Key result
The threefold increase in TH and twofold increase in NET mRNA seen in SD rats 1 week after ischemia-reperfusion was absent in TGR(ASrAOGEN) rats lacking postinfarct sympathetic hyperactivity.
Population
TGR transgenic rats and Sprague Dawley control rats
Comparison
Ischemia-reperfusion (myocardial infarction model) vs Unoperated rats and wild-type Sprague Dawley…
Design
Preclinical
Follow-up
1 week
Authors
Loading...
Supports sympathetic hyperactivity driving post-MI neuronal gene changes in rats; hypothesis-generating, clinical translation unknown.
Postinfarct sympathetic hyperactivity is the major stimulus driving the increased expression of tyrosine hydroxylase and norepinephrine transporter in cardiac neurons after myocardial infarction.
Parrish et al. (2007) studied Myocardial infarction. TGR(ASrAOGEN) transgenic genotype vs. Sprague Dawley (SD) controls was evaluated on TH and NET mRNA and protein levels. The threefold increase in TH and twofold increase in NET mRNA seen in SD rats 1 week after ischemia-reperfusion was absent in TGR(ASrAOGEN) rats lacking postinfarct sympathetic hyperactivity.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: