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C Patrono

Publications and source records attributed to C Patrono.

At least 199 records · Page 11Linked to original sources
PubMed1979

Evidence for an extra-renal origin of urinary prostaglandin E2 in healthy men.

In order to verify the validity of the assumption that male urinary Prostaglandin (PG) E2 reflects its renal production, PGE2 and PGF2 alpha concentrations were measured by radioimmunoassay in the renal venous plasma (RVP) and urine (U) of 12 male and 4 female healthy volunteers. While women had a similar PGE2/PFG2 alpha ratio in RVP (0.59 +/- 0.18) and U (0.41 + 0.06), men and a significantly (P less than 0.05) higher ratio in U (1.43 +/- 1.72) as compared to RVP (0.54 +/- 0.16). This was largely due to considerably higher and more variable U-PGE1 concentrations (roughly 6 times higher than female values), despite almost identical RVP levels. The possibility of an increased U excretion of a cross-reacting member of the PG-system, as a cause of such apparently high PGE2-like immunoreactivity (LI), was ruled out by TLC characterization of PGE2-LI with three different anti-PGE1 sera. Thus, male U-PGE2 may variably reflect an extra-renal source, such as contamination with trace amounts of seminal fluid. It is concluded that, unless such a contamination can be monitored and corrected for, measurement of male U-PGE1 should be considered of questionable relevance to renal PG-synthesis.

Chromatography, Thin Layer↗
PubMed1978

Aspirin intolerance: unaltered susceptibility of platelet cyclo-oxygenase to inhibition by aspirin in vitro.

Inhibition of prostaglandin (PG) biosynthesis has been proposed as a mechanism of aspirin-induced asthma. In order to verify the existence of a generalized abnormal sensitivity of the PG cyclo-oxygenase in intolerant patients, we have compared the inhibitory effects of aspirin on platelet PGE2 and PGF2alpha spontaneous formation in vitro, in 10 healthy subjects, 10 aspirin-sensitive asthmatics, and 10 nonasthmatic aspirin-sensitive patients. No statistically significant differences were found in the pattern nor in the absolute concentrations of both PGs in the control platelet superfusates. Moreover, the synthesis and release of both PGs were inhibited by aspirin with the same potency in the three groups studied.

Adult↗
PubMed1975

Release of prostaglandin F1alpha and F2alpha from superfused platelets: quantitative evaluation of the inhibitory effects of some aspirin-like drugs.

The release of PGF1alpha and PGF2alpha from superfused blood platelets was studied by the combined use of two radioimmunoassay systems with different specificities. PGF1alpha only accounted for approximately 30% of the total immunoreactivity. A substantially similar pattern of release was obtained with platelets of rat and human origin, although the latter released considerably lower amount of both compounds. Indomethacin, Femoprofen, Ditazole and Aspirin all inhibited PGF2alpha release from rat platelets in descending order of potency. Hydrocortisone was partically inactive. The release of PGF1alpha and PGF2alpha was inhibited to the same extent by both Indomethacin and Fenoprofen. Moreover, a quite similar inhibitory effect by the same drug on rat and human platelets was found in preliminary experiments. In agreement with a previous similar finding, Aspirin displayed a higher inhibitory activity than that reported in other tissues. The use of superfused platelets seems to provide a simple and reproducible model for studying pharmacologic influences upon PG formation.

Animals↗
PubMedDate not supplied

Radioimmunoassay measurement of prostaglandins E2 and F2alpha in human urine.

Techniques are described in detail for the radioimmunological measurement of prostaglandin (PG) E2 and F2alpha in human urine. 50 ml urine samples are extracted with an organic solvent system and then purified by silicic acid column chromatography. The overall recovery after extraction and purification, calculated with labeled as well as unlabeled compounds, is in the order of 70%. The column eluates are assayed at 1:12-1:60 dilution in the "standard diluent" of the assay: 8 pg PGE2 or PGF2 alpha/ml of whole urine represents the lowest measurable concentration. A urine blank and a solvent blank were evaluated separately, subjecting 50 ml of urine obtained from an indomethacin treated subject ("PG-free" urine) or 50 ml of distilled water, respectively, to the extraction-purification procedures. Both were found not to interfere with the antigen-antibody reaction. Urinary PG-like immunoreactivity (LI) was characterized in terms of immunochemical and thin-layer chromatographic (TLC) behavior. Both urinary PGE2-LI and PGF2 alpha-LI behaved as authentic PGE2 and PGF2 alpha, upon dilution and on TLC. In 33 healthy female subjects (aged 19-58 yr), urinary excretion rates averaged 178 +/- 80 (mean +/- SD) ng/day for PGE2 and 498 +/- 181 ng/day for PGF2 alpha. In a group of 8 healthy men, both PGE2 and PGF2 alpha excretion rates were higher and more scattered than the female values. When two healthy women were given indomethacin (200 mg/day), urinary PGE2 and PGF2 alpha dropped to undetectable levels during the 4th day of drug therapy. Intravenous injection of furosemide (50 mg) in a female volunteer was followed by an immediate rise of urinary sodium, PGE2, PGF2 alpha and PGE2/PGF2 alpha ratio and plasma renin activity. In a 10 year old girl with Bartter's syndrome, urinary PG excretion rate was elevated with a 3 times higher than normal PGE2/PGF2 alpha ratio. Indomethacin therapy resulted in a prompt drop of PG excretion rate and of plasma renin activity. These results show that a combination of adequate purification steps and antisera with optimal characteristics provides a reliable method for measuring PGE2 and PGF2 alpha in urine, and therefore a valuable tool to further our knowledge of the physiology and physiopathology of the renal PG-system.

Adult↗
PubMedDate not supplied

Role of platelet activation in dementia.

Platelets play an important role in atherosclerosis, and increased platelet activation is associated with stroke. Stroke is an important risk factor for dementia, as approximately 25% of the patients are demented after stroke. In this review, we describe platelet activation studies in patients with stroke and with dementia. In addition, we review the few studies that have investigated the effect of antiplatelet medication such as aspirin and non-steroidal anti-inflammatory drugs on cognitive function and the occurrence of dementia. We conclude that further studies are needed to characterize the mechanisms and determinants of platelet activation in relation to the development of dementia. Furthermore, the efficacy and safety of antiplatelet intervention will have to be assessed in properly designed randomized trials.

Aging↗