Different, tissue-dependent antiaggregatory properties of endothelial cells are suggested by in vitro findings, which show different spectra and amounts of arachidonic acid products to be synthesized by vessels of different type and origin. Platelet aggregation was assessed in vivo in native arterioles of the hamster cheek pouch and in arterioles of heart transplants by intravascular excitation of fluorescein isothiocyanatedextran (FITC-d). The time to aggregate appearance (TAA) was determined, i.e. the interval from onset of FITC-d excitation until the first aggregate was seen to adhere to the vessel wall. Two groups were pretreated with 100 μg/kg nafazatrom and 100 mg/kg acetylsalicylic acid (ASA), both potent antithrombotic drugs. Nafazatrom has been shown to stimulate prostacyclin release from endothelial cells, whereas ASA blocks cyclooxygenase both in platelets and vessel walls. TAA was the same for native arterioles of both types. Nafazatrom was equally effective in both vessels, and about three orders of magnitude more potent than ASA in prolonging TAA. ASA was twice as effective in arterioles of the heart as it was in those of the skin type, indicating that tissue-dependent mechanisms achieve the antiaggregatory potency of the vessel walls. It is concluded that further in vivo studies on platelet aggregation and thrombus formation should be performed on cardiac vessels directly and not on vessels of different origin. The presented model may be a useful tool for investigating the mentioned tissue-dependent mechanisms of thrombus formation in vivo