Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0151814 (coronary occlusion)
 3,687 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A number of heparin-binding growth factors, including basic (bFGF) and acidic (aFGF) fibroblast growth factors have been shown to promote angiogenesis in vivo. In this study, we employed a sustained-release polymer extravascular delivery system to evaluate the angiogenic efficacy of a novel form of genetically modified aFGF in the setting of chronic myocardial ischemia. Fifteen Yorkshire pigs subjected to Ameroid occluder placement on the left circumflex (LCX) artery were treated with perivascularly administered aFGF in ethylene vinyl acetate (EVAc) polymer (10 micrograms, n = 7) or EVAc alone (controls, n = 8). Seven to nine weeks later, after coronary angiography to document Ameroid-induced coronary occlusion, all animals underwent studies of coronary flow and global and regional left ventricular function. Microsphere-determined coronary flow in the Ameroid-compromised territory was significantly increased in aFGF-treated compared with control animals, and this improvement in perfusion was maintained during ventricular pacing. Left ventricular function studies demonstrated improved global and regional function in aFGF-treated animals. We conclude that local perivascular delivery of genetically modified aFGF results in significant improvement in myocardial flow and regional and global left ventricular function.
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PMID:Angiogenic potential of perivascularly delivered aFGF in a porcine model of chronic myocardial ischemia. 953 Feb 6

The aim of this work was to examine factors that could be involved in the occurrence of apoptosis in rat hearts subjected to coronary occlusion followed by reperfusion. To this end, we studied the expression of the pro- and anti-apoptotic factors, bax and bcl-2, respectively, in reperfused ischemic hearts and in hearts injected with bFGF or saline. In anesthetized rats the left coronary artery was occluded for 45 min, the anesthesia withdrawn and the occlusion removed to allow reperfusion; in sham-operated rats the occlusion was omitted. After 4 hours the rats were decapitated and the heart excised. Sections from the left ventricle were stained with anti-bcl-2-antibody and anti-bax-antibody using the TUNEL method which detects apoptosis. Fragmentation of DNA isolated from reperfused ventricles was examined by agarose electrophoresis. In reperfused hearts no bcl-2 staining was observed in the discrete area in which many cardiomyocyte nuclei were stained by the TUNEL method; outside this area staining for bcl-2 was more marked than in sham-operated rats. Sections from reperfused hearts were stained for bax protein over a wide area including the apoptotic region; sham-operated hearts showed little reaction. Staining for bcl-2 was demonstrable in some nuclei in hearts from saline-injected rats; the numbers were unaffected by i. v. bFGF. Ischemia/reperfusion increases the overall expression of both bcl-2 and bax proteins, but bcl-2 is lost from the reperfused area as indicated by TUNEL staining. Accordingly, the ratio of bcl-2 to bax was reduced in the reperfused area, indicating a pro-apoptotic trend. The marked increase in bcl-2 outside the reperfused area could be a mechanism with which to salvage surviving cardiomyocytes.
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PMID:Coronary reperfusion following ischemia: different expression of bcl-2 and bax proteins, and cardiomyocyte apoptosis. 1193 25

Early mechanisms involved in improving capillarity and oxygen transport to cardiac tissue exposed to transient coronary ischemia followed by reperfusion were studied in rats. Under ether anaesthesia, the left coronary artery was mechanically occluded for 3 min after which it was released, and the rats allowed to recover. After 2, 24 or 48 h the rats were sacrificed and the hearts frozen in liquid nitrogen. Frozen cross-sections were stained immunohistochemically for proliferating cell nuclear antigen (PCNA) and for the growth factors, VEGF and bFGF. No reaction for PCNA was seen in sections of sham-operated hearts but an inhomogeneous reaction occurred in annular structures in the occluded hearts at 48 h reperfusion. The stain appeared to be located in proliferating nuclei, and in the cytosol of endothelial cells. It is suggested that PCNA is stimulated by the increase in growth factors that is known to occur within 2 h after the end of the coronary occlusion. It is concluded that the increase in capillarity, indicated by the nuclear proliferation of endothelial cells, will improve the transport of oxygen to the cardiac tissues.
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PMID:Expression of proliferating cell nuclear antigen in rat hearts subjected to transient ischemia followed by reperfusion. 1456 55