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

1 Endotoxin is known to confer a delayed protection against myocardial infa rction. Lipopolysaccharide (LPS) treatment also induces the de novo synthes is of kinin B-1-receptors that are not present in normal conditions. The ai m of this study was to evaluate whether LPS-induced B-1-receptors are impli cated in the reduction of infarct size brought about by LPS. 2 Rabbits were submitted to a 30-min coronary artery occlusion and 3-h repe rfusion sequence. Six groups were studied: pretreated or not (control anima ls) with LPS (5 mug 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 m g kg(-1) h(-1)), the B-1-agonist Sar-[D-Phe(8)]-des-Arg(9)-bradykinin (15 m ug kg(-1) h(-1)) or vehicle (saline). Infarct size and area at risk were as sessed by differential staining and planimetric analysis. 3 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-pr etreatment 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 modifie d by B-1-receptor antagonism (7.4+/-2.2%, NS) or stimulation (5.2+/-1.2%, N S). Neither antagonist nor agonist modified infarct size in control animals . 4 In conclusion, these data suggest that LPS-induced myocardial protection in the rabbit is not related to concomitant cte novo B-1-receptor induction .