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longitudinally divided, and the lumen inspected under the operating microscope. This allowed to exclude errors in performing the microvascular anastomoses. White mural thromboses were demonstrated as the cause of occlusion.
In the second part of the study, a group of 16 grafts were implanted after the rabbits were given Heparine (500 \mathrm{U}) in bolus. PT and PTT values were obtained before the injection of heparine and at different intervals (1 hr, (3 \mathrm{hrs}). (12 \mathrm{hrs}, 24 \mathrm{hrs})), at the same time as the assessment of the patency. Heparin delayed the occlusion time up to 48 hrs, well after its effects were already disappeared, as demonstrated by the PTT values. Nevertheless, occlusion occurred in all grafts at some time. We believe that the thrombosis model here presented may be useful in studying antithrombotic drugs when considering increasing the patency rates of small diameter PTFE prostheses. In this study, a single injection of heparine just before declamping was sufficient to reverse a strong tendency of the graft towards a rapid thrombosis and to mantain patency for at least 24 hours. This study has potential clinical implications. However, further studies are needed before traslating these results into the clinical setting.
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