Effect of chlorothiazide upon aldosterone excretion and sodium and potassium balance in essential hypertension.
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Haemodialysis treatment comprises the removal of surplus body water, mainly by ultrafiltration. Frequent complications, such as hypotension, are believed to be related to an imbalance between blood volume reduction, based upon ultrafiltration, and vascular refilling. The control of fluid balance can be achieved by the measurement of blood volume changes. A new method of determining total blood protein concentration by ultrasonic means facilitates continuous monitoring of blood volume changes during haemodialysis. Blood volume monitoring was undertaken during 38 haemodialysis treatments (19 patients) in order to achieve a better adjustment of the patient's estimated dry weight. The relative change in blood volume was registered in 11 patients who were first ultrafiltrated to their estimated dry weight. In a following session the ultrafiltration was increased by 10%. The relative change in blood volume, normalized to the change in total body water, increased significantly from 1.16 +/- 1.11% (normal ultrafiltration) to 1.67 +/- 0.8% (normal ultrafiltration + 10%) (p less than 0.05). Thus, normalized blood volume reduction may serve as an approximation to adjust the patient's dry weight.
The distribution and transport of fluid, ions, and other solutes (plasma proteins and glucose) are described in a mathematical model of unresuscitated hemorrhage. The model is based on balances of each material in both the circulation and its red blood cells, as well as in a whole-body tissue compartment along with its cells. Exchange between these four compartments occurs by a number of different mechanisms. The hemorrhage model has as its basis a validated model, due to Gyenge et al., of fluid and solute exchange in the whole body of a standard human. Hypothetical but physiologically based features such as glucose and small ion releases along with cell membrane changes are incorporated into the hemorrhage model to describe the system behavior, particularly during larger hemorrhages. Moderate (10%-30% blood volume loss) and large (> 30% blood loss) hemorrhage dynamics are simulated and compared with available data. The model predictions compare well with the available information for both types of hemorrhages and provide a reasonable description of the progression of a large hemorrhage from the compensatory phase through vascular collapse.
1. In the unanaesthetized Rhesus monkey, solutions containing sodium, calcium, potassium or magnesium in excess of the normal concentration of extracellular fluid were perfused from a lateral to the fourth ventricle through chronically implanted cannulae.2. Sodium (11.0-88.0 mM in excess of the physiological concentration) perfused through the ventricles, caused an immediate rise in body temperature which was accompanied by vasoconstriction, piloerection and shivering. The latency of the hyperthermia was related directly to the rate of perfusion and the concentration of sodium, whereas the magnitude of the response depended upon the concentration only. When the perfusion was terminated, shivering ceased and the temperature of the monkey returned to the base line level.3. When calcium ions were perfused in concentrations 2.5-47.9 mM in excess of that of extracellular fluid, a fall in the temperature of the animal occurred. The magnitude of the decreases depended upon the concentration of calcium in the perfusion fluid. Vasodilatation, sedation and a reduction in withdrawal reflexes accompanied the calcium-induced hypothermia. After the perfusion ended, the temperature continued to fall until the monkey began to shiver and vasoconstriction was observed in many skin areas.4. The perfusion through the cerebral ventricles with modified Krebs solution alone or with the Krebs solution which contained potassium or magnesium ions in concentrations five to ten times normal had virtually no effect on the temperature of the monkey.5. Since the temperature of the monkey was unchanged as long as the physiological ratio of sodium to calcium in the perfusion fluid remained constant, we conclude that the balance between these two essential cations within the brain stem could determine the neural mechanism whereby the set-point for body temperature of the primate is established.
BACKGROUND: For unclear reasons, life-threatening water intoxication often coincides with acute psychosis in polydipsic schizophrenic patients with chronic hyponatremia. In contrast, most polydipsic schizophrenic patients are normonatremic and never manifest hyponatremia. To explore whether the effect of acute psychosis on water balance differs in these 2 schizophrenic subgroups, we compared their responses to drug-induced psychotic exacerbations. METHODS: Matched polydipsic schizophrenic patients with (n = 6) and without (n = 8) hyponatremia were identified based on past and current indexes of fluid intake and hydration. A transient psychotic exacerbation was induced with an infusion of the psychotomimetic methylphenidate hydrochloride (0.5 mg/kg of body weight over a 60-second period). Antidiuretic hormone levels, subjective desire for water, and factors known to influence water balance were measured at 15-minute intervals for 2 hours. RESULTS: Except for the expected differences in plasma osmolality and sodium, basal measures were similar in the 2 groups. Following methylphenidate administration, antidiuretic hormone levels increased more in the hyponatremic patients (P < .02), despite their consistently lower plasma osmolality (P < .007). No known or putative antidiuretic hormone stimulus could account for this finding. Only basal positive psychotic symptoms (P < .09) and plasma sodium (P < .18) were even marginally associated with the peak antidiuretic hormone responses, but neither factor could explain the difference in the response by the 2 groups. CONCLUSION: Psychotic exacerbations are associated with enhanced antidiuretic hormone secretion, for unknown reasons, in schizophrenic patients with hyponatremia and polydipsia, thereby placing them at increased risk of life-threatening water intoxication.
UNLABELLED: After neurosurgical treatment, surgeons sometimes observe decreased hematocrit (Ht), though fluid as well as blood transfusions were properly given during and after surgery. This study was performed to investigate the effects of osmotic change on the decrease in Ht. MATERIAL AND METHODS: Subjects were 153 patients who underwent neurosurgical treatment. Group 1: 39 patients with parasellar tumor. Group 2: 35 patients with anterior cerebral aneurysm. Group 3: other 79 patients with brain tumor or aneurysm except Group 1 and 2. As the controls, 50 patients undergoing intraabdominal operations. During the pre- and postoperative course, blood examination (Ht, RBC, blood glucose, BUN, electrolyte and blood gases), measurements of osmotic pressure (of serum, urine and cerebrospinal fluid), and checks of blood and water balance and vital signs were performed. RESULTS: As compared with the control group in which Ht decreased clearly but slightly, the neurosurgically-treated groups showed marked decreases in Ht on the 2nd to 4th day after surgery. Of them, groups 1 and 2 showed more prominent decreases. On the 1st to 4th day after surgery, serum sodium levels of groups 1, 2 and 3 increased more clearly than that of the control group. Urine volumes of groups 1 and 2 were larger during one postoperative week, and cases of diabetes insipidus were included. No significant difference was found in water balance and urinary osmotic pressure. Relationships between the serum osmotic pressure and serum sodium content, cerebrospinal fluid osmotic pressure and serum sodium content, and cerebrospinal fluid and serum osmotic pressure were seen. We lay stress on the inverse correlation between the decrease in Ht and the time-course of serum osmotic pressure.(ABSTRACT TRUNCATED AT 250 WORDS)
In an effort to describe the influence of both high (HNA) and low (LNA) dietary sodium (399 vs. 98 mEq Na+ X d-1) on body fluids during heat acclimation (HA), nine untrained males underwent 8 d of HA twice (90 min treadmill walking, 5.6 km X h-1, 6% grade) in an environmental chamber (40.1 degrees C, 23.5% RH). Mean wholebody Na+ balance calculations indicated that HNA resulted in an increase of Na+ of $916 mEq per 8 days per subject, whereas LNA resulted in a relative Na+ deficiency of -230 mEq per 8 days per subject. Subjects exhibited typical HA adaptations of decreased heart rate (HR), decreased rectal temperature (Tre) during exercise, and an increase in resting plasma volume (PV) during both diets. Significant HNA vs. LNA differences (p less than 0.05) were observed in HR (days 3-5), Tre (days 3-6), PV (day 4), plasma osmolality (day 4), plasma Na+ (day 4), urine Na+ (days 2-8), and sweat Na+ (days 4 and 8). The between-diet differences in HR, Tre and PV were not detectable by the end of each dietary-exercise regimen. Needle biopsy samples (20-50 mg, lateral aspect of the gastrocnemius) indicated that muscle Na+ and muscle water were similar on all days, except day 9 when intracellular fluid expansion during LNA was noted. Change in body weight was not strongly correlated with delta PV (R2 = 0.47, 0.10) and neither osmotic forces nor plasma protein movements explained all PV shifts adequately.(ABSTRACT TRUNCATED AT 250 WORDS)
The RAS is part of an extremely powerful feedback system for long-term control of arterial pressure and volume homeostasis as illustrated in Figure 4. Disturbances that tend to lower blood pressure such as heart failure, cirrhosis, and peripheral vasodilation, cause sodium and water retention until blood pressure returns to normal due in large part to the combined actions of ANGII and reduced renal perfusion pressure. In response to disturbances such as high sodium intake, suppression of ANGII greatly amplifies the effectiveness of the basic pressure natriuresis and diuresis mechanism, thereby preventing large increases in body fluid volumes and blood pressure. In circumstances in which the RAS is inappropriately activated, the sodium-water retaining effects of ANGII necessitate increased blood pressure to maintain sodium and water balance via pressure natriuresis. The sodium retaining actions of the RAS are mediated by intrarenal as well as extrarenal mechanisms. The intrarenal actions of ANGII include a direct effect on tubular sodium transport as well as a potent constrictor action on efferent arterioles which increases tubular reabsorption by altering peritubular capillary physical forces. The constrictor action of ANGII on efferent arterioles also plays an important role in stabilizing GFR and therefore in preventing fluctuations in excretion of metabolic waste products that depend upon a high GFR for excretion. ANGII is known to stimulate proximal reabsorption, but the effects on more distal tubular segments have not been completely elucidated. The primary extra-known to stimulate proximal reabsorption, but the effects on more distal tubular segments have not been completely elucidated. The primary extra-renal effect of ANGII which influences sodium excretion is stimulation of aldosterone secretion. Current evidence, however, suggests that the various intrarenal actions of ANGII are quantitatively more important in causing sodium retention than those mediated by changes in aldosterone secretion. However, the combined intrarenal and extrarenal actions of ANGII on sodium reabsorption provide the body with one of its most potent feedback systems for long-term regulation of body fluid volumes and arterial pressure.
The fetal lung, filled with fluid during intrauterine life, is recognized as a site of fluid production, significantly contributing to amniotic fluid volume. To assess possible hormonal control of lung liquid production, we studied the effect of intravenous vasopressin or vasotocin on lung liquid production in chronically catheterized fetal sheep. Both vasopressin and vasotocin infusion resulted in a significant decrease in lung fluid production (38% and 40%, respectively) when compared to that in control animals receiving saline infusion. There was no significant change in lung fluid osmolality, sodium, or potassium. These findings suggest that lung liquid production in utero may be regulated by the fetus and that vasopressin or vasotocin may be of physiologic importance in lung fluid dynamics during the third trimester of ovine pregnancy and perhaps during parturition.
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Both chemo- and mechanosensitive receptors are involved in detecting changes in the signals that reflect the status of body fluids and of blood pressure. These receptors are located in the systemic circulatory system and in the sensory circumventricular organs of the brain. Under conditions of body fluid deficit or of marked changes in fluid distribution, multiple inputs derived from these humoral and neural receptors converge on key areas of the brain where the information is integrated. The result of this central processing is the mobilization of homeostatic behaviors (thirst and salt appetite), hormone release, autonomic changes, and cardiovascular adjustments. This review discusses the current understanding of the nature and role of the central and systemic receptors involved in the facilitation and inhibition of thirst and salt appetite and on particular components of the central neural network that receive and process input derived from fluid- and cardiovascular-related sensory systems. Special attention is paid to the structures of the lamina terminalis, the area postrema, the lateral parabrachial nucleus, and their association with the central nucleus of the amygdala and the bed nucleus of the stria terminalis in controlling the behaviors that participate in maintaining body fluid and cardiovascular homeostasis.
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