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Antioxidant effect of lidocaine and procaine on reactive oxygen species-induced endothelial dysfunction in the rabbit abdominal aorta.

Lee JM, Suh JK, Jeong JS, Cho SY, Kim DW - Korean J Anesthesiol (2010)

Bottom Line: The aortic rings were pretreated with lidocaine or procaine (10(-5) M to 3 x 10(-3) M) to compare their effects, as well as ROS scavengers, catalase, mannitol, sodium salicylate, and deferoxamine, and a catalase inhibitor, 3-amino-1,2,4-triazole (3AT).The 3AT pretreated procaine (3 x 10(-3) M) group decreased more significantly than the un-pretreated procaine group (P < 0.05).These findings suggest that lidocaine and procaine dose-dependently preserve endothelium-dependent vasorelaxation against ROS attack, potentially via hydrogen peroxide scavenging.

View Article: PubMed Central - PubMed

Affiliation: Department of Anesthesiology and Pain Medicine, College of Medicine, Catholic University of Korea, Seoul, Korea.

ABSTRACT

Background: Reactive oxygen species (ROS) induce lipid peroxidation and tissue damage in the endothelium. We tested the antioxidant effect of lidocaine and procaine on ROS-induced endothelial damage in the rabbit aorta.

Methods: Aortic rings isolated from rabbits were suspended in an organ bath filled with Krebs-Henseleit (K-H) solution bubbled with 5% CO(2) and 95% O(2) at 37.5. After precontraction with phenylephrine (PE, 10(-6) M), changes in tension were recorded following a cumulative administration of acetylcholine (ACh 3 x 10(-8) to 10(-6) M). Differences were measured as percentages of ACh-induced relaxation of aortic rings before and after exposure to ROS as generated by electrolysis of the K-H solution. The aortic rings were pretreated with lidocaine or procaine (10(-5) M to 3 x 10(-3) M) to compare their effects, as well as ROS scavengers, catalase, mannitol, sodium salicylate, and deferoxamine, and a catalase inhibitor, 3-amino-1,2,4-triazole (3AT).

Results: Lidocaine and procaine dose-dependently maintained endothelium-dependent relaxation induced by ACh despite ROS activity (P < 0.05 vs control value). The 3AT pretreated procaine (3 x 10(-3) M) group decreased more significantly than the un-pretreated procaine group (P < 0.05).

Conclusions: These findings suggest that lidocaine and procaine dose-dependently preserve endothelium-dependent vasorelaxation against ROS attack, potentially via hydrogen peroxide scavenging.

No MeSH data available.


Related in: MedlinePlus

Effect of low doses of lidocaine pretreatment (L-5: 10-5, L3x-5: 3 × 10-5, L-4: 10-4 M) on the reactive oxygen species (ROS) attack. Data are presented as mean ± SE. ACh: acetylcholine, EL(-): before electrolysis. *P < 0.05, compared with ACh 10-7 to 10-6 M of EL(-), †P < 0.05, compared with ACh 10-7 to 10-6 M of the lidocaine 10-5 M (L-5) group.
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Figure 2: Effect of low doses of lidocaine pretreatment (L-5: 10-5, L3x-5: 3 × 10-5, L-4: 10-4 M) on the reactive oxygen species (ROS) attack. Data are presented as mean ± SE. ACh: acetylcholine, EL(-): before electrolysis. *P < 0.05, compared with ACh 10-7 to 10-6 M of EL(-), †P < 0.05, compared with ACh 10-7 to 10-6 M of the lidocaine 10-5 M (L-5) group.

Mentions: Lidocaine dose-dependently reduced the relaxation by ACh 10-7, 3 × 10-7, and 10-6 M after ROS exposure (P < 0.05, Fig. 2 and 3). Similarly, procaine dose-dependently reduced the relaxation induced by ACh when compared with that before the ROS exposure (P < 0.05, Fig. 4 and 5).


Antioxidant effect of lidocaine and procaine on reactive oxygen species-induced endothelial dysfunction in the rabbit abdominal aorta.

Lee JM, Suh JK, Jeong JS, Cho SY, Kim DW - Korean J Anesthesiol (2010)

Effect of low doses of lidocaine pretreatment (L-5: 10-5, L3x-5: 3 × 10-5, L-4: 10-4 M) on the reactive oxygen species (ROS) attack. Data are presented as mean ± SE. ACh: acetylcholine, EL(-): before electrolysis. *P < 0.05, compared with ACh 10-7 to 10-6 M of EL(-), †P < 0.05, compared with ACh 10-7 to 10-6 M of the lidocaine 10-5 M (L-5) group.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC2926425&req=5

Figure 2: Effect of low doses of lidocaine pretreatment (L-5: 10-5, L3x-5: 3 × 10-5, L-4: 10-4 M) on the reactive oxygen species (ROS) attack. Data are presented as mean ± SE. ACh: acetylcholine, EL(-): before electrolysis. *P < 0.05, compared with ACh 10-7 to 10-6 M of EL(-), †P < 0.05, compared with ACh 10-7 to 10-6 M of the lidocaine 10-5 M (L-5) group.
Mentions: Lidocaine dose-dependently reduced the relaxation by ACh 10-7, 3 × 10-7, and 10-6 M after ROS exposure (P < 0.05, Fig. 2 and 3). Similarly, procaine dose-dependently reduced the relaxation induced by ACh when compared with that before the ROS exposure (P < 0.05, Fig. 4 and 5).

Bottom Line: The aortic rings were pretreated with lidocaine or procaine (10(-5) M to 3 x 10(-3) M) to compare their effects, as well as ROS scavengers, catalase, mannitol, sodium salicylate, and deferoxamine, and a catalase inhibitor, 3-amino-1,2,4-triazole (3AT).The 3AT pretreated procaine (3 x 10(-3) M) group decreased more significantly than the un-pretreated procaine group (P < 0.05).These findings suggest that lidocaine and procaine dose-dependently preserve endothelium-dependent vasorelaxation against ROS attack, potentially via hydrogen peroxide scavenging.

View Article: PubMed Central - PubMed

Affiliation: Department of Anesthesiology and Pain Medicine, College of Medicine, Catholic University of Korea, Seoul, Korea.

ABSTRACT

Background: Reactive oxygen species (ROS) induce lipid peroxidation and tissue damage in the endothelium. We tested the antioxidant effect of lidocaine and procaine on ROS-induced endothelial damage in the rabbit aorta.

Methods: Aortic rings isolated from rabbits were suspended in an organ bath filled with Krebs-Henseleit (K-H) solution bubbled with 5% CO(2) and 95% O(2) at 37.5. After precontraction with phenylephrine (PE, 10(-6) M), changes in tension were recorded following a cumulative administration of acetylcholine (ACh 3 x 10(-8) to 10(-6) M). Differences were measured as percentages of ACh-induced relaxation of aortic rings before and after exposure to ROS as generated by electrolysis of the K-H solution. The aortic rings were pretreated with lidocaine or procaine (10(-5) M to 3 x 10(-3) M) to compare their effects, as well as ROS scavengers, catalase, mannitol, sodium salicylate, and deferoxamine, and a catalase inhibitor, 3-amino-1,2,4-triazole (3AT).

Results: Lidocaine and procaine dose-dependently maintained endothelium-dependent relaxation induced by ACh despite ROS activity (P < 0.05 vs control value). The 3AT pretreated procaine (3 x 10(-3) M) group decreased more significantly than the un-pretreated procaine group (P < 0.05).

Conclusions: These findings suggest that lidocaine and procaine dose-dependently preserve endothelium-dependent vasorelaxation against ROS attack, potentially via hydrogen peroxide scavenging.

No MeSH data available.


Related in: MedlinePlus