Figure 1.
Pathohistological manifestations of AMI heart.
TTC staining showing that the viable myocardium stained brick red (A) and the infarct appeared as pale white (B); Hematoxylin-eosin (HE) stain showing the microstructure of myocardium in control (C) and AMI (D) rats. C and D; scale bar = 10 µm.
Table 1.
Hemodynamic parameters in control and AMI rats at day 5 post-ligation.
Table 2.
Heart rate variability (HRV) analysis in rat with different treatment.
Figure 2.
Expression of OXA in LHA of the control and AMI group.
A to C showing OXA-IR expressed in control group and D to F showing the AMI group, respectively; the positive cellular morphology indicated by arrows; the number and relative optical density (ROD) of OXA-IR neurons in AMI increased markedly as compared with those of the control rats(G); mRNA level of PPO in the hypothalamus in AMI group increased (H); values as mean±S.E.M (n = 7); * P<0.05, **P<0.01 when compared with the control group; scale bars = 50µm in A and D; 20µm in B and E; 10µm in C and F LH: lateral hypothalamic area; F: fornix.
Figure 3.
Expression of OX1R in RVLM of the control and AMI group.
A to C showing OX1R expressed in the control group; D to F showing the OX1R-IR expressed in AMI group; the positive cellular morphology indicated by arrows; the number and relative optical density (ROD) of OX1R -IR neurons in AMI increased significantly when compared with those of the controls (G) (n = 7); Western blot showing the change of OX1R expressions in RVLM in the control and AMI group (H) (n = 4); values as mean+S.E.M; * P<0.05, ** P<0.01 when compared with the control group; scale bars = 50µm in A and D; 20µm in B and E; 10µm in C and F VLM: ventrolateral medulla.
Figure 4.
Effects of SB-408124 or TCS OX2 29 on OXA-induced cardiovascular responses in AMI rats.
Exogenously administrated OXA into the RVLM evoking pressor and tachycardiac responses; SB-408124 (100 pmol/100 nl) or TCS OX2 29 (100 pmol/100 nl) followed by OXA (100 pmol) partly abolishing the pressor and tachycardiac responses of exogenously administrated OXA into the RVLM; values as means ± S.E.M, n = 7; *P<0.05, **P<0.01 when compared with aCSF group; #P<0.05, ##P<0.01 when compared with OXA group.
Figure 5.
Co-localization of OX1R and NADPH oxidase subunits in RVLM.
Double immunofluorescent staining showing the OX1R and NADPH oxidase subunit gp91 phox or p47 phox co-localized in RVLM; the OX1R shown in red (A, D, G and J), and the gp91 phox (B and E) or p47 phox (H and K), in green; the merged images showing yellow color (C, F, I and L); scale bars = 10µm in A, B, C, G, H and I, 5µm in D, E, F, J, k and L. RVLM: rostral ventrolateral medulla.
Figure 6.
Measurements O2− production and the mRNA of gp91phox and p47phox in RVLM.
The results showing a significant increase in RVLM of OXA-treated rats than in that of the controls; SB-408124 (100pmol/100nl) or apocynin (APO, 100pmol/100nl) followed by OXA (100pmol) reducing the production in the RVLM; values as means ± S.E.M, n = 7; **P<0.01,*P<0.05 when compared with that of control+aCSF group; ##P<0.01,#P<0.05 when compared with AMI+aCSF group; ▴P<0.05 when compared with AMI+OXA group.
Figure 7.
Effects of apocynin on OXA-induced cardiovascular responses in AMI rats.
Exogenously administrated OXA into the RVLM evoking pressor and tachycardiac responses; apocynin (APO, 100 pmol/100 nl) followed by OXA (100 pmol) partly abolishing the pressor and tachycardiac responses of exogenously administrated OXA into the RVLM; values as means ± S.E.M, n = 7; *P<0.05, **P<0.01 when compared with aCSF group; #P<0.05, ##P<0.01 when compared with OXA group.