Abstract
BackgroundThe uses of engineered nanomaterials have expanded in biomedical technology and consumer manufacturing. Furthermore, pulmonary exposure to various engineered nanomaterials has, likewise, demonstrated the ability to exacerbate cardiac ischemia reperfusion (I/R) injury. However, the influence of particle size or capping agent remains unclear. In an effort to address these influences we explored response to 2 different size gold core nanosilver particles (AgNP) with two different capping agents at 2 different time points. We hypothesized that a pulmonary exposure to AgNP induces cardiovascular toxicity influenced by inflammation and vascular dysfunction resulting in expansion of cardiac I/R Injury that is sensitive to particle size and the capping agent.MethodsMale Sprague–Dawley rats were exposed to 200 μg of 20 or 110 nm polyvinylprryolidone (PVP) or citrate capped AgNP. One and 7 days following intratracheal instillation serum was analyzed for concentrations of selected cytokines; cardiac I/R injury and isolated coronary artery and aorta segment were assessed for constrictor responses and endothelial dependent relaxation and endothelial independent nitric oxide dependent relaxation.ResultsAgNP instillation resulted in modest increase in selected serum cytokines with elevations in IL-2, IL-18, and IL-6. Instillation resulted in a derangement of vascular responses to constrictors serotonin or phenylephrine, as well as endothelial dependent relaxations with acetylcholine or endothelial independent relaxations by sodium nitroprusside in a capping and size dependent manner. Exposure to both 20 and 110 nm AgNP resulted in exacerbation cardiac I/R injury 1 day following IT instillation independent of capping agent with 20 nm AgNP inducing marginally greater injury. Seven days following IT instillation the expansion of I/R injury persisted but the greatest injury was associated with exposure to 110 nm PVP capped AgNP resulted in nearly a two-fold larger infarct size compared to naïve.ConclusionsExposure to AgNP may result in vascular dysfunction, a potentially maladaptive sensitization of the immune system to respond to a secondary insult (e.g., cardiac I/R) which may drive expansion of I/R injury at 1 and 7 days following IT instillation where the extent of injury could be correlated with capping agents and AgNP size.Electronic supplementary materialThe online version of this article (doi:10.1186/s12989-016-0159-z) contains supplementary material, which is available to authorized users.
Highlights
The uses of engineered nanomaterials have expanded in biomedical technology and consumer manufacturing
We investigated the unique cardiovascular toxicity associated with pulmonary exposure to AgNP
In order to evaluate the cardiovascular toxicity endpoints following pulmonary instillation of AgNP we evaluated vascular responses in the aorta and coronary artery, as well as investigated the impact of AgNP on cardiac ischemia reperfusion (I/R) injury
Summary
The uses of engineered nanomaterials have expanded in biomedical technology and consumer manufacturing. In an effort to address these influences we explored response to 2 different size gold core nanosilver particles (AgNP) with two different capping agents at 2 different time points. We hypothesized that a pulmonary exposure to AgNP induces cardiovascular toxicity influenced by inflammation and vascular dysfunction resulting in expansion of cardiac I/R Injury that is sensitive to particle size and the capping agent. The diverse physiochemical properties of ENM have been utilized in a multitude of industrial, commercial and consumer applications and have raised concerns over potential human or animal toxicity. Nano-silver particles have innate antimicrobial properties [3] and as a result have been utilized in biomedical applications: wound dressings, silver impregnated catheters, vascular prosthetics, surgical mesh [4, 5]; and consumer applications: clothing and undergarments, air filters, laundry detergents, toiletries, and water taps [6]. Pulmonary responses to ENMs have been a key focus regarding investigation routes [2, 9, 10], and a large body of evidence describing AgNP and pulmonary interactions [11,12,13,14,15]
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