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Updated: Aug 12, 2026
13:42
A Murine Closed-chest Model of Myocardial Ischemia and Reperfusion
Published on: July 17, 2012
Postischemic anti-inflammatory effects of bradykinin preconditioning
S Shigematsu1, S Ishida, D C Gute
1Department of Molecular and Cellular Physiology, Louisiana State University Health Sciences Center, School of Medicine in Shreveport, Shreveport, Louisiana 71130, USA.
American Journal of Physiology. Heart and Circulatory Physiology
|December 21, 2000
Summary
Bradykinin preconditioning (BK-PC) protects microvessels from ischemia/reperfusion injury by activating B2 receptors and nonconventional protein kinase C (PKC) to generate nitric oxide (NO). This prevents leukocyte adhesion and leakage.
Area of Science:
- Physiology
- Pharmacology
- Microcirculation Research
Background:
- Ischemia/reperfusion (I/R) injury causes microvascular dysfunction.
- Bradykinin preconditioning (BK-PC) may prevent this damage.
Purpose of the Study:
- To elucidate the mechanisms of BK-PC in preventing postischemic microvascular dysfunction.
- To identify the receptors and signaling pathways involved in BK-PC's protective effects.
Main Methods:
- Intravital videomicroscopy in rat mesentery.
- Quantification of leukocyte-endothelial interactions and albumin leakage.
- Pharmacological blockade of B1/B2 receptors, nitric oxide synthase (NOS), cyclooxygenase (COX), and protein kinase C (PKC) isoforms.
Main Results:
- BK-PC prevented I/R-induced leukocyte recruitment and albumin leakage.
- These effects were mediated by B2 receptors, nonconventional PKC, and nitric oxide (NO) formation during reperfusion.
- B1 receptor blockade, COX inhibition, or conventional PKC inhibition did not affect BK-PC's protective action.
Conclusions:
- BK-PC protects mesenteric postcapillary venules against I/R injury.
- The mechanism involves B2 receptor activation, nonconventional PKC signaling, and subsequent NO production.
- This highlights a novel pathway for pharmacological preconditioning of microvasculature.
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