Key result
Exogenous angiotensin-I enlarges myocardial ischemia by ~35%, an effect completely prevented by captopril.
Why the study?
The endogenous activity of the local renin-angiotensin system and the anti-ischaemic properties of captopril in isolated rabbit hearts were unclear.
Does captopril inhibit the deleterious effect of exogenous angiotensin-I on regional ischemia in isolated rabbit hearts?
Population
Electrically driven rabbit Langendorff hearts with induced myocardial ischaemia
Comparison
Exogenous angiotensin-I with or without captopril versus absence of exogenous angiotensin-I or captopril alone
Design
Preclinical experimental study
Authors
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Captopril blocks angiotensin-I worsening of ischemia in rabbit hearts; leaves open direct cardioprotection and human translation.
Does captopril inhibit the deleterious effect of exogenous angiotensin-I on regional ischemia in isolated rabbit hearts?
p-value: p=<0.05
In isolated rabbit hearts, captopril prevents the exacerbation of myocardial ischemia induced by exogenous angiotensin-I but lacks direct cardioprotective properties independent of ACE inhibition.
Rump et al. (1993) studied Myocardial ischaemia. Exogenous angiotensin-I and captopril vs. Absence of exogenous angiotensin-I / captopril alone was evaluated on Extent of regional myocardial ischaemia (p=<0.05). Exogenous angiotensin-I significantly enlarged myocardial ischaemia by 35% (P<0.05), an effect that was completely prevented by the addition of captopril.
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