Table 1.
Model | Study design¥ | Cardiac remodeling | Ref | |||||
---|---|---|---|---|---|---|---|---|
Structural/functional | Inflammation | Oxidative stress | Apoptosis | Metabolic impairment | Others | |||
C57BL/6J mice: 32 weeks of CS exposure | CS effect on LV remodeling in mice | ↑ SBP, DBP ↑ HW : BW ratio, LVM ↓ EDV and CO |
N/A | ↑ ROS in white blood cells | N/A | N/A | ↑ NO decay ↑ ED |
[22] |
(i) Impaired LV P-V relationship at high afterload | ||||||||
| ||||||||
S-D rats: 1 week CS exposure prior to abdominal aortocaval fistula surgery and for 6 weeks thereafter |
CS effect on LV remodeling in volume overloaded heart | ↑ LV dilation ↓ LVPWT, eccentric index, FS ↔ HR, CO, BP |
N/A | N/A | N/A | N/A | ↓ collagen deposition ↓ ET-1, HIF1α, VEGF, TGF-β protein levels ↑ MMP-9, TIMP-1 protein levels ↔ MMP-2 protein levels |
[29] |
| ||||||||
S-D rats: 5 weeks of CS exposure |
CS effect on LV remodeling in rats | ↑ LVEDD, LVESD, E/A ↑ HW : BW ratio ↓ FS ↔ LVPWT |
N/A | N/A | N/A | N/A | ↑ urinary NE levels ↑ Pp38/total p38 ↑ PERK1/2/ERK1/2 ↔JNK levels |
[23] |
| ||||||||
Rabbit-mouse VM exposed to 0.1% aqueous extract of cig smoke | Effects of aqueous extract of cigs on isolated VM | ↑ ischemic injury ↑ myocyte contracture |
N/A | ↑ ROS | N/A | ↑ susceptibility to mPTP opening | ↑ myocyte mito [Ca2+]m uptake ↑ myocyte cytosolic [Ca2+]i during ischemia |
[89] |
| ||||||||
Wistar rats: 20 cigs/day first week then 40 cigs/day for 4 weeks |
CS effect on cardiac Cx43 | ↔ LVW, RVW, CSA | N/A | N/A | N/A | N/A | ↔ Cx43 distribution at intercalated disks ↓ Cx43 intensity at intercalated disks ↑ Cx43 dephosphorylation ↑ lateralization ↔ total Cx43 levels ↔ CVF |
[27] |
| ||||||||
Wistar rats: 20 cigs/day first week then 40 cigs/day until 2 months |
CS effect on LV remodeling | ↑ LA area, CSA ↑ LVSV ↓ EF, FS |
N/A | ↑ ROS ↓ SOD and GSHPx activities |
↑ apoptosis | ↓ OHDAH, CS activities ↑ LDH activity ↑ serum VLDL, LDL, TG, myocardial TG ↓ serum HDL |
↔ PPAR-α, PGC-1α | [24] |
| ||||||||
Wistar rats: 6 months of CS exposure starting at 48 hours post-MI |
CS effect on LV remodeling post-MI | ↑ HR, LA area, E/A, DA, SA ↑ RVW : BW ratio, LW |
N/A | ↑ GSH, GSSG ↓ GSH/GSSG ratio ↔ LOOHs levels |
N/A | N/A | ↔ CVF | [25] |
| ||||||||
C57BL/6 mice: 20 cigs/day for 1 month |
CS effect on LV remodeling | ↑ BP, LVH, HW : BW ratio ↔ HR |
↑ IL-6, TNF-α serum levels ↔ IL-6, TNF-α |
N/A | N/A | N/A | ↑ eNOS, iNOS, sGCα, sGCβ, pVASP, cGMP ↑ mRNA β-MHC ↔ PKG, PDE5 ↓ H2S producing enzymes |
[124] |
| ||||||||
C57BL/6 mice: 20 cigs/day for 1 month |
CS effect on LV remodeling followed by NoC, PreC or PostC I/R | ↔ infarct size (NoC, PreC) ↑ infarct size (PostC) |
N/A | ↔ PC, MDA (NoC, PreC) ↑ PC, MDA (PostC) |
N/A | N/A | ↔ Akt, eNOS, cGMP activation (PreC) ↓ Akt, eNOS, cGMP activation (PostC) ↔ Akt, ↑ eNOS, and cGMP (NoC) ↓ pVASP (PostC and PreC) ↑ pVASP (NoC) ↓ nitrate + nitrite (PostC and PreC) ↔ nitrate + nitrite (NoC) |
[124] |
¥Results presented in this table are in comparison with nonsmoking same conditioning treatment. CS: chronic tobacco smoking; S-D: Sprague-Dawley; N/A: not available; ↑, increase; ↓, decrease; ↔, no changes; SBP: systolic blood pressure; DBP: diastolic blood pressure; LV: left ventricle; LVM: left ventricular mass; EDV: end-diastolic volume; CO-Hb: carboxyhemoglobin; LV P-V: LV pressure-volume; ED: endothelial dysfunction; HW : BW: heart weight : body weight; ROS: reactive oxygen species; NO: nitric oxide; LVPWT: left ventricular wall thickening; FS: fractional shortening; HR: heart rate; BP: blood pressure; ET-1: endothelin 1; HIF1α, hypoxia inducible factor; VEGF: vascular endothelial growth factor; TGF-β: transforming growth factor; MMP: matrix metalloproteinases; TIMP-1: tissue inhibitors of metalloproteinase-1; LVEDD: left ventricular end-diastolic diameter; LVESD: left ventricular end-systolic diameter; E/A: E: peak velocity of early ventricular filling, A: peak velocity of transmitral flow during atrial contraction; NE: norepinephrine; p38: p38 kinase; Pp38: phosphorylated p38 kinase; ERK: extracellular-regulated kinase; PERK: phosphorylated extracellular-regulated kinase; JNK: c-Jun NH2-terminal protein kinase; MPT: mitochondrial permeability transition; [Ca2+]i: intracellular calcium; [Ca2+]m: mitochondrial calcium; VM: ventricular myocytes; CVF: collagen volume fraction; RVW: right ventricular weight; CSA: cross sectional area; Cx43: connexin 43; LA: left atria; LVSV: left ventricular systolic volume; EF: ejection fraction; OHDAH: 3-hydroxyacyl coenzyme-A dehydrogenase; LDH: lactate dehydrogenase; LDL: low-density lipoprotein; VLDL: very low-density lipoprotein; TG: triacylglycerols; HDL: high-density lipoprotein; PGC-1α: peroxisome proliferator-activated receptor gamma coactivator 1 alpha; PPAR-α: peroxisome proliferator-activated receptor alpha; DA: diastolic area; SA: systolic area; LOOHs: lipid hydroperoxides; LVH: left ventricular hypertrophy; RVW : BW: right ventricular weight : body weight; LW: lung weight; eNOS: endothelial nitric oxide synthases; iNOS: inducible NOS; IL: interleukin; TNF: tumor necrosis factor; sGC: soluble guanylate cyclase; VASP: vasodilator-stimulated phosphoprotein; pVASP: phosphorylated VASP; cGMP: cyclic guanosine monophosphate; mRNA: messenger RNA; β-MHC: myosin heavy chain beta; PKG: protein kinase G; PDE5: phosphodiesterase type 5 inhibitor; H2S: hydrogen sulfide; PC: protein carbonyl; NoC: no conditioning, PreC: preconditioning; PostC: postconditioning; I/R: ischemia reperfusion; MDA: malondialdehyde; Akt: RAC-alpha-serine/threonine-protein-kinase.