OAGB is a simple, safe and effective operation with less perioperative risk than conventional gastric bypass, quicker return to normal activities, and better quality of life.
This study demonstrates that the anesthetic propofol increases one of the most important mechanisms against cellular damage, the glutathione system. The study was performed in several tissues of healthy rats. This could be applied as a possible protection in surgical patients suffering from an ischemic process (cerebrovascular disease, coronary ischemia, etc.).
To help clarify the mechanism of propofol-induced vasodilation, we investigated whether propofol, at concentrations ranging from 10(-6) to 10(-3) M, inhibited platelet aggregation in human whole blood. Propofol inhibited platelet aggregation induced by adenosine diphosphate, collagen, or arachidonic acid in a concentration-dependent manner, with a 50% inhibited concentration (micromol/L) of 136 +/- 9.8 for adenosine diphosphate, 77.8 +/- 6.6 for collagen, and 71.8 +/- 5.4 for arachidonic acid. In platelet-rich plasma, propofol had no significant antiaggregant effect except when arachidonic acid was used as the aggregant (50% inhibited concentration 105 +/- 9.9 micromol/L). The antiaggregant effect of propofol in platelet-rich plasma was increased in the presence of red blood cells or leukocytes in a cell number-dependent manner. We conclude that propofol reduces the platelet activity in human whole blood in vitro.
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