In Vivo CNT Toxicity to Cardiovascular Homeostasis

If persistent, these molecules (coding for inflammation, oxidative stress, remodeling, and thrombosis) can cause endothelial dysfunction and acceleration of arthrosclero-sis progression [117]. SWNTs were shown also to alter the cardiac activity by affecting the arterial baroreflex function (BRF) of sinus mode in rats exposed by intratracheal instillation [118]. 

Radomski et al. [113] demonstrated that the CNTs were efficient in causing platelet aggregation both in vitro and in vivo, accelerating significantly the rate of development of carotid artery thrombosis in rats. Platelet aggregation was likely to result from MMP-dependent activation of GPIIb/IIa receptor. 

These findings suggest that CNT exposure should be evaluated as a potential cardiovascular risk factor. It should be noted, however, that no thrombosis or other adverse effects on the cardiovascular homeostasis were reported after intravenous injection in healthy animals, when this administration route was used for investigating the biokinetics of CNTs [119-126]. 

---