostaglandin E2, at a concentration which would been synthesized in the absence of inhibitor, reversed the effect of indomethacin, one of the cyclo-oxygenase inhibitors, on cyclic AMP. It is concluded that endogenous prostaglandin E2 production in these transformed cells influences their cellular cyclic AMP levels.

5,8,11,14-Eicosatetraynoic Acid↗
PubMed1977

Inhibition of prostaglandin synthesis in mouse 3T3 fibroblasts and human platelets by substituted phenols.

Several substituted phenols with antioxidant properties were potent reversible inhibitors of prostaglandin synthesis in 3T3 cell cultures. The ID50's for prostaglandin (PG) E2 synthesis in these cells were 0.1 muM for 2,6-xylenol, 5 muM for tricresol, 6 muM for p-cresol, 7 muM for o-cresol, 15 muM for 3,5-xylenol, 30 muM for m-cresol and 100 muM for phenol. The corresponding values for aspirin and indomethacin were 4 muM and 0.02 muM, respectively. The substituted phenols also inhibited serotinin release, aggregation and prostaglandin synthesis in human platelets induced by arachidonic acid but not by PGG2.

Animals↗
PubMed1976

Detection of ototoxicity from drugs applied topically to the middle ear space.

This paper summarizes data obtained from two separate studies done in our laboratory. Both studies were done to investigate the possibility that drugs commonly applied to the middle ear space could be the cause of sensori-neural hearing loss. The two drugs that were felt to be the most likely candidates for the studies were neomycin and polymyxin B. In the neomycin study, the various drug concentrations were administered three times a day for four weeks. In the polymyxin B study, the administration was three times a day for two weeks. Cochlear function was evaluated electrophysiologically and by examination of surface preparations of the organ Corti. The data show that both neomycin and polymyxin B can, in concentrations similar to those found in commercially available otic drops, induce cochlear damage when they are applied to the middle ear space of guinea pigs. The degree of damage produced is related. In the case of neomycin, it was shown that the effect worsens as the duration of the dosage administration is extended...

Animals↗