Why the study?
Does alloxan-induced diabetes improve endothelial cell regrowth and morphology after balloon catheter injury in rabbits compared to euglycemia?
Does alloxan-induced diabetes improve endothelial cell regrowth and morphology after balloon catheter injury in rabbits compared to euglycemia?
In a rabbit model, alloxan-induced diabetes paradoxically improved endothelial cell regrowth and morphology after balloon catheter injury compared to euglycemia, though vasoreactivity remained impaired.
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These rabbit findings should not guide clinical practice; leaves open whether diabetes accelerates endothelial recovery after injury in humans.
Neointimal thickening after catheter injury has been reported to be influenced by the integrity of the vascular endothelium. We have previously shown that neointimal thickening is significantly reduced in alloxan-induced diabetic New Zealand White rabbits after catheter injury compared with euglycemic rabbits. In the present study, it was hypothesized that endothelial cell regrowth, morphology, and endothelium-dependent vasoreactivity after catheter injury are improved in the diabetic rabbit (glucose >/=400 mg/dl) compared with the euglycemic rabbit. Two weeks after catheter injury, the percent endothelial regrowth was significantly increased in diabetic animals compared with euglycemic animals (32.1 +/- 2 and 15.6 +/- 1, respectively; P < 0.05). The endothelial cell morphology analyzed by scanning electron microscopy was also restored 2 wk after catheter injury in thoracic aortas from the diabetic animals compared with vessels from euglycemic animals. Endothelium-dependent relaxation to ACh in vessels from diabetic and euglycemic rabbits was attenuated 2 wk after injury, and, although improved by 4 and 8 wk, relaxation remained significantly depressed. These results suggest that endothelial cell regrowth and morphology in diabetic animals was improved compared with euglycemic animals; however, endothelium-dependent vasoreactivity remained impaired. Thus the attenuated neointimal thickening seen in the diabetic rabbit may be a function of the rate and degree of regrowth rather than the normalization of ACh-induced relaxation.
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Schiller et al. (1999) studied this question.
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