Buffer capacity and acid-base balance of blood. Effects of blood loss and some infusion fluids on rabbit blood.
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To study the effects of atrial natriuretic peptide (ANP) on body fluid volume regulation, we estimated the changes in intra- and extravascular fluid volume by measuring hematocrit (Hct), plasma protein concentration and water balance, and the changes in intra- and extracellular fluid volume by the electrical impedance method during intravenous infusion of ANP. We did two studies, as follows: ANP was infused into 18 patients with essential hypertension, 29 with renal parenchymal hypertension and 15 normotensives at 0.025 microgram/kg/min for 40 min. Both hypertensive groups showed greater natriuretic responses to ANP than normotensives. ANP infusion into essential hypertensive patients increased the urinary excretion of water by 125%, Na by 205%, Hct by 4.2% and plasma total protein (TP) by 5.2% (each P less than .001). In 9 patients (1 with renal hypertension and 8 normotensives) who did not show a natriuretic response (-2.1%), the infusion of ANP also significantly increased Hct (3.8%) and plasma TP (3.1%, each P less than .01). The electrical impedance method was applied to 12 subjects to simultaneously detect the intracellular (Ri) and extracellular resistivities (Re), of which reciprocals reflect the fluid volume in the extra- and intracellular spaces, respectively. ANP infusion increased Re in all subjects (3.96 +/- 0.16 [SE] v 4.03 +/- 0.16 omega.m, P less than .05), but decreased Ri in 7. Changes in urinary Na excretion correlated positively with those in both Re (r = 0.62, P less than .05) and Ri (r = 0.75, P less than .01).(ABSTRACT TRUNCATED AT 250 WORDS)
Since its first description in 1985, two opposing theories have evolved to explain the etiology of symptomatic hyponatremia of exercise. The first holds that the condition occurs only in athletes who lose both water and sodium during exercise, and fail to fully replace their sodium losses. The second theory holds that the symptomatic form of this condition occurs in athletes who generate a whole body fluid overload as a result of an excessive fluid intake during prolonged exercise. It is argued that the promotion of the idea that athletes should drink as much as possible during exercise has produced, rather than prevented, the recent increase in the incidence of this condition. A series of case reports and laboratory studies reported in the past 2 years have established that it is a whole body fluid overload, resulting from sustained high rates of fluid intake, that causes the symptomatic hyponatremia of exercise. There is no evidence that, in the absence of fluid overload, the usual sodium deficits generated during exercise can cause this condition. These findings confirm that the potentially fatal condition of symptomatic hyponatremia would be eliminated from sport immediately if all athletes were advised of the dangers of ingesting as much fluid as possible during any exercise that lasts more than 4 hours.
The purpose of this study was to investigate the effects of beverage ingestion on fluid balance during 1.5 hr of low intensity cross country skiing. In Part I, 6 skiers drank water ad libitum during ski training. In Part II, 10 skiers were matched by body weight (BW) and assigned to ingest 2.5 ml.kg-1 BW of water or a carbohydrate/electrolyte (CE) beverage every 2.5 km. Skiing speed averaged 11.5 km.hr-1 for 90 min around a 5 km groomed track. Following 20 min of seated rest, blood samples were collected immediately before and approximately 30 min after skiing. Part I data indicated that subjects ingested 576 +/- 189 ml of fluid and produced 266 +/- 205 ml of urine; BW, plasma and urine osmolality, and plasma protein decreased significantly. In Part II, the CE group produced less urine (135u75 vs. 450 +/- 262 ml) and had smaller decreases in plasma osmolality (-1.0 +/- 1.0 vs. -7.0 +/- 2.4 mOsm.kg H2O) and protein (-0.11 +/- 08 vs. -0.42 +/- 0.24 gL-1) than the water group. No differences were observed for BW loss, % change in PV, FWC, or change in urine osmolality. It was concluded that ad lib water ingestion was inadequate to minimize fluid balance disruption. Plain water ingestion also led to significant dilution of the plasma and increased urine output. However, the ingestion of CE led to attenuation of fluid balance disruption, presumably due to the maintenance of osmotic balance in the plasma.
The Schlager genetically hypertensive mouse has been shown to be a valuable animal model with which to study human essential hypertension. Previous studies have characterized renal morphology, juxtaglomerular index, hematocrit, prostaglandin levels, brain catecholamines, social behavior, and patterns of inheritance. The present study continues the phenotypic characterization of this animal model. Using desiccation, isotope dilution, and clearance, the total body water, extracellular fluid volume, and glomerular filtration rate (GFR) in hypertensive and normotensive animals during normal postnatal development were measured. Additionally, using an electron microscopic tracer, the relative permeabilities of the glomerular filter in these animals were assessed. The data indicate a volume expansion in the young hypertensive animals along with a reduction in GFR. As the animals mature the volume expansion in the hypertensives subsides and is eventually reversed resulting in a lower than normal fluid volume level. The significance of the reduced GFR in the hypertensives is also diminished with age although not to the same degree as that of the fluid volume. The indication of a reduced glomerular permeability may account for the above in light of Guyton's cascade hypothesis.
An incorrect fluid therapy can lead to serious complications considerably more rapidly in children, especially in newborns and infants, than in adults. The pediatric patient has a limited range of compensation for maintenance of fluid and electrolyte balance. Precise knowledge of the physiological age-dependent fluid balance, i.e. the large extracellular space, the developing renal function, the increased metabolism, the acid-base state, the electrolyte balance with the relatively higher sodium and chloride requirements must be the basis of an adequate fluid therapy. The basic fluid requirement (normal fluid and electrolyte requirement) varies with age and is influenced considerably by environmental conditions, body temperature and metabolism. For substitution of this basic fluid requirement one-third to one-half strength electrolyte solution in 5% dextrose is used, the amount depending on age. The perioperative fluid requirement, however, has to be calculated with due consideration for the characteristic changes in fluid and electrolyte balance during anaesthesia and surgery, the preoperative fasting period, drug effects of anesthetics, hormonal changes and ventilation; it is higher than the basic fluid requirement (infants 6-8 ml.kg-1.h-1, toddlers 4-6 ml.kg.h-1, schoolchildren 2-4 ml.kg-1.h-1). For intraoperative fluid therapy infusions with an increased sodium concentration (70-100 mmol/l) or Ringer's lactate (Na+ = 130 mmol/l) must be used. On no account must electrolyte-free solutions, e.g., 5-10% glucose, be used intraoperatively, as they can lead to water intoxication. The third-space requirements compensate for the additional losses by drainage, third-space deficits by evaporation and gastric and enteral secretions.(ABSTRACT TRUNCATED AT 250 WORDS)
The quantity of given fluids was guided by the Evans rule but with no limitations of infusion above 50 p. cent of burns. Fluid was concentrated human serum albumine made isotonic by infusion through a Y pathway with 5 p. cent glucose, natrium (6 g/l) and carbo-hydrate for caloric needs. Under these conditions, clinical and biological parameters show the keeping of a good hemodynamic and hydroelectrolytic balance, with a level of blood proteins very near of the normal one, and a raise in body weight much lower than usually described in literature. Beyond this, the time needed to lower the body weight to its initial level is short and the quantity of infused liquid is much lower than that requisited by resuscitation utilising only cristalloid fluids for the first 24 hours.
Estimates of energy expenditure using both isotope-labelled (2H2(18)O) water and dietary intake/body composition changes were made during an attempt by two men (MS and RF) to walk to the North Pole. The isotope-labelled water technique gave mean estimates of daily energy expenditure for the 48-day expedition of 28.05 MJ (MS) and 32.38 MJ (RF), which compared with estimates of 25.66 MJ (MS) and 24.86 MJ (RF) from the intake/body composition measurements. Fluid retention and peripheral oedema probably caused a considerable underestimate of the losses in body energy stores when applying the energy balance method, whereas in the isotope method, uncertainty in the measurements of isotopic background led to minimum errors of -4.9% to +4.0% of the means for MS and -12.7% to +8.2% for RF (95% confidence limits).
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This chapter reviews alterations in volume and sodium homeostasis and osmoregulation during human pregnancy. Pregnant women undergo extracellular and plasma volume increases of 50-70%, and these changes accompany marked cumulative sodium retention shared by both mother and fetus. Pregnancy alters several factors with opposing effects on renal salt handling; however, mechanisms by which gestational sodium accumulation and volume expansion are achieved remain obscure. Furthermore, despite substantial increases in absolute blood volume, considerable uncertainty exists as to how this volume is sensed, particularly in late pregnancy when a rapid increase in volume is associated with decreases in peripheral resistance and blood pressure. Attempts to assess 'effective' intravascular volume suggest that pregnant women sense their volume as normal. Osmoregulation is also changed. Body tonicity and the osmotic thresholds for AVP release and thirst decrease by about 10 mosm/kg. The mechanisms responsible for the osmoregulatory changes are obscure. Haemodynamic stimuli such as decrements in blood pressure and of 'effective circulating volume' do not seem to account for them. Of the many increments in hormone levels known to accompany gestation, only hCG has so far been implicated in these changes. Pregnant women experience three- to fourfold increments in AVP disposal rates between early and mid pregnancy; this may be caused by the striking rise in circulating cystine-aminopeptidase (vasopressinase) which also occurs during this period. The increments in MCR may be one reason why the hormonal response to a given osmotic stimulus appears to decrease in late pregnancy. All these alterations permit speculation on the manner in which the decrease in Posm occurs and is maintained within narrow limits. Lowering the osmotic threshold to drink stimulates a rise in water intake and dilution of body fluids. Since AVP release is not suppressed at the usual level of hypotonicity, AVP continues to circulate at levels sufficient to permit water retention. Posm continues to decline until it decreases below the new osmotic thirst threshold, when a new steady state is established. At this point water turnover, too, resembles that in the non-pregnant state. The change in MCR and the marked increment in plasma vasopressinase may explain certain observations regarding disordered water metabolism during late pregnancy. These are the transient DI syndromes due either to subclinical hypothalamic disease or to a disorder peculiar to pregnancy which is AVP-resistant but dDAVP-responsive; the latter analogue resists degradation by vasopressinase.
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1. The role of the area postrema (AP) in the long-term control of body fluid homeostasis and arterial pressure under conditions of increased dietary salt intake is reviewed. A model is proposed in which sympathetic nerve activity is suppressed when dietary salt is increased. It is hypothesized that the AP acts as an essential integrative site in the hind-brain for this response. 2. An essential component of the hypothesis is that basal levels of circulating angiotensin II support arterial pressure in animals consuming a normal salt diet by acting on the AP to drive sympathetic nerve activity. This hypothesis is supported by the observation that the long-term hypotensive response to losartan, the AT1 receptor antagonist, is attenuated in AP-lesioned (APx) rats. 3. The role of hepatoportal sodium receptors in signalling the AP about changes in dietary salt intake is discussed. Intragastric hypertonic saline infusion increases portal venous, but not systemic plasma, osmolality and increases Fos-like immunoreactivity in the AP, nucleus tractus solitarius and the supraoptic, paraventricular and lateral parabrachial nuclei. Other studies have shown that stimulation of these receptors decreases renal sympathetic nerve activity. 4. The hypothesis that the AP is critical in long-term control of arterial pressure and body fluid homeostasis under conditions of altered dietary salt intake was studied. The responses of arterial pressure and sodium and water balance to changes in dietary salt intake were measured in intact and APx rats. Contrary to the hypothesis, APx rats did not exhibit impaired regulation of arterial pressure or water balance. However, APx rats did demonstrate an impaired ability to excrete sodium when salt intake was elevated. 5. Based on these observations, it is concluded that the AP is important in the control of sodium balance, but not arterial pressure, when dietary salt intake is altered.
Out of 332 patients with a confirmed diagnosis of RDS, 214 were mechanically ventilated more than 48 hours and 118 less than 48 hours. The incidence of a hemodynamically active persistent ductus arteriosus (PDA) revealed a significant difference for both groups. (54% versus 4,2%). The distribution of PDA did not seem to correlate with birthweight but rather with the severity of RDS, defined by the duration of artificial ventilation. Between three selected groups of 214 patients with longterm ventilation (1. RDS-PDA with surgical ligation - 2. RDS-PDA with spontaneous closure - 3. RDS without PDA) we found significant differences only in the values of inspiratory pressures on mechanical ventilation. No significant differences were found in the time of exposure to high levels of oxygen, the fluid balance, and the application of furosemide.