What question did this study set out to answer?

To delineate the contribution of bradykinin to the cardioprotective effects of angiotensin-converting enzyme inhibitors during cardiac ischemia and reperfusion.

January 1, 1990Journal of Cardiovascular PharmacologyOpen Access

Local Inhibition of Bradykinin Degradation in Ischemic Hearts

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Why the study?

Does bradykinin administration or local inhibition of its degradation improve cardioprotection in ischemia-reperfusion injury in animal models?

Population

Rats and anesthetized dogs

Comparison

Bradykinin perfusion/infusion, ramiprilat, and… vs Control/baseline or antagonist administration

Design

Preclinical

Follow-up

90 min occlusion and 30 min reperfusion (dogs)

Authors

WLWolfgang LinzOntario Brain Institute PMPiero A. MartoranaUniversity of Siena BSBernward A. SchölkensGoethe University Frankfurt

Discussion

Member takes

Implication

Supports bradykinin cardioprotection in animal reperfusion models; leaves open translation to human ischemia-reperfusion or ACE inhibitor use.

Key Points

To delineate the contribution of bradykinin to the cardioprotective effects of angiotensin-converting enzyme inhibitors during cardiac ischemia and reperfusion.
Tested isolated perfused working rat hearts undergoing regional ischemia with bradykinin, ramiprilat, angiotensin II, and a bradykinin antagonist.
Infused bradykinin (1 ng/kg/min) into the left anterior descending coronary artery of anesthetized dogs during 90 minutes of occlusion and 30 minutes of reperfusion.
In rat hearts, bradykinin reduced the incidence and duration of reperfusion ventricular fibrillation, lowered lactate dehydrogenase and creatine kinase leakage, and showed marked cardioprotection when combined with subthreshold ramiprilat.
In dogs, intracoronary bradykinin decreased coronary sinus lactate and lactate dehydrogenase levels while preserving myocardial glycogen and energy-rich phosphates in the infarcted area.

Structured PICO

Does bradykinin administration or local inhibition of its degradation improve cardioprotection in ischemia-reperfusion injury in animal models?

Population

Rats (isolated perfused working hearts with regional myocardial ischemia) and anesthetized dogs (with 90 min LAD occlusion and 30 min reperfusion)

Intervention

Bradykinin (BK) perfusion/infusion (various concentrations, e.g., 1 ng/kg/min in dogs), ramiprilat, and combinations

Comparator

Control/baseline or antagonist administration

Outcome

Cardioprotective effects including coronary flow, incidence and duration of reperfusion ventricular fibrillation, and metabolic parameters (LDH, creatine kinase, lactate)surrogate

Bradykinin mediates the cardioprotective effects of ACE inhibitors during ischemia-reperfusion injury in animal models.

Cite This Study

Linz et al. (1990) studied this question.

synapsesocial.com/papers/6a71d3b75671bbf00bc2f6fe https://doi.org/10.1097/00005344-199000156-00018

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Implication

Supports bradykinin cardioprotection in animal reperfusion models; leaves open translation to human ischemia-reperfusion or ACE inhibitor use.

Local Inhibition of Bradykinin Degradation in Ischemic Hearts

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

Local Inhibition of Bradykinin Degradation in Ischemic Hearts

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

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