The reaction of the myocytes to ischemic stress is described on the molecular and
cell-biological level in this review. It is shown that signalling cascades are activated,
that originate most probably simultaneously from cell membrane receptors and from
the metabolic derangement in the cytosol. A multitude of Signals is transmitted to
the nucleus and to the cell membrane which exert different effects with regards to
survival and cell death. We describe that death-promoting pathways exist that can
be blocked pharmacologically, which leads to an increase in the survival time of ischemic
myocardium. In spite of the shortage of energy new mRNA can be produced by ischemic
myocardium and hypoxia-specific gene expression also occurs is described. A major
difficulty is discussed: mRNA stability can change under hypoxic conditions, which
can simulate altered transcription.
Myocardial ischema - Reperfusion - Stunning - Gene expression - Heat shock protein
- Proto-oncogene
