Skip to main content
. 2018 Jun 21;115(1):168–178. doi: 10.1093/cvr/cvy157

Figure 4.

Figure 4

Isoflurane (ISO)-induced increase in nitric oxide (NO) production were blocked by either neutralizing antibody against vascular endothelial growth factor (nVEGF) or hypoxia-inducible factor (HIF1α) shRNA in endothelial cells (ECs) and co-cultured ECs and cardiomyocytes (CMs). (A) Effects of IgG, nVEGF, and L-NMMA (L-NG-monomethyl arginine) on ISO-induced increases in NO production in ECs; (B) effects of IgG, nVEGF, and L-NMMA on ISO-induced increases in NO production in co-cultured ECs and CMS; (C) effects of HIF1α shRNA, scrambled HIF1α shRNA sequence (SCR), and recombinant VEGF (rVEGF) on ISO-induced increases in NO production in ECs; (D) effects of HIF1α shRNA, SCR, and rVEGF on ISO-induced increases in NO production in co-cultured ECs and CMS. The values of the control groups were arbitrarily defined as one in each batch of experiments. Data are presented as mean ± SEM. Kruskal–Wallis test followed by Dunn’s test was used to analyse multiple group comparisons. *P < 0.05 vs. CON (control); †P < 0.05 vs. ISO; ‡P < 0.05 vs. shRNA + ISO (n = 5).