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Biomedical subjects

B A Peskar

Publications and source records attributed to B A Peskar.

At least 181 records · Page 10Linked to original sources
PubMed1981

Prostacyclin-thromboxane interactions in the platelet-perfused in vitro heart.

A preparation of an isolated platelet-perfused guinea pig heart is described, which was utilized to study prostacyclin-thromboxane interrelationships. Infusion of washed human platelets (4 X 10(8)/min) through the coronary vascular bed stimulated the vascular PGI2 production from 114 +/- 27 to 350 +/- 30 pg/ml (P less than 0.01) and was associated with a significant increase in platelet cAMP from 1.2 +/- 0.4 to 2.6 +/- 0.9 pmol/10(8) platelets (P less than 0.05). Administration of arachidonic acid (AA) (45 micrograms) to the system led to a further increase (eight- to ninefold) of PGI2 and yielded marked thromboxane formation (20-25 ng/ml). Treatment of the hearts with aspirin (1 mM) prevented the PGI2 formation and AA-induced increase in platelet cAMP. Treatment of platelets with aspirin prevented thromboxane formation but did not influence AA-induced changes in platelet cAMP and vascular PGI2 production. Bioassay data of PGI2 and rabbit aortic contracting substance gave results comparable to radioimmunoassay of 6-keto-PGF1 alpha and thromboxane B2. AA always decreased the coronary vascular resistance whether thromboxanes were formed or not.

Animals↗
PubMed1980

Paracetamol does not potentiate the acetylsalicylate inhibition of prostaglandin release from macrophages.

Prostaglandin (PGE2 and PGI2) synthesis can be stimulated in macrophages by the tumour promotor 12-O-tetradecanoylphorbol-13-acetate (TPA) and inhibited by acetylsalicyclic acid (IC50 = 8.2 x 10(-6) M) and paracetamol (IC50 = 1.9 x 10(-4) M). When mixture of both drugs were tested only an additive effect was observed. This result is in contrast to recent reports describing both potentiation of acetylsalicylate-induced PG synthesis inhibition and enhancement of PG production by paracetamol.

Acetaminophen↗
PubMed1980

Enhanced 6-oxo-PGF1 alpha levels in plasma during hemodialysis.

The activation of platelets due to foreign surface interaction is a well known fact. Earlier, we found an increase of circulating platelet microaggregates (method of Wu and Hoak) during hemodialysis. Since this phenomenon might cause a PGI2-release by lung and/or vascular tissue, we studied the plasma 6-oxo-PGF 1 alpha-levels in 6 patients during hemodialysis. We found an initial increase of plasma 6-oxo-PGF 1 alpha. Coincidently, hypoxemia, fall in platelet and lekocyte count and a decrease in platelet count ratio were observed. An effect of heparin was excluded in a control group. The findings support the hypothesis that PGI2 acts as a defense mechanism against platelet deposition on vascular wall by a temporary increased synthesis which could be monitored by a temporarily enhanced plasma 6-oxo-PGF 1 alpha-level during the initial phase of hemodialysis.

6-Ketoprostaglandin F1 alpha↗
PubMed1980

Prostaglandins and prostaglandin metabolites in human gastric juice.

Human gastric juice contains higher concentrations of PG metabolites than of unmetabolized PG indicating that local metabolism might play a role in limiting the biological activity of PG in gastric mucosa and has to be considered when investigating endogenous gastric PG. A major fraction of the 15-keto-13,14-dihydro-PGE2 (KH2PGE2) formed in gastric mucosa and released into the gastric lumen seems to be rapidly dehydrated to a compound co-chromatographing with KH2PGA2, while the amounts of the bicyclic degradation product 11-deoxy-13,14-dihydro-15-keto-11,16-cyclo-PGE2 (11-deoxy-KH2-cyclo-PGE2), as measured by radioimmunoassay, in freshly extracted gastric juice are negligible. Stimulation of secretion with pentagastrin does not influence significantly the concentrations of PG and PG metabolites in human gastric juice, but total output tends to increase parallel to the increase in secretion volume. Levels of immunoreactive 6-keto-PGF1 alpha in human gastric juice are much lower than those of PGE2. Since human gastric mucosa synthesizes conciderable amounts of PGI2 and 6-keto-PGF1 alpha in vitro, the low levels of 6-keto-PGF1 alpha in gastric juice might indicate that PGI2 formed by gastric mucosa in vivo is, like PGE2 and PGF2 alpha, rapidly metabolized and/or removed preferentially via the blood stream.

6-Ketoprostaglandin F1 alpha↗
PubMed1980

Effect of prostaglandins and thromboxane A2 on the contractility of rabbit splenic capsular smooth muscle.

The effect of various prostaglandins (PGs) and a thromboxane A2 (TXA2)-generating system on the contractility of rabbit splenic capsular smooth muscle has been investigated. PGI2 as well as higher concentrations of PGE1 and 5, 6 beta-dihydro-PGI2 inhibit noradrenaline-induced contractions of the smooth muscle preparation. The TXA2-generating system and high concentrations of PGD2, on the other hand, increase the contractions. The results support the concept that the hypothetical PGI2 receptor on the smooth muscle of the rabbit splenic capsule resembles, in its specificity, the PGI2 receptor on platelets.

Animals↗
PubMed1979

Prostaglandin D2 is the prevailing prostaglandin in the acute inflammatory exudate of urate arthritis in the chicken.

An acute inflammation was elicited in intertarsal joints of chicken by injection of urate crystals. Inflammatory exudates recovered at different times were assayed for prostaglandin D2(PGD2)E2 and F2 alpha and thromboxane B2 content by specific radioimmunoassays. We found that PGD2 was the prevailing prostaglandin reaching concentrations up to 10 times in excess of PGE2. This finding was confirmed by gas chromatography-mass spectrometry. It is concluded that PGD2 should be considered as a possible mediator of acute inflammation.

Animals↗
PubMed1979

Prostaglandins and fibroblast functions in vitro.

Secondary embryonic mouse fibroblasts synthesise mainly E-type PG. The formation of PGF2 alpha is about 10 times lower. No PGI2 formation was observed. Secondary embryonic mouse fibroblasts possess an adenylate cyclase which is stimulated by E-type PGs, but little by PGF2 alpha or PGI2. PGE1-induced stimulation of cAMP levels is dose-dependently linked to an increase in biosynthetic activity of the cells, visible in increased GAG biosynthesis and PG formation. cAMP-dependent enhancement of GAG biosynthesis does not alter the carbohydrate spectrum of the secreted GAG, indicating that only the amount, but not the quality of the secreted GAG is affected by PGE1 or cAMP. Steroidal as well as non-steroidal antirheumatic agents can affect either basal or PGE1 stimulated cAMP levels or other components of the adenylate cyclase system independent of their inhibitory action on PG formation. These effects are always reflected in a decrease or increase of GAG biosynthesis. PGE1-induced stimulation of cAMP levels is related to an inhibition of fibroblast proliferation. Reduction of endogenous PG formation for prolonged periods does not result in a prolonged decrease of intracellular cAMP followed by a decrease in GAG biosynthesis or an increase in proliferation. The initial effect of reduced endogenous PG formation is compensated for by an increased sensitivity of the cells to PG's, resulting in maintenance of basal cAMP levels and an increased sensitivity to exogenous PGE1. These effects on cAMP levels are also reflected in GAG biosynthesis and proliferative activity of the cells.

Animals↗
PubMed1978

Radioimmunological determination of prostaglandin D2 synthesis in human thrombocytes.

A specific radioimmunoassay for prostaglandin D2 was developed. Using the radioimmunoassay, prostaglandin D2 synthesis by human thrombocytes was measured. While the cyclooxygenase inhibitor indomethacin inhibits formation of prostaglandin D2, increased formation of prostaglandin D2 was observed in the presence of the thromboxane synthetase inhibitor imidazole.

Blood Platelets↗
PubMed1978

Effect of imidazole on prostaglandin and thromboxane accumulation in urate arthritis.

High concentrations of prostaglandins E2 and F2alpha and much lower concentrations of thromboxane B2 occurs in joint washes of chicken 1--3 h after intra-articular injection of urate crystals. Pretreatment with 200 mg/kg imidazole i.v. reduced the concentration of prostaglandins and of thromboxane B2 in the joint washes significantly. Simultaneously, leucocyte invasion was delayed and development of oedema was inhibited. The results suggest that in urate crystal arthritis the effect on prostaglandin and thromboxane accumulation at the site of inflammation contributes to the anti-inflammatory activity of imidazole.

Animals↗