This Article Abstract Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Wagner, J. A. Articles by Ertl, G. Search for Related Content PubMed PubMed Citation Articles by Wagner, J. A. Articles by Ertl, G.

Endogenous cannabinoids mediate hypotension after experimental myocardial infarction

^a Department of Medicine, University of Würzburg, Würzburg, Germany
^b National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, Maryland, USA

View larger version (17K): [in a new window]   Figure 1 The effects of myocardial infarction on mean arterial pressure (A) and heart rate (B) in control rats (circles; n = 16) or SR141716A-pretreated (circles, n = 12) rats. SR141716A (6.45 µmol/kg IV) was given 15 min before left coronary artery ligation, performed at 0 min. The vertical bars represent SEM. Significant differences (*p < 0.05; p < 0.01; #p < 0.001) from corresponding values in the absence of SR141716A .

View larger version (11K): [in a new window]   Figure 2 The effects of SR141716A (circles, n = 25) on early survival after myocardial infarction; SR141716A given at 0 min. The rats were treated intravenously either with 6.45 µmol/kg SR141716A or vehicle (circles, n = 20) 15 min before experimental myocardial infarction. *Significant difference (p < 0.05) from corresponding value in vehicle-treated rats.

View larger version (11K): [in a new window]   Figure 3 Changes in blood pressure of recipient rats in response to circulating monocytes and platelets isolated from rats with myocardial infarction. See Methods for details. Cells were injected into control (circles, n = 5) and SR141716A -pretreated (6.45 µmol/kg IV; circles, n = 4) rats at 0 min. Basal mean arterial pressure (MAP) and heart rate were 116 ± 5 mm Hg and 402 ± 19 beats/min before and 114 ± 7 mm Hg and 383 ± 36 beats/min after SR141716A , respectively *Significant difference (p < 0.05) from corresponding control value.

View larger version (15K): [in a new window]   Figure 4 Relaxations induced by acetylcholine (A) and sodium nitroprusside (SNP) (B) in phenylephrine-preconstricted aortic rings from rats 2 h after myocardial infarction (), as compared with sham-operated animals (solid and open circles). The rats were treated with either vehicle (open circles and open downward triangles) or SR141716A (6.45 µmol/kg intravenous 15 min before myocardial infarction (solid circles and). The results are expressed as the mean value ± SEM from 8 to 12 separate experiments. **p < 0.01 for vehicle used in rats with myocardial infarction vs. vehicle used in sham-operated rats vs. SR141716A used in rats with myocardial infarction.