thromboxane-a2 and Carotid-Stenosis

To compare the results of computer estimation of atherosclerotic plaque with biochemical data and ascertain any relationship with the occurrence of stroke.. The study involved 20 atherosclerotic plaques causing 70-99% stenosis of internal carotid arteries (ICA). Ultrasonographic examination (USG) images of plaques were analyzed using a computer program. A histogram was obtained for each plaque and a gray scale median (GSM) was determined for each histogram in order to measure the echogenicity of an examined plaque. Then the plaques, collected during endarterectomy, were examined with regard to the concentration of prostaglandins E2 (PGE2), thromboxane A2 (TXA2), and 8 - epi-prostaglandin F2α. This data was compared with GSM and the occurrence of stroke.. The statistical analysis showed significant correlations between low GSM and the occurrence of strokes. Out of 10 plaques with GSM<35, 6 (60.0%) were associated with a stroke. In contrast, out of 10 plaques with GSM>35, only 1 (10.0%) had a stroke. In addition, there were significant differences in the plaque content of PGE 2, (P<0.05) and (TXA2, P<0.011) between groups.. High levels of PGE2 and TXA2, correlated with the low GSM values, may be the features of unstable plaques and that may be associated with a risk for stroke.

Topics: Aged; Biomarkers; Carotid Artery, Internal; Carotid Stenosis; Dinoprost; Female; Humans; Logistic Models; Male; Middle Aged; Pilot Projects; Plaque, Atherosclerotic; Prostaglandins E; Risk Factors; Stroke; Thromboxane A2; Ultrasonography, Doppler, Duplex

The aim of the study was to determine the quantity of produced mediators of inflammation (cytokines and eicosanoids), during carotid endarterectomy (CEA), which are factors of ischemic damage of the brain.. Two groups (A and B) of 15 patients each, with internal carotid backpressure >30 mmHg were operated in our institution. We did not use a shunt in Group A during CEA and group B was operated upon with a shunt. Plasma concentrations of Interleukin-1b (IL-1b), Thromboxane B2 (TXB2), Prostaglandin E2 (PGE2) and tumor necrosis factor-a (TNFa) were measured by enzyme-linked immunosorbent assay (ELISA) technique.. We measured gradual increase of levels of IL-1b and TXB2 during cross-clamping and during reperfusion in group A (P<0.05). The levels of TNFa increased only during reperfusion (P<0.05). The concentration of IL-1b and TNFa remained almost stable in group B, whereas the concentration of TXB2 reduced but not significantly (P>0.05). The levels of PGE2 remained stable in both groups.. We should consider the increase of proinflammatory mediators during carotid cross-clamping when no shunt is used. The critical concentration of these mediators that threaten the brain's vitality is not yet detected. However, the clinical significance of this is unclear, since there were no perioperative strokes.

Topics: Brain Ischemia; Carotid Stenosis; Constriction; Dinoprostone; Endarterectomy, Carotid; Enzyme-Linked Immunosorbent Assay; Female; Greece; Humans; Inflammation Mediators; Interleukin-1beta; Male; Thromboxane A2; Tumor Necrosis Factor-alpha; Up-Regulation

Prostacyclin (PGI2), a metabolite of arachidonic acid, has the vasoprotective effects of vasodilation, anti-platelet aggregation, and inhibition of smooth muscle cell proliferation. We hypothesized that an overexpression of endogenous PGI2 may accelerate the recovery from endothelial damage and inhibit neointimal formation in the injured artery. To test this hypothesis, we investigated in vivo transfer of the PGI2 synthase (PCS) gene into balloon-injured rat carotid arteries by a nonviral lipotransfection method. Seven days after transfection, a significant regeneration of endothelium was observed in the arteries transfected with a plasmid carrying the rat PCS gene (pCMV-PCS), but little regeneration was seen in those with the control plasmid carrying the lacZ gene (pCMV-lacZ) (percent luminal circumference lined by newly regenerated endothelium: 87. 1+/-6.9% in pCMV-PCS-transfected vessels and 6.9+/-0.2% in pCMV-lacZ vessels, P<0.001). BrdU staining of arterial segments demonstrated a significantly lower incorporation in pCMV-PCS-transfected vessels (7. 5+/-0.3% positive nuclei in vessel cells) than in pCMV-lacZ (50. 7+/-9.6%, P<0.01). Moreover, 2 weeks after transfection, the PCS gene transfer resulted in a significant inhibition of neointimal formation (88% reduction in ratio of intima/media areas), whereas medial area was similar among the groups. Arterial segments transfected with pCMV-PCS produced significantly higher levels of 6-keto-PGF1alpha, the main metabolite of PGI2, compared with the segments transfected with pCMV-lacZ (10.2+/-0.55 and 2.1+/-0.32 ng/mg tissue for pCMV-PCS and pCMV-placZ, P<0.001). In conclusion, this study demonstrated that an in vivo PCS gene transfer increased the production of PGI2 and markedly inhibited neointimal formation with accelerated reendothelialization in rat carotid arteries after balloon injury.

Topics: 6-Ketoprostaglandin F1 alpha; Animals; Aorta; Carotid Arteries; Carotid Artery Injuries; Carotid Stenosis; Catheterization; Cell Division; Cytochrome P-450 Enzyme System; Endothelium, Vascular; Gene Expression Regulation, Enzymologic; Gene Transfer Techniques; Genes, Reporter; Intramolecular Oxidoreductases; Lac Operon; Male; Muscle, Smooth, Vascular; Rats; Rats, Sprague-Dawley; Thromboxane A2; Transformation, Genetic; Tunica Intima