Extent of damage in ischemic, nonreperfused, and reperfused myocardium of anesthetized rats

Abstract

To investigate the localization of the earliest damage in ischemic and ischemic-reperfused myocardium, anesthetized rats were subjected to coronary occlusion for 15, 30, 45, or 90 min. One-half of the animals in each group had no reperfusion, whereas the other half was reperfused for 14 min. With the use of histological methods, preferentially in the periphery of the area at risk, localized zones were detected that lacked the hypoxia-specific increase in NADH fluorescence. The extent of these areas displaying injured tissue was found to be significantly smaller in the ischemic-nonreperfused hearts than in the ischemic-reperfused organs (15-min ischemia: 0.22 +/- 0.12% vs. 43.0 +/- 5.0%; 30-min ischemia: 5.7 +/- 2.7% vs. 64.6 +/- 2.9%; 45-min ischemia: 5.6 +/- 1.2% vs. 66.0 +/- 7.5%; 90-min ischemia: 39.3 +/- 5.5% vs. 86.7 +/- 1.8% of the area at risk). The results point to a localized initiation of the damage close to the surrounding oxygen-supplied tissue during ischemia and an expansion of this injury by intercellular actions into yet-intact areas upon reperfusion.

Impairment of ultrastructure and cytoskeleton during progression of cardiac hypertrophy to heart failure

“…Areas of ultrastructural damage were assessed according to a four-point scale for all of these parameters. 5 The EM pictures were read by blinded readers, who were not aware of the groups or genotypes of the mice.…”

“…However, whether the injury is reversible and the cells ultimately recover or whether membrane disruptions occur, resulting in irreversible injury and death of the cell, depends on the intensity of these factors. 5 In human hearts, the structural basis of the progression from well-compensated hypertrophy to HF is still largely unknown, and the correlation between morphological alterations and molecular changes during the different phases of the transition to HF has not yet been fully described. 6 Studies from ultrastructural changes in patients with endstage dilated cardiomyopathy (DCM) have shown an increase in fibrosis, degeneration of hypertrophied myocardial cells, and alterations of the cytoskeleton.…”

Controlled regional hypoperfusion in Langendorff heart preparations

“…Reduced or completely blocked blood flow during the early phase of ischemia elicits profound changes in the metabolism and electrical activity of cardiac myocytes (Vetterlein et al 2003). Such changes are highly heterogeneous and can lead to arrhythmia (Pogwizd and Corr 1987).…”

Phosphorylation of Extrajunctional Cx43 in Ischemic-Preconditioned Rat Hearts

“…Based on such investigations in an earlier study [16] as well as in the present one, experiments were performed in which propidium iodide was intravenously injected in anesthetized rats in order to trace the dye's distribution in the ischemic myocardial tissue. Due to its polar character, the dye distributes itself in the extracellular space; however, it is normally unable to gain access to the intracellular compartment.…”

“…Afterwards, the hearts were exposed to 45 min of ischemia; FITC-albumin was injected, the heart was removed, and frozen [16]. Since processing for immunostaining induces extraction of propidium iodide, NADH, and FITC-albumin from the tissue, parallel sections were prepared, one for immunostaining of Cx43, and one for detection of the dyes named above.…”