Key result
In a porcine model of balloon angioplasty, the nitric oxide donor SIN-1 significantly reduced platelet adhesion (15.1 vs 53.6 x 10^6/cm2, P<0.01) and mural thrombosis (17% vs 71%, P<0.05).
Why the study?
Does the nitric oxide donor SIN-1 reduce platelet and neutrophil adhesion and vasoconstriction in a porcine model of balloon angioplasty?
Does the nitric oxide donor SIN-1 reduce platelet and neutrophil adhesion and vasoconstriction in a porcine model of balloon angioplasty?
In a porcine model of balloon angioplasty, the nitric oxide donor SIN-1 significantly reduced platelet and neutrophil adhesion, mural thrombosis, and postangioplasty vasoconstriction.
Does not support clinical use of SIN-1 in angioplasty; hypothesis-generating for nitric oxide donors in vascular injury models.
Nitric oxide has been reported to modulate platelet and neutrophil interactions with the arterial wall. In this study, we investigated the effects of the nitric oxide donor 3-morpholino-sydnonimine (SIN-1) on platelet and neutrophil adhesion, and the vasomotor response, in a porcine model of angioplasty. Carotid arterial injury was produced by balloon dilation in control (n = 10) and treated (SIN-1; 10 micrograms/kg + 1 microgram/kg/min, i.v.) (n = 8) pigs. At the site of deep arterial injury, the average platelet adhesion was 53.6 +/- 11.3 x 10(6)/cm2 in the control animals and was significantly inhibited by more than 70%, to 15.1 +/- 4.1 x 10(6)/cm2 (P < .01), by SIN-1. Neutrophil adhesion was also decreased by SIN-1, from 255.9 +/- 29.7 to 101.8 +/- 19.7 x 10(3)cm2 (P < .001). Mural thrombosis was found in 12 (71%) of the 17 injured arteries in the control group but in only 2 (17%) of the 12 injured arteries in the SIN-1-treated group (P < .05). Concomitantly, SIN-1 reduced platelet and neutrophil adhesion to the site of endothelial injury distally. The internal diameter of the carotid arteries was similar between the two groups before dilation but was 40% greater at the site of endothelial injury distally in SIN-1-treated animals after dilation (P < .05), as compared with controls. Accordingly, postangioplasty vasoconstriction was significantly attenuated from 46.3 +/- 2.9% in control pigs to 32.5 +/- 4.8% (P < .05) in SIN-1-treated animals. The beneficial effects of SIN-1 were associated with inhibition of neutrophil-mediated whole blood aggregation and of neutrophil-endothelium interactions. The potent antiadhesive and antithrombotic properties of SIN-1 in vivo were confirmed in ex vivo superfusion experiments. These results indicate that administration of a nitric oxide donor may be effective in preventing the acute pathophysiological responses to arterial injury by angioplasty.
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Provost et al. (1997) studied Arterial injury by balloon angioplasty (n=18). 3-morpholino-sydnonimine (SIN-1) vs. Control was evaluated on Platelet adhesion at the site of deep arterial injury (x 10^6/cm2) (p=< .01). In a porcine model of balloon angioplasty, the nitric oxide donor SIN-1 significantly reduced platelet adhesion (15.1 vs 53.6 x 10^6/cm2, P<0.01) and mural thrombosis (17% vs 71%, P<0.05).
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