Upregulation of vascular endothelial growth factor receptor-1 contributes to sevoflurane preconditioning-mediated cardioprotection

Figures & data

Figure 1 A schematic representation of the experimental protocol.

Abbreviations: I/R, ischemia–reperfusion; KHB, Krebs–Henseleit buffer; PIGF, placental growth factor; SPC, sevoflurane preconditioning.

Table 1 The basal hemodynamics of isolated hearts

Group	HR (beats/min)	LVDP (mmHg)	+dp/dt (mmHg/ms)	−dp/dt (mmHg/ms)	LVEDP (mmHg)
Sham	199.5±10.1	101.5±5.1	1,843.6±33.6	1,727.6±38.8	5.8±0.4
I/R	201.2±10.6	102.1±5.2	1,821.6±37.2	1,741.2±35.3	6.2±0.3
SPC	198.8±11.2	103.4±3.9	1,809.6±34.5	1,726.8±39.6	5.7±0.3
SPC+MF1	200.3±10.8	100.5±4.4	1,815.6±31.9	1,738.4±37.5	6.0±0.4
SPC+PIGF	201.4±10.3	102.3±4.5	1,837.6±36.4	1,714.3±33.4	5.9±0.3

Note: All values are expressed as mean ± SEM (n=12).

Abbreviations: +dp/dt, maximum LVDP increase rate; −dp/dt, maximum LVDP decrease rate; HR, heart rate; I/R, ischemia–reperfusion; LVDP, left ventricular developed pressure; LVEDP, left ventricular end-diastolic pressure; PIGF, placental growth factor; SEM, standard error of the mean; SPC, sevoflurane preconditioning.

Figure 2 Pretreatment with 2.5% sevoflurane improved the cardiac LV function after I/R injury.

Notes: (A–D) The LV function parameters including LVDP, ±dp/dt, and LVEDP during reperfusion (n=12). Values are presented as mean ± SEM. **P<0.01 vs the sham group; ‡P<0.01 vs the I/R group; ^##P<0.01 vs the SPC group.
Abbreviations: +dp/dt, maximum LVDP increase rate; −dp/dt, maximum LVDP decrease rate; I/R, ischemia–reperfusion; LV, left ventricle; LVDP, left ventricular developed pressure; LVEDP, left ventricular end-diastolic pressure; PIGF, placental growth factor; SEM, standard error of the mean; SPC, sevoflurane preconditioning.

Figure 3 Pretreatment with 2.5% sevoflurane limits the myocardial infarct size and reduces cardiac enzyme release.

Notes: (A) Representative myocardial cross sections of TTC-stained hearts for the five groups (n=6, five slices per heart). Red-stained areas indicate viable tissue, and unstained pale areas indicate infarct tissue. (B) Myocardial infarct size of hearts in the five groups. (C–E) Total CK-MB, LDH, and cTnI release in coronary effluent after 2 h reperfusion. Values are expressed as mean ± SEM. **P<0.01 vs the sham group; ^‡P<0.01 vs the I/R group; ^##P<0.01 vs the SPC group.
Abbreviations: CK-MB, creatine kinase-MB, cTnI, cardiac troponin-I; I/R, ischemia–reperfusion; LDH, lactate dehydrogenase; PIGF, placental growth factor; SEM, standard error of the mean; SPC, sevoflurane preconditioning; TTC, triphenyl tetrazolium chloride.

Figure 4 Representative immunoblots (top panel) of VEGFR-1 in isolated rat hearts. Values are presented as mean ± SEM.

Notes: **P<0.01 vs the I/R group; ^##P<0.01 vs the SPC group.
Abbreviations: I/R, ischemia–reperfusion; PIGF, placental growth factor; SEM, standard error of the mean; SPC, sevoflurane preconditioning; VEGFR-1, vascular endothelial growth factor receptor 1.

Figure 5 Pretreatment with 2.5% sevoflurane attenuates the inflammatory cytokine release after I/R.

Notes: (A) The release of TNF-α after 2 h reperfusion. (B) The release of IL-6 after 2 h reperfusion. Values are presented as mean ± SEM. **P<0.01 vs the sham group; ^‡P<0.01 vs the I/R group; ^##P<0.01 vs the SPC group.
Abbreviations: IL-6, interleukin 6; I/R, ischemia–reperfusion; PIGF, placental growth factor; SEM, standard error of the mean; SPC, sevoflurane preconditioning; TNF-α, tumor necrosis factor-alpha.