Vitamin E kinetics and the function of tocopherol regulatory proteins.

Plasma and tissue alpha-tocopherol concentrations are remarkably stable, which suggests that they are regulated. alpha-Tocopherol transfer protein, tocopherol-associated protein, and tocopherol-binding protein bind alpha-tocopherol. These proteins might function as tocopherol regulatory proteins, although only tocopherol transfer protein has been shown to influence plasma and tissue alpha-tocopherol concentrations. Tissue alpha-tocopherol concentrations likely depend on tocopherol regulatory protein function and tissue lipid content, vitamin E uptake and efflux, oxidative stress, and interactions between vitamin E and other antioxidants. Pharmacokinetic models often divide tissues into rapidly perfused, slowly perfused, and very slowly perfused compartments. Tissue vitamin E concentrations might equilibrate more rapidly in tissues with greater perfusion, greater vitamin E uptake, increased amounts or activities of tocopherol regulatory protein, and lower lipid contents. The rate at which tissue concentrations approach equilibrium, however, does not predict the final equilibrium concentrations because of redistribution among tissues. Redistribution of vitamin E to adipose tissue from other tissues may be significant. Intracellular trafficking of vitamin E might occur in conjunction with membrane recycling because membrane constituents rapidly recycle between the plasma membrane and intracellular endocytic compartments. Thus, tocopherol regulatory proteins may modulate rather than directly regulate vitamin E tissue distribution and intracellular trafficking.

Effects of anesthetic agents on the drift of a transcutaneous oxygen tension sensor.

Both halothane and nitrous oxide can be reduced at the cathode of a polarographic oxygen electrode, causing the electrode current to drift upward and report falsely high oxygen tension. Because transcutaneous oxygen tension is measured by a heated oxygen electrode, there is a potential for significant upward drift of these values. To examine the clinical significance of this drift, the following study was performed. Transcutaneous oxygen tension sensors were calibrated at oxygen tensions of 0 mm Hg and 157 mm Hg (room air) just before clinical use during anesthesia. This calibration was rechecked immediately upon removal of the sensor from the patient at the end of the anesthesia. The predominant anesthetic agent used and the duration of monitoring were noted from the record. Data were collected from 208 patients representing a total of 463.6 hours of anesthesia. The patients were divided into five groups based on anesthetic administered: halothane, enflurane, isoflurane, nitrous oxide-narcotic, and local/regional. The mean zero point recalibration value was 0.4 mm Hg or less for all agents except halothane, for which it was 1.8 +/- 3.2 mm Hg. This halothane drift was significantly greater than that for the other agents (P less than 0.01). Room air recalibration was not significantly different in any of the five groups, varying from 160 +/- 4.9 mm Hg for halothane to 157 +/- 4.9 mm Hg for enflurane. All these drift values are within the manufacturer's specifications. We conclude that the drift of the transcutaneous oxygen tension sensor due to anesthetic agents is not clinically significant. However, caution should be exercised when halothane is used during an extremely long period of anesthesia.