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Biomedical subjects

A Uzan

Publications and source records attributed to A Uzan.

121 records · Page 7Linked to original sources
PubMedDate not supplied

Enoxaparin reduces cerebral edemaafter photothrombotic injury in the rat.

This study investigates the effect of enoxaparin (Lovenox, Klexane), a low-molecular-weight heparin, on edema following a photothrombotic lesion using rose bengal dye in the rat. An area of cerebral ischemia was provoked in the right hemisphere of rats. Edema developed over 24 h after the lesion, as seen comparing water content of a core sample from the right hemisphere to that of a similar sample from the left hemisphere of each rat. Enoxaparin at 0. 5 mg/kg i.v. plus 2 mg/kg s.c. reduced edema 24 h after lesion induction by 32% (p < 0.01) when the treatment was started 2 h after photothrombotic insult, with maintenance doses of 2 mg/kg s.c. enoxaparin at 6 and 18 h. When the same initial treatment with enoxaparin was started 18 h after insult, there was still a significant reduction of 20% (p < 0.01) in cerebral edema. Administration of enoxaparin 18 h after insult reduced cerebral edema in a dose-dependent manner. There was no evidence of intracranial hemorrhages in any of the animal groups and when the hemoglobin content of the brain samples was assayed by the method of Drabkin, no increase in hemoglobin content was seen compared to sham-operated animals.

Animals↗
PubMedDate not supplied

Combination of enoxaparin and fibroblast growth factor-1 increases myocardial blood flow and capillary density after myocardial infarction in rabbits.

OBJECTIVE: The effect of enoxaparin and fibroblast growth factor-1 (FGF-1) on post-infarction capillary density and regional myocardial blood flow (RMBF) was examined. METHODS: New Zealand White rabbits received an intramyocardial injection of either physiological saline, FGF-1 + enoxaparin, FGF-1 or enoxaparin directly after ligation of the left anterior descending artery. RMBF and capillary density were investigated using fluorescent microspheres and histological examination. RESULTS: One week after infarction a significant difference in the number of capillaries could be demonstrated within the FGF-1 + enoxaparin group (p < 0.001 versus the control group), the FGF-1 group (p < 0.01) and the enoxaparin group (p < 0.05). Treatment with FGF-1 + enoxaparin resulted in a significantly increased number of capillaries compared to treatment with FGF-1 (p < 0.05) and enoxaparin (p < 0.05) alone. Additionally, all groups treated with FGF-1 and/or enoxaparin showed a significant increase of microvessel density in the treated ischemic border zone compared to the non-treated ischemic border zone (p < 0.001 for FGF-1 + enoxaparin, p < 0.01 for FGF-1, p < 0.05 for enoxaparin). RMBF was significantly increased within the FGF-1 + enoxaparin group compared to the control group (p < 0.05). Moreover, perfusion rates within the FGF-1 + enoxaparin-treated area did not significantly differ from the pre-infarction values. CONCLUSION: Treatment with either enoxaparin or FGF-1 or FGF-1 + enoxaparin resulted in increased microvessel growth. However, only the combination of enoxaparin with FGF-1 promotes capillary growth and RMBF. Thus, we conclude that enoxaparin enhances the angiogenic potential of intramyocardially injected FGF-1 in the acutely infarcted rabbit heart.

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PubMedDate not supplied

Modulation of voltage-operated, but not receptor-operated, calcium channels in the rabbit aorta by PK 11195, an antagonist of peripheral-type benzodiazepine receptors.

We compared the effects of PK 11195, an antagonist of peripheral benzodiazepine receptors, on contractions of rabbit aorta by activation of either voltage-operated calcium channels (VOC) using BAY K 8644 (a calcium "agonist") and KCl or receptor-operated channels (ROC) using phenylephrine and B-HT 920, (alpha 1- and alpha 2-adrenoceptor agonist, respectively). In partially depolarized muscle strips, BAY K 8644 induced contractions that were noncompetitively inhibited by PK 11195 (pD'2 = 5.6 +/- 0.15). The effect of this calcium agonist was also antagonized by nitrendipine (competitively) and by yohimbine (noncompetitively), while prazosin was inactive. Contractions induced by KCl were inhibited by nitrendipine and, weakly, by PK 11195. Contractions induced by phenylephrine and B-HT 920 were inhibited competitively by prazosin and yohimbine and noncompetitively by nitrendipine, while PK 11195 was ineffective. It is concluded that PK 11195 behaves as an antagonist of VOC activated by BAY K 8644 and to a lesser extent by KCl depolarization but not of ROC coupled to alpha 1- and alpha 2-receptors.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMedDate not supplied

[Biochemical characterization and study by quantitative autoradiography of the binding sites of indalpine, a 5-HT uptake inhibitor, in cat brain].

The [3H]indalpine binding sites have been characterized in slide-mounted cat brain sections. This inhibitor of 5-HT reuptake binds with a very high affinity to sites which have the pharmacological properties of the serotonin carrier. These sites can, however, be differentiated from the [3H]imipramine binding sites by their Na+ dependency and competitive inhibition by serotonin. Quantitative autoradiographic studies demonstrate that indalpine binding sites are localized in structures rich in serotonergic neurons. The widespread distribution of indalpine binding sites in limbic and associative areas is consisted with its well characterized antidepressant activity in human.

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