Inhibitory Effect of Lidocaine on Cultured Porcine Aortic Endothelial Cell-dependent Antiaggregation of Platelets

Abstract

Our results suggest that lidocaine has an inhibitory effect on antiaggregation derived from endothelial cells, caused by the inhibition of NO and PGI2 released from endothelial cells.

Self‐limiting enhancement by nitric oxide of oxygen free radical‐induced endothelial cell injury: evidence against the dual action of NO as hydroxyl radical donor/scavenger

“…The bradykinin concentration-dependent increase in the intracellular calcium (EC50 1 nM; ECI 00 100 nM) was confirmed by fura-2 fluorescence spectrometry as described previously (Az-ma et al, 1995a). EDNO release from the cells was also examined by the inhibition of collagen-induced platelet aggregation as described by Az-ma et al (1995b): addition of the incubation buffer from bradykininstimulated PAE cells to platelets caused anti-aggregation, which was inhibited by the co-treatment of the cells with NGmethyl-L-arginine.…”

Differential action of spasmolytic vasodilators on platelet aggregation and endothelial cell‐dependent anti‐aggregation

“…Porcine aortic endothelial (PAE) cells were isolated and cultured as described previously ( 17, 18). The obtained PAE cells were grown to passage 3–4 (split ratio, 1:3) in RD medium [1:1 (v/v) RPMI 1640 medium/Dulbecco’s modified Eagle’s medium (DMEM)] supplemented with bicarbonate (2 mg/ml), N‐[2‐hydroxyethyl] piperazine‐N′‐[2‐ethanesulfonic acid] (HEPES, 15 mM), ampicillin (90 μg/ml), kanamycin (90 μg/ml), and 10% (v/v) fetal bovine serum under a humidified atmosphere of 5% CO 2 in air at 37°C.…”

“…Effects of various vasodilators on platelet aggregation provoked by collagen were measured by the turbidimetric technique using an aggregometer equipped with a thermostat adjusted at 37°C (CAF‐100, Japan Spectroscopic Co.) ( 17). Vasodilators dissolved in PSS (100 μl) at various concentrations were added to PRP (800 μl) stirred at 1000 rpm in a siliconized glass chamber at 5 min prior to the addition of collagen (100 μl, at a final concentration of 4 μg/ml).…”

“…Adherence of platelets to a defective endothelial cell monolayer at the site of anastomosis causes the release of potent vasoconstricting agonists such as thromboxane A 2 and serotonin from platelets stimulated with sub‐endothelial stimuli, including collagen. To prevent these adverse effects, endothelial cells physiologically release vasodilatory and anti‐aggregatory agents, e.g., nitric oxide (NO) and prostacyclin (PGI 2 ) ( 15–17).…”

“…We have previously reported that one of the most frequently used topical vasodilators, lidocaine, concentration‐dependently inhibits endothelial cell dependent anti‐aggregation of platelets stimulated by collagen ( 17). However, little is known about the interactions of other vasodilators with platelet/endothelial cell functions.…”