The role of nitric oxide as an endogenous regulator of platelet and neutrophil activation within the pulmonary circulation of the rabbit

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Abstract
1 Intravenous (i.v.) administration of adenosine diphosphate (ADP), platelet activating factor (PAF) and thrombin induced a dose-related accumulation of 111indium-labelled platelets within the thoracic region of anaesthetized rabbits. 2 I.v. administration of the inhibitor of NO biosynthesis, l-NG-nitro arginine methyl ester (l-NAME; 10 mg kg−1) significantly potentiated the peak platelet accumulation induced by ADP, PAF and thrombin. Additionally l-NAME prolonged the disaggregation of platelets in comparison to d-NAME (10 mg kg−1). Such changes were reversible by the administration of l-arginine (900 mg kg−1). 3 I.v. administration of PAF induced a small accumulation of 111indium-labelled neutrophils within the pulmonary circulation which could be greatly potentiated by pretreatment of the animals with l-NAME. In contrast, thrombin administration did not cause significant accumulation of 11indium-labelled erythrocytes in the pulmonary circulation of anaesthetized rabbits. 4 Intracarotid (i.c.) administration of thrombin induced a marked accumulation of radiolabelled platelets within the cranial vasculature which was not potentiated by the prior administration of l-NAME (at either 10 mg kg−1 or 100 mg kg−1). 5 These results suggest that endogenous NO may regulate platelet and polymorphonuclear leukocyte activation within the pulmonary but not the cerebral circulation of rabbits.