Time-resolved X-ray diffraction diagnostic development for the National Ignition Facility.

We present the development of an experimental platform that can collect four frames of x-ray diffraction data along a single line of sight during laser-driven, dynamic-compression experiments at the National Ignition Facility. The platform is comprised of a diagnostic imager built around ultrafast sensors with a 2-ns integration time, a custom target assembly that serves also to shield the imager, and a 10-ns duration, quasi-monochromatic x-ray source produced by laser-generated plasma. We demonstrate the performance with diffraction data for Pb ramp compressed to 150 GPa and illuminated by a Ge x-ray source that produces ∼7 × 1011, 10.25-keV photons/ns at the 400 µm diameter sample.

Upgrade of the gated laser entrance hole imager G-LEH-2 on the National Ignition Facility.

A major upgrade has been implemented for the ns-gated laser entrance hole imager on the National Ignition Facility (NIF) to obtain high-quality data for Hohlraum physics study. In this upgrade, the single "Furi" hCMOS sensor (1024 × 448 pixel arrays with two-frame capability) is replaced with dual "Icarus" sensors (1024 × 512 pixel arrays with four-frame capability). Both types of sensors were developed by Sandia National Laboratories for high energy density physics experiments. With the new Icarus sensors, the new diagnostic provides twice the detection area with improved uniformity, wider temporal coverage, flexible timing setup, and greater sensitivity to soft x rays (<2 keV). These features, together with the fact that the diagnostic is radiation hardened and can be operated on the NIF for high neutron yield deuterium-triterium experiments, enable significantly greater return of data per experiment.

Somatosensory evoked potentials during hypoxia and hypocapnia in conscious humans.

PURPOSE: The objective of the study was to evaluate the effects of moderate hypoxia and hypocapnia on the latency and amplitude of cortical somatosensory evoked potentials (SSEPs) in conscious human subjects. METHODS: In ten volunteers the amplitude and latency of the cortical somatosensory evoked potentials were recorded during stimulation of the left posterior tibial nerve. Measurements of SSEPs and respiratory variables were made breathing ambient air, air containing a reduced oxygen percentage (17% O2, 14% O2 (n = 6) or 11% O2 (n = 10)), and again during voluntary hyperventilation breathing ambient air (PETCO2 = 20 mmHg, n = 10). RESULTS: Hypoxia (11% O2) caused mild stimulation of ventilation (P < 0.05) but had no effects on the latency or amplitude of the SSEP. Lesser degrees of hypoxia had no effects. Hyperventilation caused a small (2-4%) decrease) in the latency of the SSEP and an increase in the amplitude of the SSEP (P < 0.05). CONCLUSIONS: These findings in conscious subjects were consistent with previous observations in anaesthetized humans and anaesthetized dogs and show that the decrease in latency of the SSEP associated with hypocapnia is not due to changes in the depth of anaesthesia. These effects of hypocapnia may contribute to small variations in the latency of the SSEP when monitoring is performed during surgery, but are unlikely to be large enough to be of clinical concern.

Regulation of plasma vasopressin by plasma osmolality and carotid sinus pressure in anesthetized rabbits.

The purpose of the experiments was to investigate the effect of changes in carotid sinus baroreceptor stimulation on plasma vasopressin (AVP) at different plasma osmolalities in the anesthetized artificially ventilated rabbit. Both carotid sinuses were isolated and perfused with blood at servo-controlled pressures. The vagus and aortic depressor nerves were sectioned bilaterally to eliminate input from atrial and aortic arch baroreceptors. Saline (0.3%, wt/vol) was infused to lower plasma osmolality, and 5% saline was infused to raise plasma osmolality. At three plasma osmolalities, the carotid sinus pressure (CSP) was changed from 100 mmHg to 40 and 140 mmHg and returned to 100 mmHg. There were no changes in plasma AVP in response to changes in CSP at low plasma osmolality (289 mosmol/kgH2O), but at medium (309 mosmol/kgH2O) and high (323 mosmol/kgH2O) osmolality, plasma AVP was higher at 40 than at 140 mmHg CSP. The relationship between plasma AVP and plasma osmolality was expressed as a linear regression at each CSP. Changes in CSP changed the sensitivity but not the threshold of the osmotic control of AVP release.