Pharmacological modification of thromboxane and prostaglandin release in cardiac anaphylaxis.
Isolated perfused sensitized guinea pig hearts release relatively large amounts of radioimmunologically measurable thromboxane B2 (TXB2) as well as smaller amounts of prostaglandin (PGs) after antigenic challenge. Using thin layer chromatography the major PG released was shown to cochromatograph with PGD2, while smaller amounts of immunoreactive PGF2alpha were found. The TX-synthetase inhibitor imidazole (100 microgram/ml) significantly decreased TXB2 release and simultaneously increased PG release during cardiac anaphylaxis. On the other hand, the beta-sympathomimetic drug isoproterenol decreased both TXB2 and PG release from the anaphylactic hearts. While isoproterenol significantly diminished anaphylactic coronary flow reduction, imidazole was without effect in this respect. PGD2 (0.5 microgram/min and 5.0 microgram/min) infused intraaortally into non-sensitized guinea pig hearts reduced coronary flow dose-dependently. These results are compatible with the view that release of TX and PGs might contribute to coronary flow reduction in cardiac anaphylaxis.
D000707:Anaphylaxis / Q000378:metabolism* / Q000503:physiopathology; D000818:Animals; D003326:Coronary Circulation / Q000187:drug effects; D006168:Guinea Pigs; D007093:Imidazoles / Q000494:pharmacology; D066298:In Vitro Techniques; D007545:Isoproterenol / Q000494:pharmacology; D009206:Myocardium / Q000378:metabolism*; D011453:Prostaglandins / Q000378:metabolism*; D011457:Prostaglandins D / Q000494:pharmacology; D013929:Thromboxane B2 / Q000378:metabolism*; D013931:Thromboxanes / Q000378:metabolism*
D007093:Imidazoles; D011453:Prostaglandins; D011457:Prostaglandins D; D013931:Thromboxanes; D013929:Thromboxane B2; D007545:Isoproterenol