What question did this study set out to answer?

To determine whether myocardial angiotensin II receptor expression changes immediately after ischemia-reperfusion and contributes to acute cardiac dysfunction.

August 5, 1997Circulation

Increase in Angiotensin II Type 1 Receptor Expression Immediately After Ischemia-Reperfusion in Isolated Rat Hearts

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Why the study?

Does ischemia-reperfusion alter myocardial Angiotensin II receptor expression and does losartan attenuate resulting cardiac dysfunction in isolated rat hearts?

Population

Isolated buffer-perfused Sprague-Dawley rat hearts (n=20)

Comparison

25 minutes of global ischemia followed by 30… vs Continuous perfusion (control)

Design

Preclinical

Follow-up

30 minutes of reperfusion

Authors

BYBaichun YangChina Geological Survey MPM. Ian PhillipsCalifornia Institute of Technology PAP. E. J. AmbuehlUniversity of Florida

Discussion

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Implication

AT1 upregulation may drive acute post-ischemic dysfunction in rat hearts; leaves open whether AT1 blockade improves human ischemia-reperfusion outcomes.

Key Points

To determine whether myocardial angiotensin II receptor expression changes immediately after ischemia-reperfusion and contributes to acute cardiac dysfunction.
Isolated buffer-perfused Sprague-Dawley rat hearts were assigned to continuous perfusion (control, n=5) or to 25 minutes of global ischemia followed by 30 minutes of reperfusion (n=10).
An interventional group of isolated rat hearts (n=5) was perfused with buffer containing the AT1 receptor antagonist losartan (10⁻⁵ mol/L) during ischemia-reperfusion.
Hemodynamic measurements and myocardial autoradiographic binding analysis were performed to evaluate AT1 and AT2 receptor expression.
Ischemia-reperfusion caused severe cardiac dysfunction, marked by elevated coronary perfusion pressure and left ventricular end-diastolic pressure, along with decreased developed left ventricular pressure.
Total myocardial angiotensin II receptor expression was significantly higher post-reperfusion than in controls (P < .05), driven by an increase in AT1 receptor expression (34.6 ± 6.5 vs 18.2 ± 4.4 fmol/g, P < .05) without changes in AT2 expression.
Perfusion with losartan attenuated ischemia-reperfusion-induced cardiac dysfunction and blocked the increase in myocardial AT1 receptor binding.

Structured PICO

Does ischemia-reperfusion alter myocardial Angiotensin II receptor expression and does losartan attenuate resulting cardiac dysfunction in isolated rat hearts?

Population

Isolated buffer-perfused Sprague-Dawley rat hearts (n=20)

Intervention

25 minutes of global ischemia followed by 30 minutes of reperfusion, with or without losartan (10(-5) mol/L)

Comparator

Continuous perfusion (control)

Outcome

Myocardial Angiotensin II receptor expression (AT1 and AT2) and cardiac hemodynamics (coronary perfusion pressure, left ventricular end-diastolic pressure, and developed left ventricular pressure)surrogate

Myocardial AT1 receptor expression increases immediately after ischemia-reperfusion and contributes to cardiac dysfunction, which can be attenuated by AT1 receptor blockade with losartan.

Cite This Study

Yang et al. (1997) studied this question.

synapsesocial.com/papers/6a70552826770c2b8de0785e https://doi.org/10.1161/01.cir.96.3.922

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Implication

AT1 upregulation may drive acute post-ischemic dysfunction in rat hearts; leaves open whether AT1 blockade improves human ischemia-reperfusion outcomes.

Increase in Angiotensin II Type 1 Receptor Expression Immediately After Ischemia-Reperfusion in Isolated Rat Hearts

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

Increase in Angiotensin II Type 1 Receptor Expression Immediately After Ischemia-Reperfusion in Isolated Rat Hearts

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

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Also Consider