title: Delayed myocardial protection induced by endotoxin does not involve kinin B(1)-receptors.
abstract: 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 microgram 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 microgram 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.
authors.affiliation: Laboratoire Stress Cardiovasculaires et Pathologies Associées, Université Grenoble I, France.
authors.forename: C
authors.initials: C
authors.lastname: Mazenot
authors.forename: F
authors.initials: F
authors.lastname: Gobeil
authors.forename: C
authors.initials: C
authors.lastname: Ribuot
authors.forename: D
authors.initials: D
authors.lastname: Regoli
authors.forename: D
authors.initials: D
authors.lastname: Godin-Ribuot
mesh_terms: D000818:Animals; D006321:Heart / Q000187:drug effects*; D006439:Hemodynamics / Q000187:drug effects; D008050:Lipid A / Q000031:analogs & derivatives / Q000494:pharmacology; D008070:Lipopolysaccharides / Q000494:pharmacology*; D008297:Male; D009203:Myocardial Infarction / Q000188:drug therapy; D011817:Rabbits; D043783:Receptor, Bradykinin B1; D018002:Receptors, Bradykinin / Q000502:physiology*
chemical_list: D008050:Lipid A; D008070:Lipopolysaccharides; D043783:Receptor, Bradykinin B1; D018002:Receptors, Bradykinin; C048436:monophosphoryl lipid A