Experimental myocardial infarction. III. Recovery of left ventricular function in the healing phase. Contribution of increased fiber shortening in noninfarcted myocardium

摘要: Abstract In the presence of focal myocardial damage, stroke volume may be maintained by ventricular dilatation, resulting in an increased left end-diastolic volume, or fiber shortening noninfarcted muscle. Relative contribution these factors was examined 5 shamoperated and 10 coronary-ligated dogs studied 4 to 7 days after surgery. Utilizing spherical formulas, (SV), (EDV), infarct size (IS) as a fraction weight ventricle were measured vivo at postmortem, fiber-shortening (FSF) muscle calculated: FSF = [l − 3 1 ( SV EDV ] (1 IS ) When pressure kept range mm. Hg, well with small (infarct less than 20 per cent ventricle) large greater infarcts, did not differ from shams. However, calculation gave values 0.17 ± 0.03 (S.E.M.) for shams, 0.22 0.01 animals 0.36 0.07 indicating Left enddiastolic increased; on contrary, 36 ml. 100 Gm. 35 compared 51 2 suggesting that compliance is reduced infarcted This study shows hemodynamic compensation acute infarction occur nonifarcted