September 1, 2001AJP Heart and Circulatory Physiology
Bradykinin elicits “second window” myocardial protection in rat heart through an NO-dependent mechanism
Population
Conscious rats whose hearts were subsequently Langendorff perfused and subjected to 35 min of regional…
Comparison
Bradykinin preceded 15-20 min earlier by saline… vs Saline
Design
Preclinical
Follow-up
24 hours after pretreatment, followed by 35 min ischemia…
Authors
Discussion
Loading...
Member takes
Implication
Bradykinin pretreatment confers NO-dependent delayed cardioprotection in rats; hypothesis-generating for clinical translation in ischemia-reperfusion injury.
Key Points
- This study aims to investigate the effects of bradykinin on delayed myocardial protection and its dependence on nitric oxide generation.
- Conscious rats received bradykinin (40 microg/kg iv) or saline preceding NO synthase inhibitor (L-NAME, 10 mg/kg ip) or saline.
- Hearts were Langendorff perfused after 24 hours and subjected to 35 min of regional ischemia and 120 min of reperfusion.
- Infarct size was assessed using tetrazolium staining and expressed as a percentage of the risk zone.
- Bradykinin pretreatment reduced the infarct-to-risk ratio from 53.5 +/- 3.2% to 29.1 +/- 4.7% (P < 0.01).
- Pre-administration of L-NAME before bradykinin eliminated delayed protection with infarct size at 52.3 +/- 5.0%.
- L-NAME alone did not influence infarct size (53.5 +/- 4.8%).
Structured PICO
P
Population
Conscious rats whose hearts were subsequently Langendorff perfused and subjected to 35 min of regional ischemia and 120 min of reperfusion
I
Intervention
Bradykinin (40 microg/kg iv) preceded 15-20 min earlier by saline or NO synthase inhibitor L-NAME (10 mg/kg ip)
C
Comparator
Saline
O
Outcome
Infarct size assessed using tetrazolium staining and expressed as a percentage of the risk zonesurrogate
Bradykinin evokes a delayed, NO-dependent enhancement of myocardial tolerance to ischemia in a rat model.
Cite This Study
Ebrahim et al. (2001) studied this question.