Why the study?
Does modulation of NO and ET-1 pathways improve cardiac function and reduce injury in a rat heart model of ischaemia/reperfusion?
Population
Rat hearts perfused at 9 ml/min per g, subjected to 15 min total global ischaemia and reperfused for 30 min
Comparison
L-arginine, the NO donor S-nitroso-N-acetyl-DL-pe… vs Vehicle administered from 5 min pre-ischaemia to…
Design
Preclinical
Follow-up
30 minutes of reperfusion
Authors
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NO/ET-1 modulation improves rat reperfusion function; leaves open translation to human cardioprotection.
Does modulation of NO and ET-1 pathways improve cardiac function and reduce injury in a rat heart model of ischaemia/reperfusion?
In a rat model of ischaemia/reperfusion, ET-1 causes cell necrosis and L-arginine outflow without compromising NO synthesis, while NO donors and ET receptor antagonists improve cardiac function.
Friedrich Brünner (1997) studied this question.
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