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Figure 5 | Particle and Fibre Toxicology

Figure 5

From: Pulmonary diesel particulate increases susceptibility to myocardial ischemia/reperfusion injury via activation of sensory TRPV1 and β1 adrenoreceptors

Figure 5

Pulmonary TRPV1 blockade in vivo prevented the effects of intratracheal DEP on infarct size, myocardial apoptosis and cell viability ex vivo . Co-instillation of the TRPV1 antagonist AMG 9810 (hatched columns, 30 mg/kg) with DEP in vivo prevented the increase in myocardial infarct size (expressed as a percentage of area at risk; AAR) induced by DEP (0.5 mg, black column, a). AMG9810 had no effect on infarct size when present only in the perfusate ex vivo (1 μM, hatched column, (a) inset panel). When co-administered in vivo AMG 9810 also prevented the greater levels of apoptosis (TUNEL staining, b) and loss of cell viability (TTC staining, c) associated with pulmonary DEP exposure. Results are expressed as mean ± SEM (n = 3-5), **P < 0.01 versus saline; ##P < 0.01 versus DEP without AMG 9810; two-way ANOVA followed by Bonferroni post-hoc test.

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