Pharmacological Study and Pharmaceutical Intervention to Reduce Intravenous Injection-induced XXXX .

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Intravenous injection often causes vasc @entity1317 h as veno @entity146 sc @entity158 d phle @entity3527 sc @entity1317 eriorates the pati @entity1 OL and sometimes limits the continuation of injection therapy. Pharmaceutical intervention and pharmacological mechanisms used to reduce vasc @entity1317 uced by vino @entity1206 epir @entity1259 e reviewed. A multivariate logistic regression analysis revealed that the dose of vino @entity1206 40 mg) was a significant predictor for veno @entity146 teration of the volume of normal saline for vino @entity1206 solution, from 50 to 100 mL, significantly decreased the grade of veno @entity146 the other hand, the phle @entity3527 res were significantly higher in pati @entity1 ated with epir @entity1259 dy-to-use solution compared with lyophilized powder. The change of formulation of epir @entity1259 lyophilized powder decreased the risk of veno @entity146 e concentration inducing 50% cell viability inhibition was lower in the order of vesicant, irritant, and nonvesicant drugs on porcine aorta endothelial cells (PAECs), suggesting that the injuring effects of anticancer drugs on PAECs may be relevant as an indicator of the frequency of their vasc @entity1317 e exposure to vino @entity1206 PAECs rapidly depleted intracellular glut @entity2041 els and increased intracellular reactive oxyg @entity26 cies production. Moreover, exposure to epir @entity1259 reased intracellular lipid pero @entity2625 els and enhanced the phosphorylation of p38 @entity1435 ogen-activated protein kinase. These results demonstrate that oxidative stress plays an important role in vino @entity1206 d epir @entity1259 uced endo @entity130 d may therefore increase the potential for vasc @entity1317 n intravenous injection.
