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Biomedical subjects

F Martelli

Publications and source records attributed to F Martelli.

45 records · Page 3Linked to original sources
PubMed1986

The co-operative action of hyaluronidase and urokinase on the isoproterenol-induced myocardial infarction in rats.

The effects of the intravenous administration of hyaluronidase (HY; 2,500 IU/kg) and urokinase (UK; 20,000 and 40,000 IU/kg), alone or in combination, on the isoproterenol (ISP) induced myocardial infarction (MI) in rats, were studied. The severity of infarction was determined by measuring the levels of serum enzymes (CPK, GOT, LDH) and by evaluating the extent of the injured areas and the incidence of mortality. Plasma thromboxane B2 (TXB2) levels were also determined. All the treatments reduced the infarction area and the enzyme levels (increased by ISP) to a varying degree. However, a definite potentiating activity was obtained when HY was combined with the highest dose of UK. This combination was also capable of reducing the mortality rate. Finally, both HY and UK or the combined preparation brought the plasma TXB2 levels back to normal. These findings suggest the possibility of complementary activities of HY and UK in the treatment of experimental MI.

Animals↗
PubMed1986

[Digoxin-propafenone interaction: values and limitations of plasma determination of the 2 drugs. Anti-arrhythmia effectiveness of propafenone].

Propafenon's influence on the pharmacokinetic and actions of digitalis and viceversa have been evaluated in 27 patients (25 with ventricular hyperkinetic arrhythmias and 2 with paroxismal atrial fibrillation). Patients were divided in two groups according to whether the drug firstly administered were digoxin or propafenon. Plasmatic digoxin and/or propafenon's concentrations, these last performed only in 12 patients, were determined before and during the association and after propafenon's interruption at 7.55-9-11 and at 3-8 p.m. During drug's association area under the plasmatic digoxin concentration curve (AUC 12h) increased on the average by 13.8% (from 19.27 +/- 6.002 ng hours/ml to 21.94 +/- 6.198 ng hours/ml: P less than 0.05) and by 19% at the first hour. Neverthless individual behaviour was not homogeneous since the plasmatic digoxin concentration (PDC) increased in 22 cases (81.4%) and decreased in 5 (18.6%). In 6 patients mean increase was 38.8% (from 16.72 +/- 3.0 ng hours/ml to 23.21 +/- 5.44 ng hours/ml) without signs of digoxin intoxication. Another patient with congestive heart failure and basal PDC 1.87 ng/ml experienced digoxin poisoning with fatal ventricular fibrillation after propafenon. Digoxin administration in the second group's patients produced a not significant increase of plasmatic propafenon concentration (PPC). There was a good correlation among propafenon's absolute amount and plasmatic concentration and antiarrhythmic effect and no correlation among PPC and body-weight related dose. Propafenon's to digitalis association induced, in propafenon's steady state, significant P-R longation from 170 to 190 ms (P less than 0.01) but HR, QRS and QTc didn't show any important change (P greater than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1983

The vascular protection of ditazole and its effect on arachidonic acid metabolism.

Ditazole (4,5-diphenyl-2-bis-(2-hydroxyethyl)-aminoxazol) is a weak anti-inflammatory drug and has been shown to inhibit thrombus formation following electrically stimulated vascular damage in the microcirculation of the hamster cheek pouch. The drug was found to inhibit thromboxane A2 (TXA2) production ex vivo as determined by radioimmunoassay (RIA) and to reversibly antagonise the effect of TXA2 on smooth vascular tissue. However, in contrast to acetylsalicylic acid (ASA), it does not inhibit vessel cyclooxygenase. The apparent vascular protective effect of ditazole could not be ascribed to an enhanced production of vascular prostacyclin (PGI2) since the latter, when estimated ex vivo by RIA, was not enhanced following oral treatment with the drug. It is suggested that the mode-of-action of ditazole may be different from the cyclo-oxygenase/PG synthetase blocking action of most other non-steroidal anti-inflammatory drugs.

Animals↗
PubMedDate not supplied

Ability of recombinant human TNF binding protein-1 (r-hTBP-1) to inhibit the development of experimentally-induced endometriosis in rats.

The aim of this study was to assess whether r-hTBP-1 (recombinant human tumor necrosis factor binding protein-1), the soluble form of tumor necrosis factor-alpha (TNF) receptor type 1 might be effective in counteracting the proliferation of ectopic endometrium using an in vivo experimental model of endometriosis. The in vivo model involved transplanting a square fragment of autologus uterine tissue onto the inner surface of the abdominal wall in rats. r-hTBP-1 was administered for 1 week at 10 mg/kg, s.c. divided into two daily injections. The gonadotropin-releasing hormone antagonist antide was used for reference and given at the dose of 2 mg/kg, s.c. every 3 days for 1 week. The animals were killed 2 and 9 days after the last treatment and the size of endometriotic implants measured. Blood samples and spleens were also taken for assessment of estradiol-17beta levels and natural killer (NK) activity in vitro against murine YAC cells, respectively. The results of this study indicate that r-hTBP-1 is effective in reducing the size of the endometriotic-like foci mainly at the later sacrifice time-point when they were significantly decreased by 64% as compared to control animals. As expected, antide induces an almost complete and statistically significant remission both at the 2-day (94%) and the 9-day (88%); sacrifice time-point. Histological examination indicates that, compared to controls, r-hTBP-1 induces a slightly increased degeneration of the stromal tissues of the implants at both examination times and, limitedly to the earlier observation time, of the mucosal epithelium. No differences in the spleen cell NK activity were observed at either sacrifice time-points in any treatment group. Estradiol-17beta concentrations are significantly decreased in the antide-treated groups only at 9 days while no statistically significant changes are found in the animals receiving r-hTBP-1. The results of this study carried out in a rat experimental model of endometriosis provide evidence of the potential effectiveness of r-hTBP-1 in this pathological condition and support the role of TNF in its development.

Animals↗
PubMedDate not supplied

Coenzyme Q10, exercise lactate and CTG trinucleotide expansion in myotonic dystrophy.

Steinert's myotonic dystrophy (DM) is a genetic autosomal dominant disease and the most frequent muscular dystrophy in adulthood. Although causative mutation is recognized as a CTG trinucleotide expansion on 19q13.3, pathogenic mechanisms of multisystem involvement of DM are still under debate. It has been suggested that mitochondrial abnormalities can occur in this disease and deficiency of coenzyme Q 10 (CoQ10) has been considered one possible cause for this. The aim of this investigation was to evaluate, in 35 DM patients, CoQ10 blood levels and relate them to the degree of CTG expansion as well as to the amount of lactate production in exercising muscle as indicator of mitochondrial dysfunction. CoQ10 concentrations appeared significantly reduced with respect to normal controls: 0.85 +/- 0.25 vs. 1.58 +/- 0.28 microg/ml (p < 0.05). Mean values of blood lactate were significantly higher in DM patients than controls (p < 0.05) both in resting conditions (2.9 +/- 0.55 vs. 1.44 +/- 1.11 mmol/L) and at the exercise peak (6.77 +/- 1.79 vs. 4.90 +/- 0.59 mmol/L), while exercise lactate threshold was anticipated (30-50% vs. 60-70% of the predicted normal maximal power output, p < 0.05). Statistical analysis showed that serum CoQ10 levels were significantly (p < 0.05) inversely correlated with both CTG expansion degree and lactate values at exercise lactate threshold level. Our data indicates the occurrence of reduced CoQ10 levels in DM, possibly related to disease pathogenic mechanisms associated with abnormal CTG trinucleotide amplification.

Adult↗
PubMedDate not supplied

[Basic behavior and behavior after stimulation of inflammatory cellular response, leukocytary chemotaxis and phagocytosis in aged subjects with depression of cellular immunity].

A larger group of 70--75 years aged subjects was studied by means of various cutaneous tests, by E-rosette formation and by blastogenic response and 18 people showing a depressed cellular immunity were selected. These subjects and a similar control group with normal C.M.I. were further investigated in various condition of stimulation for cellular response in inflammation, chemotaxis, phagocytic activity and polysaccharide content in the granulocyte citoplasm. In general the former activity was not depressed, chemotaxis and phagocytic values were deficient, polysaccharide content appeared the same in the normal (control) and in the immune deficient group.

Age Factors↗