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J Monasterio

Publications and source records attributed to J Monasterio.

39 records · Page 3Linked to original sources
PubMedDate not supplied

Effects of recombinant hirudin on D dimer levels before and after experimental venous thrombosis.

In a randomized, blind study, the effect of saline, a low-molecular-weight heparin (Fragmin), and a recombinant hirudin (CGP 39393) on thrombin-antithrombin (TAT) complexes and D dimer (DD) levels were studied in 60 rabbits. The drugs were always injected subcutaneously 2 h before the induction of thrombosis in the jugular vein by a combination of endothelial damage and flow reduction. A sample of blood was obtained just before surgery, and a further sample was obtained 10 min after thrombus formation. No significant differences were found in TAT plasma levels between the different study agents, either before or after thrombus development. However, 2 h after drug administration DD values were significantly lower in hirudin-treated animals (292 +/- 69 vs. 372 +/- 138 ng/ml; p < 0.05). Then, after thrombus formation, DD levels significantly increased in all three groups of animals, as compared to baseline levels. But the increase was significantly higher in hirudin-treated rabbits; DD levels after thrombus development were significantly higher in this group as compared to placebo (779 +/- 188 vs. 664 +/- 152 ng/ml; p < 0.05). There are no previous reports in the literature about the effect of hirudin on DD levels. Our hypothesis is that the effect of hirudin on DD may be the result of its ability to inhibit the thrombin-induced thrombus growth. If the thrombus is not allowed to grow then it will lyse more quickly, producing more DD and the process will not be impaired by the constant deposition of fibrin.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMedDate not supplied

[Correlation between the expression of proinflammatory cytokines and matrix metalloproteinases in the acute phase of an ischemic stroke].

INTRODUCTION: Proinflammatory cytokines are the main responsible for the onset of postischemic inflammatory cascade. Recently, the deleterious effect of matrix metalloproteinases (MMPs) in the acute phase of stroke has been described. Animal models suggest a link between both families. OBJECTIVE: We aimed to investigate possible relations between the MMP overproduction and proinflammatory cytokine expression after human ischemic stroke. PATIENTS AND METHODS: From all consecutive stroke patients attended during a 10 months period, we selected and prospectively studied those presenting as a cardioembolic stroke involving the MCA territory. MMP 9, MMP 2 and IL 6 were serially measured by means of ELISA at study entry and at 12, 24 and 48 hours after symptoms onset. RESULTS: A total of 39 patients were studied. A positive correlation was found between mean expression of both MMPs and IL 6 (r= 0.33, p= 0.040 for MMP 2 y r= 0.45, p= 0.004 for MMP 9). From all measured timepoints, the best obtained correlation was that of MMP 9 with IL 6 at 24 hours (r= 0.418, p= 0.010). At 24 h a peak value of IL 6 was observed. Baseline MMP 2 and MMP 9 levels showed a trend to correlate with that peak of IL 6 (r= 0.329, p= 0.061 for MMP 2 y r= 0.325, p= 0.061 for MMP 9). CONCLUSION: MMP expression correlates with the inflammatory cascade activation after acute cardioembolic stroke.

Acute Disease↗