PubMed Health⌕ Search

Biomedical subjects

B A Peskar

Publications and source records attributed to B A Peskar.

At least 199 records · Page 11Linked to original sources
PubMed1978

Chemiluminescence and immune cell activation. I. Early activation of rat thymocytes can be monitored by chemiluminescence measurements.

Immediately after the addition of concanavalin A, rat thymocytes respond, in the presence of luminol, with a burst of chemiluminescence (CL) that can be conveniently monitored in an ordinary liquid scintillation spectrometer. Peak CL is reached after 50 sec. Addition of catalase suppresses 65% of the CL, suggesting that H2O2 generation may be its major source. CL with different kinetic characteristics can also be generated by the calcium ionophore A23187. Our rat thymocytes contain approximately 0.1% endogenous macrophages. Bone marrow-derived rat macrophages also respond to concanavalin A or A23187 stimulation with a burst of CL. However, the kinetic properties of CL as well as the inhibition of CL by catalase in these cells differ markedly from those of thymocyte preparations, suggesting that the major portion of the CL in rat thymocytes actually originates in T lymphocytes. Because CL measurements allow the monitoring of very early events in cell activation and because of the simplicity of the technique, CL measurements may become a useful method for the study of lymphocyte activation, of macrophage-lymphocyte interactions, as well as for the rapid screening for specificity and reactivity of T lymphocyte populations.

Animals↗
PubMed1978

Pharmacological modification of thromboxane and prostaglandin release in cardiac anaphylaxis.

Isolated perfused sensitized guinea pig hearts release relatively large amounts of radioimmunologically measurable thromboxane B2 (TXB2) as well as smaller amounts of prostaglandin (PGs) after antigenic challenge. Using thin layer chromatography the major PG released was shown to cochromatograph with PGD2, while smaller amounts of immunoreactive PGF2alpha were found. The TX-synthetase inhibitor imidazole (100 microgram/ml) significantly decreased TXB2 release and simultaneously increased PG release during cardiac anaphylaxis. On the other hand, the beta-sympathomimetic drug isoproterenol decreased both TXB2 and PG release from the anaphylactic hearts. While isoproterenol significantly diminished anaphylactic coronary flow reduction, imidazole was without effect in this respect. PGD2 (0.5 microgram/min and 5.0 microgram/min) infused intraaortally into non-sensitized guinea pig hearts reduced coronary flow dose-dependently. These results are compatible with the view that release of TX and PGs might contribute to coronary flow reduction in cardiac anaphylaxis.

Anaphylaxis↗
PubMed1977

Radioimmunological determination of thromboxane release in cardiac anaphylaxis.

A sensitive and specific radioimmunoassay for thromboxane B2 were detected in perfusates of anaphylactic guinea pig hearts. Indomethacin decreased thromboxane B2 levels in the perfusates to below the detection limit of the radioimmunoassay and concomitantly delayed the onset of coronary vasoconstriction after antigenic challenge.

Anaphylaxis↗
PubMed1977

Angiotensin II-induced contractions of rabbit splenic capsular strips and release of prostaglandins. Use of radioimmunoassays for prostaglandins E1 and E2.

Rabbit splenic capsular strips contract in response to angiotensin II and simultaneously release prostaglandins E and F into the bath fluid. Contractions, though not sustained, and prostaglandin release are dependent on the concentrations of angiotensin II. Addition of indometacin to the bath fluid inhibits prostaglandin release and potentiates the angiotensin II-induced contractions. Similarly, 5,8,11,14-eicosatetraynoic acid, another blocker of prostaglandin synthesis, potentiates contractions elicited by angiotensin II. Exogenous prostaglandin E1 (300 ng/ml) tends to decrease angiotensin II-induced contractions, while prostaglandin E2 (300 ng/ml) as well as prostaglandin F2alpha (300 ng/ml) significantly increase the contractions produced by angiotensin II. The prostaglandin endoperoxide analogues (15S)-hydroxy-9alpha,11alpha-(epoxymethano)prosta-5Z,13 E-dienoic acid and (15S)-hydroxy-11alpha,9alpha-(epoxymethano)-prosta-5Z,13 E-dienoic acid in concentrations of 300 ng/ml are either without effect or weak smooth muscle stimulants of their own, but do not influence the effect of angiotensin II. By the simultaneous use of sensitive and specific radioimmunoassays for prostaglandins E1 and E2 the prostaglandin E-like substance released by the rabbit splenic capsular strips was found to resemble serologically much more the dienoic prostaglandin E2 than prostaglandin E1. The potentation of the effect of angiotensin II by indometacin and 5,8,11,14-eicosatetraynoic acid might be caused by inhibition of synthesis of prostaglandins or related compounds in the splenic tissue. However, an undefined sensitizing effect of indometacin and 5,8,11,14-eicosatetraynoic acid, not related to their effect on prostaglandin synthetase, on the smooth muscle preparation cannot be excluded.

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

Glucocorticoids: effects on prostaglandin release, cyclic AMP levels and glycosaminoglycan synthesis in fibroblast tissue cultures.

Glucocorticoids (GCs) reduced cyclic AMP levels and inhibited glycosaminoglycan (GAG) synthesis in secondary embryonic mouse fibroblast cultures, when cells were incubated for short periods (30 min). The order of potency was dexamethasone greater than prednisolone greater than hydrocortisone. The effect was more marked, when cyclic AMP levels and GAG synthesis were increased by addition of PGE1. Glucocorticoids exerted no longer an inhibitory effect on cyclic AMP and GAG synthesis in cultures pretreated for 48 h with the steroids. Addition of PGE1 caused a stronger rise in cyclic AMP and GAG synthesis than in controls without GC-preincubation. This enhancement was even more pronounced, when PGE1 was added together with the GCs. The reversal of the inhibitory effect of the GCs into a potentiating effect following preincubation correlated to a reducation of endogenous PGE formation in the cultures. Short-term treatment with GCs did not reduce endogenous PGE levels, but prolonged incubation markedly decreased PGE levels. PGE formation recovered following addition of fresh medium after the 48 h incubation with the steroids, but the amount of PGE formed remained significantly lower than in untreated cultures. Non-glucocorticoid steroid hormones did not decrease PGE levels. The results indicate that the apparent loss of inhibitory activity of GCs on cyclic AMP and GAG synthesis observed after prolonged incubation may result from a reduction of endogenous PGE formation which renders the cells more sensitive to the stimulatory effect of exogenous PGE1.

Animals↗
PubMed1977

Influence of prostaglandins on connective tissue cell growth and function.

Prostaglandins (PGs) are synthesized by cultured fibroblasts. PGs regulate specific cellular functions by influencing cyclic nucleotide levels. PGE1 increases cAMP levels, thus enhancing glycosaminoglycan (GAG) synthesis and reducing proliferation. Exogenous cyclic nucleotides, on the other hand, affect PG formation. Glucocorticoids (GCs) decrease cAMP content, GAG synthesis and PG formation in fibroblasts, the latter effect occurring only after prolonged incubations. The decrease in endogenous PG levels causes a sensitization of the cells to exogenous PGE1, thus counteracting the initial inhibitory effect of GCs on cAMP content and GAG synthesis. Cell proliferation shows an inverse relationship to PG-induced changes in cAMP levels.

Animals↗
PubMed1976

On the metabolism of prostaglandins by rat brain homogenate.

Using radio-immuno assays for prostaglandins and prostaglandin metabolites, three prostaglandin metabolizing enzymes were found in the 100,000 X g supernatant of rat brain, 15-hydroxy-prostaglandin-dehydrogenase, delta13-reductase and prostaglandin E-9-keto-reductase. Specific activity of the latter enzyme was highest in striatum and midbrain and lowest in cortex, cerebellum and spinal cord.

Animals↗
PubMed1976

On the metabolism of prostaglandins by human gastric fundus mucosa.

1. Specific radioimmunoassays for the prostaglandins E2, F2alpha and A2 and the metabolites 13,14-dihydro-15-keto-prostaglandin E2, 15-keto-prostaglandin F2alpha and 13,14-dihydro-15-keto-prostaglandin F2alpha were used to study the metabolism of prostaglandins by gastroscopically obtained small biopsy specimens of human gastric fundus mucosa. 2. Three prostaglandin-metabolizing enzymes were found in the 100 000 X g supernatant of human gastric fundus mucosa, 15-hydroxy-prostaglandin-dehydrogenase, delta13-reductase and delta9-reductase. The specific activity was highest for 15-hydroxy-prostaglandin-dehydrogenase and lowest for delta9-reductase. 3. Formation of prostaglandin A2 (or B2) was not observed under the same conditions. 4. None of the three enzyme activities detected in the 100 000 X g supernatant was found in the 10 000 X g and 100 000 X g pellets of human gastric fundus mucosa. 5. The results indicate that high speed supernatant derived from human gastric mucosa can rapidly metabolize prostaglandin E2 and prostaglandin F2alpha to the 15-keto and 13,14-dihydro-15-keto-derivatives. Furthermore, prostaglandin E2 can be converted to prostaglandin F2alpha, the biological activity of which, on gastric functions, differs from that of prostaglandin E2.

Adult↗
PubMed1976

On the relation between release of prostaglandins and contractility of rabbit splenic capsular strips.

Rabbit splenic capsular strips release prostaglandins E and F when contracted by noradrenaline or methoxamine. Contractions and prostaglandin release are dose-dependent. Cocaine increases significantly the effect of noradrenaline, but not that of methoxamine, on contraction of the strips and release of prostaglandin E. Release of prostaglandin F was increased by the addition of cocaine not only when noradrenaline was used as an agonist but also at two of three dose levels of methoxamine. When indometacin is added to the bath fluid, it inhibits prostaglandin release and at the same time potentiates the contractile effects of noradrenaline and methoxamine on the rabbit splenic capsular strips. The prostaglandin-synthetase blocker 5,8,11,14-eicosatetraynoic acid also potentiates the contractions induced by noradrenaline and methoxamine. Both the effects on prostaglandin synthesis and on contraction exerted by indometacin can be reversed, when indometacin is washed out. Exogenous prostaglandins E1, E2 and F2alpha in concentrations up to 150 ng/ml do not influence contractions of the strips induced by either noradrenaline or methoxamine. At higher concentrations prostaglandin E1 decreases, but prostaglandins E2 and F2alpha increase the contractions induced by both agonists. The potentiation of the effects of noradrenaline and methoxamine on rabbit splenic strips by indometacin and 5,8,11,14-eicosatetraynoic acid cannot be explained by inhibition of uptake1 or uptake2, release of endogenous noradrenaline or inhibition of metabolism of the agonists. It is suggested that the potentiation is caused by inhibition of synthesis of endogenous prostaglandins, although an undefined sensitizing effect of indometacin and 5,8,11,14-eicosatetraynoic acid cannot be completely exclused.

5,8,11,14-Eicosatetraynoic Acid↗
PubMed1975

Prostaglandin, slow-reacting substance, and histamine release from anaphylactic guinea-pig hearts, and its pharmacological modification.

Prostaglandins (Pgs), slow-reacting substance of anaphylaxis (SRS-A), and histamine were released from anaphylactic isolated perfused guinea pig hearts. Pgs were to the greatest part of the F2alpha-type. PgE2 was found in traces only. Neither PgA2, nor the metabolites 13,14-dihydro-15-keto-PgF2alpha and 13,14-dihydro-15-keto-PgE2 were detected in the perfusates. Isoproterenol reduced the PgF2alpha output significantly. This effect was increased by the addition of theophylline. Propranolol did not reverse the effect of isoproterenol, but in a high concentration (5 mug/ml) reduced the PgF2alpha output for its own. Indomethacin completely abolished the anaphylactic prostaglandin release. The histamine liberation was significantly decreased only by the combination of isoproterenol and theophylline, and also by a high concentration of propranolol (5 mug/ml). In contrast to the Pg release, the anaphylactic SRS-A and histamine liberation was not abolished by indomethacin, but rather increased. The results are discussed in view of the possible role of the released substances in the functional events of cardiac anaphylaxis.

Anaphylaxis↗