Left ventricular failure induced by myocardial infarction. II. Tissue morphometry

Abstract

Three days after myocardial infarction involving 57% of the left ventricle in rats, the viable tissue of the left ventricle expanded 29%, whereas myocardial hypertrophy in the right ventricle was 19%. To determine whether tissue oxygenation in the hypertrophied ventricles was supported by a proportional growth of the capillary network, morphometric analysis was used to measure capillary luminal volume and surface densities and the diffusion distance for O2. The volume fraction of capillary lumen and the luminal surface of capillaries, related to O2 availability and diffusion, were altered by -21 and -19%, respectively, in the left ventricle and by -23 and -20%, respectively, in the right ventricle. The path length for O2 transport was found to be increased by 12 and 15% in the left and right ventricle, respectively. In contrast, myocyte mass expanded in proportion to tissue growth in the left ventricle and exceeded tissue growth by 5% in the right ventricle. Myocyte mitochondria and myofibrils both grew in proportion to the cells, so that their volume ratio was not changed in either ventricle. The relatively inadequate adaptation of the capillary vasculature suggests that hypertrophy after severe myocardial infarction may initially leave the heart more vulnerable to additional ischemic episodes.

Noncoordinate regulation of alpha-1 adrenoreceptor coupling and reexpression of alpha skeletal actin in myocardial infarction-induced left ventricular failure in rats.

“…In particular, myocardial ischemia is characterized by a two-fold increase in alpha-l adrenoreceptor number (29) which contributes to the occurrence of malignant ventricular arrhythmias (30). Although a reduction in the oxygenation potential of the surviving myocardium early after infarction has been claimed at the level of the capillary microvasculature (3,6), measurements of coronary blood flow distribution have failed to demonstrate abnormalities in coronary perfusion consistent with myocardial ischemia (31). Moreover, the alterations in alpha-l adrenergic receptor number in congestive dilated cardiomyopathy in humans (28) occur over a period of many years of decompensated overload, whereas in the current experiments in rats, alpha-1 adrenoreceptor density was determined 1 wk after coronary occlusion.…”

“…In both cases, however, the signal that induces cellular growth is the critical factor for short and long term survival. Myocyte hypertrophy after infarction is an early event (1,3,6) that progresses with time (2) in an attempt to restore ventricular mass and improve function (1,3,6). Moreover, this growth adaptation involves augmentations in myocyte length which exceed those in cell diameter (1)(2)(3), implying that the altered hemodynamic state after infarction affects the preload more than the afterload (3).…”

cNGR: A Novel Homing Sequence for CD13/APN Targeted Molecular Imaging of Murine Cardiac Angiogenesis In Vivo

“…No CD13 upregulation was observed in non risk areas, in accordance with earlier findings that adaptation of capillary microstructure fails to occur in viable tissues after MI. 15 As a next step, we took advantage of optical sectioning, highresolution (0.5ϫ0.5ϫ1 m) and large penetration depth of TPLSM to obtain a more comprehensive picture of CD13 distribution on angiogenic and quiescent vessels in this model. 16 Indeed, TPLSM allowed us to generate 3D-images of the vasculature in the target areas (see supplemental data).…”

Is the Tissue Affinity of ACE Inhibitors of Relevance for the Remodeling of the Left Ventricular Wall following Myocardial Infarction?

“…Similar observations were made with regard to the development of noninfarcted myocardium mass (see Results). In the overall group and in the individual study groups, however, no relevant differences were found between captopril and fosinopril in their ability to influence myocardial growth and its trigger, namely systolic wall stress [37, 38]. …”