Delayed myocardial protection induced by endotoxin does not involve kinin B 1 ‐receptors

Endotoxin is known to confer a delayed protection against myocardial infarction. Lipopolysaccharide (LPS) treatment also induces the de novo synthesis of kinin B 1 ‐receptors that are not present in normal conditions. The aim of this study was to evaluate whether LPS‐induced B 1 ‐receptors are implicated in the reduction of infarct size brought about by LPS. Rabbits were submitted to a 30‐min coronary artery occlusion and 3‐h reperfusion sequence. Six groups were studied: pretreated or not (control animals) with LPS (5 μg kg −1 i.v.) 24 h earlier and treated 15 min before and throughout ischaemia–reperfusion with either the B 1 ‐antagonist R‐715 (1 mg kg −1  h −1 ), the B 1 ‐agonist Sar‐[ D ‐Phe 8 ]‐des‐Arg 9 ‐bradykinin (15 μg kg −1  h −1 ) or vehicle (saline). Infarct size and area at risk were assessed by differential staining and planimetric analysis. The presence of B 1 ‐receptors in LPS‐pretreated animals was confirmed by a decrease in mean arterial pressure in response to B 1 stimulation. LPS‐pretreatment significantly reduced infarct size (6.4±1.7%, of area at risk vs 24.1±2.5% in control animals, P <0.05). This protection was not modified by B 1 ‐receptor antagonism (7.4±2.2%, NS) or stimulation (5.2±1.2%, NS). Neither antagonist nor agonist modified infarct size in control animals. In conclusion, these data suggest that LPS‐induced myocardial protection in the rabbit is not related to concomitant de novo B 1 ‐receptor induction.British Journal of Pharmacology (2000) 131 , 740–744; doi: 10.1038/sj.bjp.0703619