Weaver LK, Howe S, Snow GL, Deru K. Arterial and pulmonary arterial hemodynamics and oxygen delivery/extraction in normal humans exposed to hyperbaric air and oxygen. J Appl Physiol 107: 336-345, 2009. First published April 30, 2009 doi:10.1152/japplphysiol.91012.2008.-Divers and hyperbaric chamber attendants breathe hyperbaric air routinely. Hyperbaric oxygen (HBO2) is used therapeutically frequently. Although much is understood about the hemodynamic physiology and gas exchange effects during hyperbaric air and HBO2 exposure, arterial and pulmonary arterial (PA) catheter data, including blood gas values during hyperbaric air and HBO2 exposure of normal humans, have not been reported. We exposed 10 healthy volunteers instrumented with arterial and PA catheters to air at 0.85, 3.0, 2.5, 2.0, 1.3 (decompression stop), 1.12 (decompression stop), and 0.85 atm abs (our altitude) and then at identical pressures breathing O2 followed by atmospheric pressure air while we measured arterial and PA pressures (PAP), cardiac output (Q ), and blood gas measurements from both arterial and PA catheters. Although hemodynamic changes occurred during exposure to both hyperbaric air and HBO2, we observed a greater magnitude of change under HBO2 conditions: heart rate changes ranged from Ϫ9 to Ϫ19% (air to O2), respiratory rate from Ϫ12 to Ϫ17%, Q from Ϫ7 to Ϫ18%, PAP from Ϫ18 to Ϫ19%, pulmonary vascular resistance from Ϫ38 to Ϫ48%, and right-to-left shunt fraction from Ϫ87 to Ϫ107%. Mixed venous CO2 fell 8% from baseline during HBO2 despite mixed venous O2 tensions of several hundred Torr. The stroke volume, O2 delivery, and O2 consumption did not change across exposures. The arterial and mixed venous partial pressures of O2 and contents were elevated, as predicted. O2 extraction increased 37% during HBO2. hyperbaric oxygen; pulmonary arterial catheter; cardiac output; oxygen extraction THOUSANDS OF PATIENTS have been treated with hyperbaric oxygen (HBO 2 ); however, the precise arterial and pulmonary arterial (PA) hemodynamic and gas exchange responses that occur during HBO 2 are not clearly known. Determining precise hemodynamic and gas exchange information requires the subject or patient to be instrumented with arterial and PA (SwanGanz) catheters, permitting measurement of intravascular pressures and blood gases, and PA catheter data collected in normal humans exposed to HBO 2 has been reported only once (24).It has long been established that heart rate (HR) falls during HBO 2 (3). Forty years ago, investigators reported that this reduction in HR was associated with decreased cardiac output (Q ) (48), an observation supported by subsequent research (Table 1) (21,24,27,29,48). Generally accepted hemodynamic effects of HBO 2 now "include mild bradycardia, leading to a proportional decline in Q and a small increase in systemic vascular resistance" (28).As (43), possibly due to high O 2 concentrations reducing myocardial relaxation factor (nitric oxide), thereby making the heart stiffer (23), or by an increase in afterload from i...
Various anatomical factors were examined which might provide passive resistance to portal venous flow and so cause portal hypertension. Methods included the measurement of portal pressure (WHVPG) in cirrhotic and non-cirrhotic patients, morphological assessment by semiquantitative grading of severity of disease, calculation of hepatocyte size indices, and assessment of volume density of hepatocytes, sinusoids, Disse's space and Disse's space collagen by electron microscopy. The wedged hepatic venous pressure gradient increased with progression of disease and portal hypertension was present before histologicaily detectable cirrhosis had developed. With increasing progression of disease towards cirrhosis, the relationship between individual and aggregated features and the WHVPG diminished and lost statistical significance. Hepatocyte size increased with progression of histological changes and correlated significantly with increase of WHVPG, both in nonalcoholic and alcoholic patients. Disse's space coliagen was increased significantly in nonalcoholic chronic active hepatitis compared with patients with near-normal liver. No significant decrease of sinusoidal space was found. Multiple factors rather than any single feature influence the development of portal hypertension.
ABSTRACT— Cholestatic and hepatitic liver cell rosettes, gland‐like formations found respectively in chronic cholestasis and in chronic active hepatitis, represent structural modifications of liver cell plates in response to injury. Differences in cytokeratin expression, ultrastructure and three‐dimensional (3‐D) configuration have been investigated. Cholestatic rosettes are considered to be a form of biliary metaplasia of hepatocytes, linking with newly‐formed bile ductules in adjacent septa and probably providing some protection from injury caused by abnormal bile constituents. Hepatitis rosettes, by contrast, are a form of liver cell regeneration developing in isolated surviving hepatocytes or small groups of hepatocytes within areas of collapse.
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