Assessing noise sources at synchrotron infrared ports.

Today, the vast majority of electron storage rings delivering synchrotron radiation for general user operation offer a dedicated infrared port. There is growing interest expressed by various scientific communities to exploit the mid-IR emission in microspectroscopy, as well as the far infrared (also called THz) range for spectroscopy. Compared with a thermal (laboratory-based source), IR synchrotron radiation sources offer enhanced brilliance of about two to three orders of magnitude in the mid-IR energy range, and enhanced flux and brilliance in the far-IR energy range. Synchrotron radiation also has a unique combination of a broad wavelength band together with a well defined time structure. Thermal sources (globar, mercury filament) have excellent stability. Because the sampling rate of a typical IR Fourier-transform spectroscopy experiment is in the kHz range (depending on the bandwidth of the detector), instabilities of various origins present in synchrotron radiation sources play a crucial role. Noise recordings at two different IR ports located at the Swiss Light Source and SOLEIL (France), under conditions relevant to real experiments, are discussed. The lowest electron beam fluctuations detectable in IR spectra have been quantified and are shown to be much smaller than what is routinely recorded by beam-position monitors.

Hypoxia causes permeability oedema in the constant-pressure perfused rat lung.

Alveolar hypoxia causes pulmonary oedema associated with increased lung capillary pressure and decreased alveolar fluid reabsorption. However, the role of altered permeability is unclear. The aim of the present study was to test whether hypoxia affects alveolar permeability and induces pulmonary oedema in rat lungs, and whether terbutaline affects oedema formation. Isolated lungs of normoxic rats were perfused at a constant pressure (12 cmH2O) and exposed to different levels of oxygenation (1.5-35% O2). Terbutaline (10-5 M) was applied as an aerosol or with the perfusate. Online measurements indicate an earlier onset of weight gain with an increasing degree of hypoxia and a shortened lung survival time (35% O2: approximately 220 min; 1.5% O2: approximately 120 min). Terbutaline did not prevent oedema formation in hypoxic lungs. The terbutaline-induced formation of cyclic adenosine monophosphate was decreased by 50% in hypoxia (1.5% O2). In experiments terminated after 75 min, bronchoalveolar lavage fluid of hypoxic lungs contained protein that originated from perfusate indicating alveolar leakage. Since lactate dehydrogenase in perfusate was not increased at the onset of oedema formation, cell damage does not explain the increased permeability. In conclusion, these results indicate the formation of a leak for macromolecules of the isolated perfused rat lung, which is accelerated by hypoxia and causes alveolar flooding even at low perfusion pressure at a rate that exceeds absorption even after stimulation with terbutaline.