Key result
Chronic periadventitial administration of bFGF normalized endothelium-dependent responses in the collateral-dependent LCX region and increased arteriolar density 4-fold compared to controls.
Why the study?
Does chronic periadventitial administration of bFGF improve endothelium-dependent relaxation in collateral-dependent coronary microcirculation in a porcine model?
Does chronic periadventitial administration of bFGF improve endothelium-dependent relaxation in collateral-dependent coronary microcirculation in a porcine model?
Chronic periadventitial delivery of bFGF preserves endothelial function and promotes angiogenesis in collateral-dependent coronary microcirculation in a porcine model.
bFGF may improve endothelial function in collateral-dependent vessels; leaves open any therapeutic role in human CAD.
The effect of chronic, periadventitial administration of basic (b) fibroblast growth factor (FGF) on endothelial dysfunction in the collateral-dependent and normally perfused coronary microcirculation was examined. Ameroid constrictors were placed on the proximal left circumflex coronary artery (LCX) in 23 pigs. In 11 pigs, bFGF was released from calcium alginate microcapsules into the perivascular space of the proximal left anterior descending coronary artery (LAD) and LCX. After 5-8 wk, coronary arterial microvessels (80-170 microns) were studied in a pressurized (40 mmHg) no-flow state with video microscopy. Receptor-mediated endothelium-dependent relaxations to ADP and serotonin were reduced while contraction to acetylcholine was enhanced in the collateral-dependent LCX microvessels of non-bFGF-treated control hearts. Relaxation of vessels to the non-receptor-mediated, endothelium-dependent agent A-23187; endothelium-independent relaxation to nitroprusside; and contraction to KCl were similar in all groups. Chronic treatment with bFGF normalized responses to ADP, serotonin, and acetylcholine in the collateral-dependent LCX region but had no effect on the responses of vessels in the normally perfused LAD region. Arteriolar density in the collateral-perfused LCX region of bFGF-treated hearts was markedly increased (4-fold compared with that in untreated hearts, suggesting a link between the angiogenic effect of bFGF and its action on endothelial preservation. Thus the periadventitial, sustained delivery of bFGF preserves receptor-mediated, endothelium-dependent responses in the collateral-dependent LCX region but has no effect on responses of microvessels in the normally perfused LAD region or on non-receptor-mediated endothelium-dependent relaxation.
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Sellke et al. (1994) studied Endothelial dysfunction in collateral-dependent coronary microcirculation (n=23). Basic fibroblast growth factor (bFGF) vs. Non-bFGF-treated control hearts was evaluated on Endothelium-dependent relaxations and arteriolar density. Chronic periadventitial administration of bFGF normalized endothelium-dependent responses in the collateral-dependent LCX region and increased arteriolar density 4-fold compared to controls.
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