Tratamiento fibrinolítico intravenoso en el manejo del ictus isquémico agudo asociado a mixoma auricular izquierdo: a propósito de un caso / Intravenous fibrinolysis for acute ischaemic stroke associated with left atrial myxoma: A case report

No disponible

The in vitro effects of propofol on tissular oxidative stress in the rat.

UNLABELLED: This study was designed to evaluate the in vitro effects of propofol on lipid peroxide formation and the glutathione antioxidant system in some tissues of Wistar rats (n = 8-10 per experiment). We measured thiobarbituric acid reactive substances (TBARS), and the activities of glutathione peroxidase (GSHpx), reductase (GSSGrd), and transferase (GSHtf). Propofol inhibited TBARS formation in a concentration-dependent manner. Etomidate and thiopental sodium 10(-6) to 10(-3) M had no effect. The effect of propofol was apparent immediately and was observed for up to 15-20 min after the start of TBARS formation. Propofol inhibited GSHpx activity by a maximum of 75.1%+/-8.4%, increased GSSGrd activity by a maximum of 188%+/-12.6%, and increased GSHtf activity by a maximum of 230%+/-20%. The solvent intralipid had no significant effect on any of the enzyme activities or on lipid peroxidation. We conclude that propofol not only inhibits lipid peroxidation, but also enhances the cellular antioxidant defense system. Propofol is thus able to prepare tissues against oxidative attack by boosting stores of reduced glutathione. IMPLICATIONS: 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.).

Effect of propofol on oxidative stress in an in vitro model of anoxia-reoxygenation in the rat brain.

Propofol, an intravenous anaesthetic, is similar in chemical structure to the active nucleus of antioxidant substances such as alpha-tocopherol (vitamin E). The present study was designed to test whether propofol had antioxidant effects in an in vitro model of anoxia-reoxygenation in slices of rat brain. We used seven experimental groups: (1) control oxygenated tissue; (2) tissue subjected to anoxia for 20 min and reoxygenation for 3 h; and tissues processed as described and incubated with (3) Intralipid (commercial solvent for propofol), or propofol at a concentration of (4) 10 micromol/l, (5) 50 micromol/l, (6) 150 micromol/l or (7) 300 micromol/l. The production of lipid peroxides was quantified as thiobarbituric acid reactive substances (TBARS); tissular glutathione production and the activities of glutathione peroxidase (GSHpx), glutathione reductase (GSSGrd) and glutathione transferase (GSHtf) were also measured. Reoxygenation led to tissular oxidative stress, which was curtailed by propofol. The anaesthetic led to a 47% reduction in TBARS, a 165% increase in the reperfusion-inhibiting glutathione content, a 47% decrease in GSHpx activity, and an 87% increase in GSHtf activity. Intralipid had no effect on any of the parameters studied here. We conclude that propofol has a clear antioxidant effect in rat brain tissue subjected to anoxia-reoxygenation.