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Blood, cerebrospinal fluid, and extracellular fluid of the parenchyma form the fluid compartments of the brain with three interfaces between--the blood-brain interface, the CSF-brain interface, and the blood-CSF interface. These and other issues are discussed in this article.
A technique for measuring glomerular filtration rate (by six-sample plasma clearance) and extracellular fluid volume is described. The results obtained for glomerular filtration rat per extracellular fluid volume with a three blood sample technique are also presented. Concurrently with the blood sample techniques measuring plasma clearance, glomerular filtration rate per extracellular fluid volume was also measured using an external radiation detector and no blood samples. The validity of expressing glomerular filtration rate per extracellular fluid volume (rather than per body weight or surface area) and the clinical utility of the results obtained with the external radiation detector are discussed.
In the steady state, urinary excretion of sodium is closely matched to dietary salt intake. Given rigorous defense of extracellular fluid osmolality, it is the quantity of sodium in the extracellular fluid that determines the volume of this compartment. Changes in extracellular fluid volume are detected by volume sensors located in the intrathoracic vascular bed, kidney and other organs. These mechanoreceptors gauge the adequacy of intravascular volume, relative to capacitance, at various sites within the circulation. The perception of a change in the normal relationship between intravascular volume and circulatory capacity evokes a host of renal effector mechanisms that lead ultimately to physiologically appropriate changes in urinary sodium excretion. These effector mechanisms involve physical adjustments in the glomerular filtration rate, renal microvascular hemodynamics and peritubular capillary Starling forces, tubule fluid composition, flow rate and transtubular ion gradients. Neural and humoral pathways are also involved and, among the latter, angiotensin II, aldosterone, prostaglandins and kinins have been studied extensively. The continuous interaction between these sensor and effector mechanisms serves to ensure near-constancy of the extracellular fluid volume, a condition essential for optimal circulatory performance.
The chronic roles of the transcapillary fluid flux and lymph flow in the distribution of extracellular fluid volume during volume-loading hypertension were investigated in five conscious dogs. Similarly, the distribution of plasma proteins across the microvasculature was evaluated. During the early phases of volume-loading hypertension the fluid balance was positive, which caused the extracellular fluid volume and the plasma volume to increase 25 and 15%, respectively. The thoracic duct lymph flow more than doubled, but the increase in transcapillary fluid flux was even greater. Therefore the interstitial fluid volume increased 30%. This fluid shift from the vasculature into the interstitium probably prevented an even greater rise in arterial pressure. In addition, the transcapillary protein flux more than doubled, but the accompanying increase in lymph protein transport prevented any change in plasma protein mass. During the latter part of the saline-infusion period, the lymph flow declined toward its control, which caused a net transfer of fluid into the interstitium. In conclusion, the transcapillary fluid flux and lymph flow play significant roles in extracellular fluid volume distribution.
To detect whether the mutual interaction occurring between the osteocytes-bone lining cells system (OBLCS) and the bone extracellular fluid (BECF) is affected by load through a modification of the BECF-extracellular fluid (ECF; systemic extracellular fluid) gradient, mice metatarsal bones immersed in ECF were subjected ex vivo to a 2-min cyclic axial load of different amplitudes and frequencies. The electric (ionic) currents at the bone surface were measured by a vibrating probe after having exposed BECF to ECF through a transcortical hole. The application of different loads and different frequencies increased the ionic current in a dose-dependent manner. The postload current density subsequently decayed following an exponential pattern. Postload increment's amplitude and decay were dependent on bone viability. Dummy and static loads did not induce current density modifications. Because BECF is perturbed by loading, it is conceivable that OBLCS tends to restore BECF preload conditions by controlling ion fluxes at the bone-plasma interface to fulfill metabolic needs. Because the electric current reflects the integrated activity of OBLCS, its evaluation in transgenic mice engineered to possess genetic lesions in channels or matrix constituents could be helpful in the characterization of the mechanical and metabolic functions of bone.
1. After overnight deprivation of water both the cellular and extracellular fluid volumes are significantly reduced in the rat. 2. In the rat with functional kidneys oral, intragastric or intravenous preloads of 10 ml. water reduce the total water intake after 1 hr by 64-69%. These preloads restore plasma osmolality to pre-deprivation levels but have little effect on plasma volume. 3. In the same rats if the plasma volume is restored with an oral, intragastric or intravenous preload of 10 ml. of an isotonic balanced salt solution which has little effect on osmolality, drinking is significantly reduced by 20-26%. The reduction of drinking correlated with the volume of the preload of balanced salt. 4. Plasma analysis shown that 1 hr after an oral preload of 10 ml. isotonic balanced salt solution, the extracellular fluid volume of the deprived rats is restored to pre-deprivation levels but osmolality is unchanged. Three hr after the balanced salt preload, extracellular fluid volume is still at pre-deprivation levels and there has been a slight decrease in osmolality due to excretion of salt. 5. In rats which had been nephrectomized or had the ureters ligated so there could be no renal modification of the preloads, the effects of the preloads of water and balanced salt are the same as in rats with intact kidneys. 6. The results indicate that after water deprivation in the rat, changes in both the cellular and extracellular fluid compartment are stimuli to drinking.
The cause of gastric mucosal cell injury induced by Helicobacter pylori (H. pylori) was investigated in vitro using gastric mucosal cells derived from the stomach of male Japanese white rabbits. In order to evaluate the contribution of potent urease activity of H. pylori to gastric mucosal cell injury, supernatant of H. pylori bacterial pellet solubilized in a 1.0% solution of n-octyl-glucoside, the H. pylori extracts, was added to the rabbit gastric mucosal cell suspension. Cell injury was expressed by LDH release into the extracellular fluid of gastric mucosal cell suspension after 30 minutes incubation at 37 degrees C. Treatment of cells by H. pylori extracts (final concentration of 0.54 mg/ml) together with urea (final concentration at 50 mM) showed a high LDH release into the extracellular fluid suggesting definite gastric mucosal cell injury. Elevation of ammonia concentration and that of extracellular fluid pH were also observed by the treatment, whereas H. pylori extracts alone and urea solution alone did not. The ammonia concentration of extracellular fluid and LDH release were distinctly elevated in accord with increasing amount of H. pylori extracts under the existence of 50 mM urea. The degree of LDH release from gastric mucosal cell by H. pylori extracts under the existence of urea was similar to that induced by the administration of the same amount of exogenous ammonia. The addition of acetohydroxamic acid (AHA), a potent specific urease inhibitor, remarkably inhibited dose dependently the ammonia production, the elevation of pH of extracellular fluid and LDH release induced by H. pylori extracts under the presence of urea. These results suggest that the ammonia produced by potent urease activity of H. pylori under the presence of urea played an important role in the pathogenesis of gastric mucosal cell injury.
Zinc homeostasis in the brain is affected by dietary zinc deficiency, and its alteration may cause brain dysfunctions. On the basis of the previous evidence that hippocampal zinc was responsive to 12-week zinc deprivation, responsiveness of hippocampal zinc to dietary zinc deficiency was examined in rats fed a zinc-deficient diet for 4 weeks. Zinc concentration in the hippocampus was not decreased by zinc deprivation for 4 weeks. However, Timm's stain was extensively attenuated in the brain of the zinc-deficient rats. In the brain of the zinc-deficient rats, moreover, zinc concentration in the hippocampal extracellular fluid was approximately 30% of that of control rats. These results demonstrate that vesicular zinc is responsive to dietary zinc and may decrease easily under zinc deficiency. Zinc concentration in the hippocampal extracellular fluid during stimulation with high K(+) was significantly increased even in zinc-deficient rats, although the increased levels of zinc were lower than the basal levels of zinc in control rats. The basal glutamate concentration in the hippocampal extracellular fluid was not significantly different between the control and zinc-deficient rats. However, glutamate concentration in the hippocampal extracellular fluid during stimulation with high K(+) was more increased in the zinc-deficient rats than in the control rats. Gamma aminobutyric acid (GABA) concentration in the hippocampal extracellular fluid during stimulation with high K(+) was increased in the control rats, but not in the zinc-deficient rats. The present study suggests that the excitability of hippocampal glutamatergic neurons is enhanced by dietary zinc deficiency.
The relationship of body fat distribution with blood pressure, fat cell weight and extracellular fluid volume was studied and compared in 20 obese hypertensive men and 20 obese hypertensive women of similar age, degree of overweight and blood pressure level. Body fat distribution, as reflected by the ratio between waist and hip circumference (W/H ratio), was significantly higher in male than in female obese patients. The W/H ratio was positively and independently correlated with systolic arterial pressure both in males and females. However, for the same W/H ratio, systolic arterial pressure was higher in females. The W/H ratio was positively correlated with gluteal fat cell weight only in males and not in females. Both in males and females, the W/H ratio was positively correlated with extracellular fluid volume, independently of the level of blood pressure level and/or the degree of obesity. The study provided evidence that the relationship between body weight and blood pressure in obese hypertensives is affected by the sex-dependence of body fat distribution with possible interferences on fat cell weight and extracellular fluid volume. Several epidemiological studies have emphasized the positive correlation observed between body weight and blood pressure in many. Many investigations have documented the association of blood pressure with body weight, weight to height, overweight or other indices of fatness such as skinfold thickness. However, the correlation coefficients of these different relationships were found constantly small, indicating that the relationship between overweight and blood pressure is somewhat complex. In patients with hypertension, body weight was shown to be strongly related with the levels of both blood pressure and extracellular fluid volume. On the other hand, patients with overweight and hypertension were found to be principally affected by hypertrophic obesity, as shown by the evaluation of fat cell weight. However these findings were exclusively observed in males. No solid data were reported in females. The relationships between body weight and extracellular fluid on one hand, and between body weight and fat cell weight on the other hand, are certainly different in males and in females. First, in females, extracellular fluid volume is submitted to cyclic changes in sodium balance involving the effect of sex steroid hormones. Second, body fat distribution, a parameter which is weakly correlated to blood pressure, is different in males and females. In males, body fat predominates in the upper part of the body while, in females, adiposity is mainly observed in the lower part of the body.(ABSTRACT TRUNCATED AT 400 WORDS)
We investigated the relationships between methylphenidate (MPD) enantiomers and endogenous dopamine (DA) levels in striatal extracellular fluid, and that between DA level and locomotor activity, after intravenous administration of racemic MPD (2, 5 or 10 mg/kg dose) or the individual enantiomers (2.5 mg/kg dose) to rats. MPD and DA levels in the extracellular fluid were measured by in vivo brain microdialysis. The maximum levels of MPD enantiomers in the striatal extracellular fluid were obtained within 15 min after administration. On the other hand, the mean maximum DA levels after administration of 2-10 mg/kg dose of racemic MPD were obtained within 10 min with values in the range of 3.0- to 8.6-fold higher than the basal DA level. The maximum DA level (4.2-fold of the basal level) after administration of (+/-)-MPD was greater than that (2.2-fold) of the same dose of (-)-MPD. A clockwise hysteresis was observed between MPD concentration and DA level in the extracellular fluid after MPD administration. Locomotor activity after administration of (+)-MPD was also greater than (-)-MPD. From these results, it was shown that the locomotor activity induced by MPD may be related to the increase of DA level in the extracellular fluid, and the degree of increase of the DA level by (+)-MPD was greater than that of the (-)-isomer.
Traditional beliefs about two aspects of glucose regulation in the brain have been challenged by recent findings. First, the absolute level of glucose in the brain's extracellular fluid appears to be lower than previously thought. Second, the level of glucose in brain extracellular fluid is less stable than previously believed. In vivo brain microdialysis was used, according to the method of zero net flux, to determine the basal concentration of glucose in the extracellular fluid of the striatum in awake, freely moving rats for comparison with recent hippocampal measurements. In addition, extracellular glucose levels in both the hippocampus and the striatum were measured before, during, and after behavioral testing in a hippocampus-dependent spontaneous alternation task. In the striatum, the resting extracellular glucose level was 0.71 mM, approximately 70% of the concentration measured previously in the hippocampus. Consistent with past findings, the hippocampal extracellular glucose level decreased by up to 30 +/- 4% during testing; no decrease, and in fact a small increase (9 +/- 3%), was seen in the striatum. Blood glucose measurements obtained during the same testing procedure and following administration of systemic glucose at a dose known to enhance memory in this task revealed a dissociation in glucose level fluctuations between the blood and both striatal and hippocampal extracellular fluid. These findings suggest, first, that glucose is compartmentalized within the brain and, second, that one mechanism by which administration of glucose enhances memory performance is via provision of increased glucose supply from the blood specifically to those brain areas involved in mediating that performance.
Peritoneal dialysis (PD) does not demand special equipment and its fluid composition can be easily changed according to the individual condition. Nine patients with chronic or acute renal failure presented severe metabolic alkalosis (MA). Hemodialysis (HD) proved virtually ineffective and the MA persisted. Physiological saline solution was adopted as the main component of the PD fluid for the treatment of MA. By this method, Cl- can be shifted from PD fluid to extracellular fluid (ECF) and HCO3- from ECF to PD fluid by ionic gradient. Therefore, pH and base excess (BE) of these patients both improved to the normal range after several fluid exchanges. The lowering effect of BE (delta BE/L) ranged from 0.99 to 2.6. Hyposaline and normo-osmol solution (Na+ 70 mEq/L) were used for one patient with hypernatremia and consciousness disturbance. Serum (S)-Na decreased from 170 to 138 mEq/L, and consciousness became almost clear with the use of 15 L of PD fluid. Hypersaline solution (Na+ 190 mEq/L) was used for two patients with hyponatremia (S-Na 113 and 121 mEq/L). S-Na rose to within the normal range after 16 and 9 L in the two cases. A fluid mixed with distilled water, 10% NaCl and 7% NaHCO3 (HCO3 34-68 mEq/L) was used to treat lactic acidosis in two patients. By this method, HCO3- can be shifted from PD fluid to ECF and lactic acid from ECF to PD fluid. Two patients recovered from prolonged shock, and pH was corrected by 10 L and 4 L, respectively. PD should be considered for application in other diseases besides renal failure.
When properties of extracellular fluids that might regulate the ability of the Lyme disease spirochete to locomote were investigated, the rate of progression correlated with viscoelasticity. Such spirochetes flexed and rotated but did not progress in relatively nonviscous fluids and migrated increasingly rapidly as the viscous characteristics of the medium increased. The viscoelastic properties of various kinds of hyaluronic acid resembled those of a methylcellulose standard. The maximum velocity that spirochetes achieved in such solutions related directly to viscoelasticity rather than to chemical composition. Spirochetes remained motile during 3 h of observation despite 100-fold dilution of the standard nutrient medium. The immobility of Lyme disease spirochetes in media less viscous in character than fixed tissue suggests dissemination via the intercellular ground substance of skin.
Glomerular hyperfiltration in established, moderately hyperglycemic, insulin-dependent diabetes has been hypothesized to be the result of mild volume expansion. Because glomerular hyperfiltration in diabetics is normalized by insulin treatment, then insulin treatment should also reduce extracellular fluid or plasma volume. Previous studies have demonstrated that acute insulin treatment in nondiabetic kidneys results in vasodilation and increased GFR. It is possible that stimuli to the diabetic kidney, as a result of insulin-induced fluid shifts that reduce extracellular fluid volume (ECF) via glucose transport, result in reduction in GFR, opposing the direct renal vasodilatory action of insulin. Awake, chronically cannulated Wistar rats were used in both nondiabetic and established, moderately hyperglycemic, streptozotocin diabetic conditions. After the initial measurements of GFR, RPF, and ECF were obtained, insulin R (5 U) was administered acutely, both groups of rats were glucose clamped at euglycemic levels, and the measurements were repeated. In nondiabetic rats, GFR increased from 0.90 +/- 0.04 to 1.12 +/- 0.06 mL/min.100 g body wt after insulin treatment (P < 0.05), whereas in diabetic rats, GFR, which was greater than in the nondiabetic rats (P < 0.05), decreased from 1.37 +/- 0.03 to 1.13 +/- 0.05 mL/min.100 g body wt (P < 0.05) after acute insulin treatment. The alterations in GFR paralleled the changes in RPF, and the GFR alterations are most likely mediated by the changes in RPF. ECF was not different between nondiabetic and diabetic rats (28 +/- 2 versus 26 +/- 2% of body wt, respectively) and was not significantly altered by acute insulin infusion. Therefore, the contrasting effects of insulin infusion on GFR and RPF in nondiabetic versus diabetic rats cannot be attributed to alterations in ECF. In addition, the data demonstrate that ECF expansion is not required to sustain glomerular hyperfiltration.
In all patients with hyponatremia, an etiologic diagnosis must be made. A diagnostic classification of hyponatremic states is proposed, which is based on extracellular fluid volume status. A spot urinary sodium concentration will be helpful in confirming the diagnosis. Treatment should concentrate on correction of etiologic factors and fluid restriction after any extracellular fluid volume depletion is treated. A regimen of rapid correction of hyponatremia is outlined for serious, symptomatic cases. It consists of diuretic induced diuresis, accompanied by hypertonic sodium replacement of urinary losses. Finally, the usefulness of demeclocycline hydrochloride is characterized.
The mammalian CNS is separated from the blood by tight junctions, collectively termed the blood-brain barrier (BBB). This imposes unique features of solvent and water movement into and out of the CNS. The basic equations for water fluxes driven by osmotic gradients are presented. The anatomy of the BBB and the physiology of the transport processes for cerebrospinal fluid production, extracellular fluid production and intercellular water and solute transport are then described. A quantitative analysis of the need for aquaporin-based water movements to accompany the known rates of CSF production is also presented. Finally, the mechanisms and roles of cellular and vasogenic edema in the CNS, especially in relation to aquaporins, are described.
CNS immune regulation is intimately dependent on the dynamics of cerebral extracellular fluid circulation. Animal models indicate that following the introduction of antigen into the CNS, normal circulation of interstitial and cerebrospinal fluids provides the opportunity for (a) delivery of CNS-derived antigen to lymphoid organs, as well as, (b) retention of immunologically significant amounts of antigen within the CNS. Thus, even in the absence of disease, CNS-derived antigen can induce antigen-specific activation of naive lymphocytes in lymphoid organs and specific reactivation of lymphoblasts that have migrated into the CNS. The initial peripheral immune response to CNS-derived antigen is induced in cervical lymph nodes and is characterized by a strong antibody response, no delayed-type hypersensitivity, and only priming for cytotoxic T-cell responses. This Th-2 type hierarchy of immune regulation is reinforced within the antigen-stimulated CNS where specific B lymphoblasts are permitted to develop their effector function but cell-mediated immunity is inhibited. Developing a paradigm for CNS immune regulation is important in understanding how CNS disorders in humans are induced, perpetuated, and may be manipulated.
BACKGROUND: Clinical management of fluid imbalance continues to be a major challenge in the long-term care industry. A proactive method of recognizing hypovolemia (reduced total body fluid) in its early stages is greatly needed. OBJECTIVES: The goals of this research were 3-fold: (1) to determine the mean total body resistance(TBR) of an unmatched population of long-term care facility (LTCF) residents and correlate increased levels of TBR with evidence of fluid imbalance; (2) to identify patients at risk for hypovolemia by using TBR measurements as an objective guide; and (3) to suggest nursing practices designed to increase hydration in LTCF residents. METHODS: Two pairs of electrocardiograph-type electrodes were placed on the right humeral-carpal junction and at the level of the right lateral malleolus of each patient. A 50-kHz signal was introduced to the outer electrode of each pair; the inner electrode detected variation of the resistance to the signal as a function of ionic conduction through the electrolyte content of body fluids. Resistance, reactance, and phase angle were measured. RESULTS: The medical records of patients in 26 LTCFs (17 urban, 9 rural) in north-central and east Texas were reviewed during 2001. The mean age of the 1225 study patients (754 women, 471 men) was 76 years; mean height was 165.8 cm, and mean body weight was 71.9 kg. The mean TBR (right wrist-right ankle) for men and women was 504.81 ohms. Based on this measurement and a measurement of 629 ohms in residents judged to be hypovolemic on the basis of abnormal clinical laboratory data, patients with a wrist-ankle resistance >550 ohms were considered at risk for hypovolemia and possibly clinically significant dehydration. Subsequent measurements of TBR revealed a reduction consistent with levels in the normal range. CONCLUSIONS: In these studies, TBR measurements correlated inversely with total body water and fluid compartments. Extracellular fluid compartments were found to be larger in females than in males, reflecting larger cellular mass in males. Total body resistivity was found to be higher in females than in males, which may have implications for body composition metrics. TBR provides a reference for comparison with both clinical and laboratory findings. The ability to identify LTCF residents at risk for hypovolemia, using noninvasive bedside measurements, may offer a definitive guideline for management of adequate fluid balance.