Why the study?
The study aimed to investigate the effect of adenosine, the role of endothelium, and potassium ion flow in non-occluded or occluded femoral arteries isolated from healthy or diabetic rats.
Does vascular occlusion restore endothelium-dependent relaxation induced by adenosine in diabetic rat femoral arteries?
Does vascular occlusion restore endothelium-dependent relaxation induced by adenosine in diabetic rat femoral arteries?
Vascular occlusion restores the endothelium-dependent relaxation effect of adenosine in diabetic rat femoral arteries, suggesting a potential protective mechanism against ischemic episodes in diabetes.
Findings in diabetic rat arteries should not change practice; hypothesis-generating for adenosine's endothelial and K+ roles.
The aim of this study was to investigate the effect of adenosine in non-occluded or occluded femoral arteries (FA) that were isolated from healthy or diabetic Wistar rats. Determining the role of endothelium, and a transmembrane flow of potassium ions in adenosine actions were also of interest. Diabetes was experimentally induced by alloxan, while the vascular occlusion was performed for 45 min on randomly selected FA. Vascular tone changes were continuously recorded. Selected markers of endothelial dysfunction were measured in animal serum. Thus, adenosine produced a concentration-dependent relaxation of rat FA, which was endothelium-dependent, too, except in a group of diabetic animals. Moreover, serum asymmetric dimethylarginine (ADMA) levels were higher in diabetic animals, thus reflecting endothelial dysfunction (ED). Still, an occlusion of FA enhanced the relaxation effect of adenosine in endothelium-intact rings from diabetic animals. Oppositely, in the presence of high potassium concentration in the buffer, adenosine-induced relaxation was significantly reduced in all of the investigated groups/subgroups. These results suggest that in diabetic animals, an occlusion of FA most probably reversed adenosine-induced relaxation from endothelium-independent into an endothelium-dependent relaxation, thus indicating the possible protective mechanism against ischemic episodes of FA in the presence of diabetes.
No takes yet. Share an insight, caveat, or question.
Stojanović et al. (2018) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: