Near-infrared spectrophotometry-determined cerebral (ScO2) and muscle oxygen saturations (SmO2) were followed in 15 volunteers during passive 50 degrees head-up-tilt-induced central hypovolaemia, and in nine volunteers during ventilatory manoeuvres affecting arterial carbon dioxide tension. During head-up tilt, mean arterial pressure [MAP, 88 (77-118) to 97 (80-136) mmHg, median and range] and heart rate [HR; 66 (49-77) to 87 (42-132) beats min-1 P < 0.01] increased, but after 22 (1-45) min they declined [to 61 (40-91) mmHg and 69 (38-109) beats min-1, respectively, P = 0.001] and pre-syncopal symptoms developed. Central hypovolaemia was indicated by an increased thoracic electrical impedance, and a decreased cardiac output and central venous oxygen saturation. The arterial oxygen saturation, pulmonal oxygen uptake and skin temperatures remained constant. The ScO2 remained stable at 72 (62-77)% until the pre-syncopal incidence, when it decreased to 62 (31-73)% (P = 0.001), and tilt down made it increase to 75 (36-87)% (P < 0.05) before the recovery value was established. In contrast, SmO2 decreased during tilting [75(70-87) to 65 (53-70)%], and recovered to 70 (53-83)%, P < 0.01) during the hypotensive episode. The end-tidal CO2 tension decreased only during tilt-up. The ScO2 decreased, and SmO2 increased during hyperventilation, and ScO2 increased during breathing of 5% carbon dioxide. Rebreathing from a bag made SmO2 decrease and resulted in a biphasic ScO2 response: it first increased and subsequently decreased. Cardiovascular changes during tilt were not reflected in skin temperature. The ScO2 reflected the maintained autoregulation of cerebral blood flow until the perfusion pressure decreased markedly. In contrast, SmO2 mirrored muscle vasoconstriction early during tilt, and vasodilatation when pre-syncopal symptoms appeared.

This study examined whether accumulated oxygen deficit depends on treadmill grade during uphill running. Oxygen uptake was measured during steady-state submaximal running. By linear extrapolation at each grade, energy demand was estimated for short exhaustive runs. Oxygen deficit was the difference between this estimate and accumulated oxygen uptake. Six subjects ran at grades of 1, 15, and 20% (study I), and five males trained for anaerobic metabolism ran at 1, 10.5, and 15% (study II). Accumulated oxygen deficit was 40 +/- 11 (SD), 72 +/- 20, and 69 +/- 8 ml O2/kg, respectively (study I), and 57 +/- 8, 78 +/- 10, and 100 +/- 7 ml O2/kg (study II). The finding that accumulated oxygen deficit became larger with treadmill inclination could reflect involvement of an increasing muscle mass. However, variation in accumulated oxygen deficit was too large to make this possibility the only explanation. More likely at small treadmill inclinations energy demand for high-intensity running is underestimated by extrapolation from oxygen uptake during submaximal exercise. At high grades of uphill running, accumulated oxygen deficit reached a maximum that may reflect the subjects' anaerobic capacity for running. This hypothesis was substantiated by an enhanced accumulated oxygen deficit in the anaerobically trained subjects during 15%, but not during 1%, uphill running.

No abstract

A previous study demonstrated a strong but short-lasting suction through the catheter eyes by a hydro-dynamically generated negative pressure fluctuation terminating bladder evacuation in some frequently occurring circumstances of indwelling catheter drainage. This report regards the biological effect. Fifteen successive evacuations on such drainage conditions in each of 4 anesthetized pigs were followed by cystectomy and histological examination. All bladders presented small swollen areas, histologically showing localized mucosal elevations dominated by edema of lamina propria and submucosa, occasionally with urothelial thinning or defects. Drainage with suction prevented in 3 animals caused normal bladders. The changes were similar to those following hydro-statical suction and much like those of the "polypoid cystitis" so commonly occurring with indwelling catheters. This suggests both types of suction by ordinary drainage as a major pathogenetic factor in the latter condition. The clinical significance and the occurrence during regimes of straight drainage or intermittent clamping are discussed.