Mapping of capillary flow, cellular redox state, and resting membrane potential in hypoperfused rat myocardium

Citation
F. Brasch et al., Mapping of capillary flow, cellular redox state, and resting membrane potential in hypoperfused rat myocardium, AM J P-HEAR, 277(5), 1999, pp. H2050-H2064
Citations number
38
Categorie Soggetti
Cardiovascular & Hematology Research
Journal title
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY
ISSN journal
03636135 → ACNP
Volume
277
Issue
5
Year of publication
1999
Pages
H2050 - H2064
Database
ISI
SICI code
0363-6135(199911)277:5<H2050:MOCFCR>2.0.ZU;2-H
Abstract
The influence on myocyte viability of ischemia-induced changes in capillary perfusion was studied in the hearts of anesthetized rats subjected to part ial occlusion of the left coronary artery for 45 min. Timed plasma labeling was applied to determine perfusion patterns. Changes in the fluorescence o f preloaded potential-sensitive dyes [tetramethylrhodamine methyl ester (TM RM) and bis-oxonol], of trypan blue, and of endogeneous NADH were utilized in characterizing myocyte viability in histological sections of the heart. Within the hypoperfused zone, localized areas appeared vascularly nonlabele d for periods of at least 10 min. Within these areas a reduction in TMRM fl uorescence occurred in 82.5% of the tissue, signaling a reduced resting mem brane potential. In the same areas 37.7% of the myocytes revealed an NADH f luorescence lower than that regularly found in anoxic tissues. This correla ted with an especially low level of TMRM, with increased fluorescence bis-o xonol and with an accumulation of trypan blue. In conclusion, in localized hypoperfusion-induced zones lacking capillary flow, an inhomogeneous patter n of reductions in myocyte viability develops, which appears to be relevant in ischemia-induced arrhythmias.