Inhibition of hypoxic pulmonary vasoconstriction by dipyridamole is not platelet mediated.
Dipyridamole, which is known to alter platelet function, has also been shown to reduce hypoxic pulmonary vasoconstriction. This latter effect could result from dipyridamole either acting on a platelet-mediated system, or acting directly on pulmonary vascular smooth muscle. To investigate these two possibilities, normal dogs were compared with dogs rendered thrombocytopenic by a platelet antiserum. Compared with the hypoxic pressor response before drug treatment, the hypoxic response following dipyridamole was only 32% as great in the normal dogs and only 38% as great in the thrombocytopenic dogs. Thus, dipyridamole was no less effective in reducing the hypoxic pressor response in the virtual absence of platelets. This supports a direct effect of dipyridamole on pulmonary vascular smooth muscle, which could be mediated by an increase in adenosine levels.
D000818:Animals; D001792:Blood Platelets / Q000276:immunology / Q000502:physiology*; D001794:Blood Pressure / Q000187:drug effects; D004176:Dipyridamole / Q000494:pharmacology*; D004285:Dogs; D005260:Female; D000860:Hypoxia / Q000150:complications / Q000503:physiopathology*; D007106:Immune Sera / Q000494:pharmacology; D008168:Lung / Q000098:blood supply* / Q000187:drug effects; D008297:Male; D013921:Thrombocytopenia / Q000150:complications / Q000503:physiopathology; D014655:Vascular Resistance / Q000187:drug effects*
D007106:Immune Sera; D004176:Dipyridamole