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M Coppo

Publications and source records attributed to M Coppo.

68 records · Page 4Linked to original sources
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Activity of dipyrone on intraplatelet arachidonic acid metabolism: an in vitro study.

The effects of dipyrone on platelet cyclooxygenase and lipoxygenase were investigated in vitro by the study of 1-14C arachidonic acid (AA) conversion by high performance liquid chromatography (HPLC) on washed platelets at seven different drug concentrations (from 5 to 300 micrograms/ml). The effects of dipyrone on thromboxane (TX) B2 generation from endogenous AA were also studied in platelet-rich plasma and in washed platelets by radioimmunoassay. In the study of 1-14C AA metabolism the inhibitory concentration (IC) 50 for TXB2 was 40 micrograms/ml. However, at the lowest drug concentration (5 micrograms/ml) a slight but significant inhibition was found (25.3%, P less than 0.001) and a complete one at 300 micrograms/ml. A relationship between TXB2 inhibition and log drug concentration was found (r = 0.97, P less than 0.001). Lipoxygenase (LO) activity showed an increase of 45.9% at 20 micrograms/ml and of 251.5% at the highest concentration (r = 0.97, P less than 0.001). The inhibition of TXB2 generation from endogenous AA by washed platelets was of the same order of magnitude of the inhibition of TXB2 production from exogenous 1-14C AA. Our results indicate that dipyrone affects intraplatelet AA metabolism at very low concentrations, however its activity, on a molar ratio basis, appears to be lower than that of other non-steroidal anti-inflammatory drugs.

Adult↗
PubMedDate not supplied

Effect of low-dose heparin treatment on fibrinolysis in patients with previous myocardial infarction.

The present study was designed to investigate whether medium-term, low-dose heparin treatment is able to affect the fibrinolytic system. In a randomized cross-over study 10 asymptomatic patients with previous (1-6 years) myocardial infarction underwent two sequential 15-day treatments, respectively, on heparin and on placebo (saline solution), preceded and separated by 10-day wash-out periods. Heparin (as calcium heparin, 12,500 IU in 0.5 ml) and saline (0.5 ml) were subcutaneously administered once a day at 8 a.m. Blood samples for fibrinolysis studies were withdrawn on the first and 15th day of each period immediately before and 4 h after heparin or saline administration before and after 10 min venous occlusion (VO) respectively. Four hours after the first heparin administration tissue plasminogen activator antigen (t-PA ag) levels significantly increased with respect to saline administration (p < 0.01 and p < 0.05, respectively). After 15-day heparin treatment a decrease in euglobulin lysis time (p < 0.05) and an increase in t-PA activity (act) (p < 0.05) and in t-PA ag (p < 0.01) in comparison with placebo were observed before VO. No statistically significant changes in plasminogen activator inhibitor-1 (PAI-1) levels were found. The variations of fibrinolytic system activity induced by heparin treatment were more marked when evaluated after VO. These results indicate that medium-term low-dose heparin treatment increases t-PA ag formation and/or release with consequent t-PA act increase.

Adult↗
PubMedDate not supplied

[Epistemology of liver cirrhosis].

Critical considerations are expressed on scientific approach to liver cirrhosis, a nosological entity based on both analytical inquiry and long term observation of a large number of cirrhotic patients. The main points taken into consideration are: the etiopathogenesis of cirrhosis; a systematic of diagnostic elements; some preventional aspects of the disease and of its major sequelae. In the histogenetical analysis, the following steps are identified and analysed: a) hepatocellular death (necrosis), b) inflammatory process, c) fibrosis, d) hepatocellular regeneration and disorganized vascular architecture as a consequence of nodular regeneration. The hepatotoxic action of the three most studied and widespread etiologic agents of cirrhosis, alcohol, HBV, iron, is also considered. Finally, as a last pathogenetic step and peculiar to liver cirrhosis, the complex vascular rearrangement that leads to a relative increase of the liver blood flow is analysed. Clinical experience suggests a distinction between active and inactive liver cirrhosis. In the former we find a chronic active hepatitis associated with nodular regeneration and subsequent compensatory blood flow rearrangement. No signs of chronic active hepatitis can be found in the latter which is characterized by irreversible alteration of the liver architecture, reduction of the liver function and hemodynamic rearrangement (portal and arterial). Both nosologic entities can be either clinically characterized or not by symptoms of the major sequelae and complications of cirrhosis. On the basis of the clinical experience, among the complications of cirrhosis spontaneous bacterial peritonitis, gastrointestinal bleeding, hepatorenal syndrome and hepatocarcinoma appear to have a great prognostic value. Association between hepatocarcinoma and liver cirrhosis, which seems to be independent of single etiologic factors of cirrhosis itself, also has a great reliance.(ABSTRACT TRUNCATED AT 250 WORDS)

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