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Figure 4 | Particle and Fibre Toxicology

Figure 4

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

Figure 4

β 1 adrenoceptor blockade in vivo prevented the effects of intratracheal DEP on infarct size, myocardial oxidant stress, apoptosis, cell viability ex vivo . Infarct size was reduced in hearts isolated from DEP instilled (filled columns) compared to controls (open columns) rats when metoprolol was co-administered in vivo (10 mg/kg, i.p., hatched columns a), but not when metoprolol was present only in the perfusate ex vivo (10 μM, hatched column, (a) inset panel). The DEP-induced changes in oxygen-derived free radicals in the coronary perfusate, (electron paramagnetic resonance; EPR, b), number of apoptotic cells (TUNEL staining, c), and loss of cardiomyocyte viability (TTC staining, d) in the left ventricle (LV) were prevented when metoprolol (10 mg/kg, i.p., hatched columns) was administered in vivo at the time of instillation. Results are expressed as mean ± SEM (n = 6), **P < 0.01, ***P < 0.001 versus saline; ##P < 0.01, ###P < 0.001 versus DEP without metoprolol; two-way ANOVA followed by Bonferroni post-hoc test.

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