A facile method for the introduction of various substituents at the C-6 position of guanosine and 2′-deoxyguanosine is reported. In a simple, 1-step transformation, tert-butyldimethylsilyl protected guanosine and 2′-deoxyguanosine were converted to the O 6 -(benzotriazol-1-yl) derivatives via reaction with 1H-benzotriazol-1-yloxy-tris(dimethylamino)phosphonium hexafluorophosphate (BOP) and 1,8-diazabicyclo[5.4.0]undec-7-ene (DBU). The easily isolated, stable and storable, O 6 -(benzotriazol-1-yl) guanosine derivatives upon exposure to range of nucleophiles, under appropriate conditions, led to the C-6 modified 2-amino purine nucleoside analogues in good yields.
Despite a remarkable expansion of microsurgery, there is still no international consensus about routinely used prophylactic antithrombotic agents. Most treatment regimens still use aspirin, heparin (low-molecular-weight and unfractionated heparin) or colloids (hydroxyphenylacetate 6%/dextran); however, clear evidence for the clinical benefit of an ideal administration regimen or one agent over the other has not yet been established. Instead of searching for the one regime that fits all, an increasing number of reviews from different disciplines describe multistep approaches that optimize what has been shown to be most promising. This includes the use of antithrombotic agents, proper risk assessment, secondary prevention and professional training to optimize microsurgical skills. In this review, we describe factors included in traditional approaches and also emphasize the value of good surgical technique, which while recognized by all to be one of the most important factors for success, receives less emphasis in reviews describing thrombosis prophylaxis in microvascular surgery.
A 34 year old male was admitted to the hospital with typical clinical symptoms of acute pulmonary embolism caused by deep vein thrombosis in the upper leg detected by phlebography. Pulmonary embolism was verified by the lung-perfusion-scintigram. The patient developed an infarct pneumonia with hemoptoe. Episodic thromboembolic phenomena occurred due to antithrombin-III deficiency (AT-III). The method, using homogenic substrates exhibited low AT-III activity of 8.6 IU/ml(25°C) due to a familiar AT-III deficit. Fiberoptic pulmonary catheter was placed into the pulmonary artery to measure pulmonary artery pressure (PAP, PCP), right ventricular pressure (RVP) and to determine cardiac output (CO) using the dye dilution technique. Heart rate (HR), central venous pressure (CVP) and aortic pressure (AOP) were recorded continuously. Patient received immediately fibrinolytic therapy, initiated by an initial dose of streptokinase (SK)(250 000 IU/20 min.), followed by a maintenance dose (100 000 IU/h), lasting 3 days. M-mode echocardiography detected before SK a moderate enlarged right ventricle and a small left ventricle, indicating a low output. After SK these values were improved. In conclusion, this case demonstrated a serious thromboembolic disorder, related to AT-III deficit. SK-therapy improved the hemodynamic situation.
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