Hypercholesterolemia attenuates postischemic ventricular dysfunction in the isolated rabbit heart

• Published in: Molecular and cellular biochemistry Vol. 273; no. 1-2; pp. 137 - 143
• Main Authors: D'Annunzio, Verónica, Donato, Martín, Sabán, Melina, Sanguinetti, Silvia M, Wikinski, Regina L W, Gelpi, Ricardo J
• Format: Journal Article
• Language: English
• Published: Netherlands Springer Nature B.V 01-05-2005
• Subjects: Aerobic conditions; Animals; Cardiology; Cholesterol; Cholesterol, Dietary - adverse effects; Heart; Heart attacks; Hypercholesterolemia - etiology; Ischemia; Myocardial Contraction - physiology; Myocardial Ischemia - etiology; Myocardial Ischemia - physiopathology; Myocardial Reperfusion Injury - etiology; Myocardial Reperfusion Injury - physiopathology; Myocardial Stunning - physiopathology; Myocardium - metabolism; Perfusion; Rabbits; Ventricular Dysfunction, Left - etiology; Ventricular Dysfunction, Left - physiopathology
• ISSN: 0300-8177; 1573-4919
• DOI: 10.1007/s11010-005-8264-6

The effects of the chronic administration of cholesterol on the stunned myocardium have not been studied. The objective was to determine the effect of a cholesterol enriched diet on postischemic ventricular dysfunction. In group 1 (G1, n = 7) isolated rabbit hearts underwent a follow up of ventricular function during 30 min in aerobic conditions. In group 2 (G2, n = 6) G1 was repeated but the animals were subjected to a 1% cholesterol enriched diet during 4 weeks (hypercholesterolemic animals). In group 3 (G3, n = 8) hearts underwent 15 min of global ischemia followed by 30 min of reperfusion. In Group 4 (G4, n = 11) G3 was repeated, but in hypercholesterolemic animals. Since cholesterol decreased the inotropism in basal situation, and this makes the comparison between groups difficult, we performed a Group 5 (G5, n = 7), in which G4 protocol was repeated but isoproterenol (8 microg/kg/min) was administered 10 min before ischemia, in order to match the preischemic inotropic state with respect to the normocholesterolemic ones. G1 and G2 maintained a stable inotropism during the 30 min of perfusion. The preischemic left ventricular developed pressure (LVDP) in G3 and G4 was 91.4 +/- 4.3 and 70.8 +/- 3.4 mmHg (p < 0.05), respectively, and after 30 min of reperfusion differences were not observed between G3 and G4. Nevertheless, when LVDP is expressed as a percentage, we detected an attenuation of postischemic systolic alterations in hypercholesterolemic animals (67.3 +/- 3.6 in G4 vs. 90.8 +/- 3.1% in G3, p < 0.05). When LVDP in G5 was increased until matching the one of G3, there were no differences after 30 min of reperfusion. Left ventricular end diastolic pressure increased 285 +/- 46%, 61 +/- 25% (p < 0.05 vs. G3 and G5) and 216 +/- 25% in G3, G4 and G5 at 30 min of reperfusion. There were no differences either in the values of tau or infarct size between groups. Thus, in hypercholesterolemic animals, a decrease of the preischemic inotropism exists and there is an attenuation of the stunned myocardium. When contractility of the normo and hypercholesterolemic animals is matched, the beneficial effect disappears.