Phosphorimeters for analysis of decay profiles and real time monitoring of exponential decay and oxygen concentrations.

A phosphorimeter which can be assembled at low cost from mainly commercially available components and which has better time resolution, data acquisition rate, sensitivity, and flexibility than commercially available instruments is described. As a phosphorescence analyzer the instrument can measure phosphorescence lifetimes ranging from approximately 30 microseconds to seconds from samples with variable intensity, excitation, and emission spectra and which may follow complex decay behavior. Configured as a phosphorescence monitor it is designed for fast, repetitive calculation of phosphorescence lifetime, assuming single-exponential decay, and can be used to calculate oxygen concentration in biological samples in real time.

A versatile and sensitive method for measuring oxygen.

Oxygen dependence of the lifetime of the excited triplet state of phosphorescent molecules can be used to measure the oxygen concentration in aqueous media. These measurements are insensitive to much of the optical interference that limits the usefulness of measurements based on the oxygen dependent quenching of luminescence intensity. The measurements also extend to significantly lower oxygen concentrations than are normally attainable using oxygen electrodes. The phosphorescence lifetimes can be accurately measured from a few microseconds to seconds, permitting a wide dynamic range of oxygen concentration measurements. With currently available probes, for example, it is possible to make continuous measurement of oxygen concentrations from 10(-4) M to 10(-8) M in a single experiment.

Cerebral energy metabolite levels and survival following exposure to low inspired oxygen concentration.

To determine the relationship between brain energy metabolites and neurologic status after ischemia-hypoxia, we measured cortical tissue levels of adenosine triphosphate (ATP), phosphocreatine, and lactate. Rats with permanent unilateral carotid occlusion were exposed to 5, 10, and 15 min of hypoxic atmosphere (FIO2 0.048) and, to examine metabolic restitution, 60 min after recovery in rats exposed to the same hypoxic mixture for 15 min. At 5 and 10 min of hypoxia, there were significant reductions in phosphocreatinine and elevations in tissue lactate, but only after 15 min of hypoxia, did ATP levels significantly decrease. By 60 min after recovery, phosphocreatinine values returned to the normal range, ATP values to 15% less than normal, and tissue lactate toward normal. In parallel survival studies, neurological status was examined following hypoxic exposure (PaO2 18 to 19 torr) for 5 an 10 min. Evidence for neurological injury in the form of posthypoxic seizures occurred at a point in time preceding significant changes in brain tissue ATP level. Since injury occurs prior to ATP reduction, changes in brain tissue ATP level may not be an appropirate endpoint for determining brain tissue injury in hypoxia.