BLOOD VOLUMES, BLOOD DISTRIBUTION AND SEA-WATER SPACES IN RELATION TO EXPANSION AND RETRACTION OF THE FOOT IN BULLIA (GASTROPODA).
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The pulsatile ac component (DeltaI) superimposed on the transmitted dc components (I: tissue plus blood) are obtained from a near-infrared finger photoplethysmogram using a wavelength of 810 nm. Only the dc component is given in an ischaemic circulatory state (I(t): tissue only). Based on Lambert-Beer's law, normalized pulse volume (NPV; =DeltaI/I) and blood volume [BV; =ln(I(t)/I)] have recently been advocated as quantitative measures. In this study, the NPV-BV relationship was examined using the finger occlusion method during rest and mental arithmetic in 16 female undergraduates. Finger vascular tone during stress was evaluated by the distance of the linear and parallel NPV-BV regression lines (D(NB)) between rest and stress conditions. A reference standard was provided by the linear regression lines of compliance index (CI=NPV/pulse pressure) and BV to the transmural pressure. The estimates at 40 mmHg of transmural pressure, as an arbitrarily chosen reference point, were calculated (CI40 and BV40). D(NB) correlated well with them (r=0.81 and 0.94, respectively). The multiple regression with mean blood pressure indicated that the combination of D(NB) and the reactivities in heart period could explain approximately 50% of valiance in pressor response. In conclusion, D(NB) is easily obtainable from the NPV-BV function and seems to be more specific and valid than NPV as an index of finger sympathetic tone, since it adjusts the mechanical effect of arterial distending pressure.
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STUDY OBJECTIVES: The objective was to correlate regional changes during brain water content with alterations in blood chemistry and cerebral pathology during hypo-osmotic edema. PARTICIPANTS: Sprague-Dawley male adult rats were used in these studies. DESIGN: Animals were block-randomized to receive either an intraperitoneal distilled water injection equivalent to 5% or 15% of their body weight or no injection (controls). Rats were sacrificed 15 or 60 minutes after water injection or at an equivalent time for controls. INTERVENTIONS: No interventions were performed. MEASUREMENTS AND MAIN RESULTS: Water content of cerebral cortical gray and white matter was calculated from measurements of tissue specific gravity. Blood plasma osmolality and sodium and potassium concentrations were determined at various times after water injection. An index of blood-brain barrier permeability was obtained by measuring brain red blood cell and plasma volumes. A qualitative assessment of edema was made from light and electron micrographs of the cerebral cortex. We found that water injection produced a dose-dependent decrease in plasma osmolality and sodium concentration within 15 minutes. Cortical water content was unchanged after this period. An influx of water into cerebral gray, and, less readily, into cerebral white matter occurred during the next 15 minutes. Whole blood specific gravity and brain blood content were unchanged and thus did not confound the measurement of cerebral water content. Hematocrit was increased 60 minutes after a 15% water injection. The blood-brain barrier remained intact throughout this period. Microscopy revealed astrocytic swelling with slight extracellular fluid accumulation 60 minutes after the water injection. CONCLUSIONS: Homeostatic mechanisms in the cerebral cortex can maintain constant water content for at least 15 minutes during maintained intravascular hypo-osmolality. Fluid that subsequently moves into the tissue primarily enters an intracellular compartment. This model will be useful in investigating physiological mechanisms of brain water regulation and the pathogenesis of brain edema, a common clinical entity in emergency conditions.
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To evaluate the influence of plasma protein concentration and colloid osmotic pressure (COP) on blood volume and blood pressure, we studied 40 patients with the nephrotic syndrome (plasma protein 41.1 +/- 5.3 g/liter, COP 10.9 +/- 2.2 mm Hg) and 43 patients with chronic renal failure (plasma protein 65.0 +/- 5.8 g/liter, COP 22.4 +/- 3.0 mm Hg) at overhydration, during gradual edema removal to normal hydration, and occasionally, to mild dehydration. The number of measure points was 113 in the nephrotic syndrome and 92 in renal failure. In both groups blood volume was normal at normal extracellular fluid volume (ECFV). Elevation of ECFV to 300% of normal in the nephrotic syndrome occurred with only a modest elevation of blood volume (NS). Elevation of ECFV to 200% of normal in the patients with renal failure was attended by a major elevation of blood volume (P less than 0.01). Reduction of ECFV to about 10% below normal was accompanied by parallel blood volume reduction in both groups. Blood pressure was comparable at normohydration, and increased to clearly hypertensive levels only in the renal failure group with increasing ECFV and blood volume (P less than 0.01). No major blood pressure difference was observed between normal and subnormal hydration, but hypotension was observed twice in the nephrotic group. Apparently, patients with severe hypoproteinemia due to the nephrotic syndrome are generally able to preserve their blood volume even when free of edema. However, their blood volume is not elevated in overhydration, in contrast to patients with renal failure who are normoproteinemic. This difference in regulation of extracellular fluid distribution is probably related to the hypoproteinemia, and its effect to reduce tissue-fluid protein.
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