The participation of cells in disturbances of acid-base balance.
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Twenty healthy pigs weighing 12-17 kg were anesthetized and the small intestines were exteriorized into saline-moistened gauze. During a 2-h period 4% of the animals' body weight was bled through an arterial cannula in six increments and replaced immediately by the fluid tested: hydroxyethyl starch 120 (HES, Plasmafusin, Orion Corp., Mw 120,000), dextran 70 (DEX) and Ringer's acetate (RA). The amount of fluid infused for replacement of blood loss was equal to the amount of blood withdrawn in the colloid groups but fourfold in the RA group. Five non-bled pigs served as controls. After the hemodilution the laparotomy was closed and the animals received only 5% dextrose (2 ml/kg/min) during a 5-h follow-up period. The synthetic colloids caused a more effective dilution of hemoglobin and albumin than did RA. The colloid osmotic pressure (COP) was well maintained by the plasma substitutes but decreased in the RA group to 64% of the initial values. A stable urinary output and no edema formation was found in the HES and DEX groups. The RA animals were unable to excrete the excess crystalloid, which resulted in a strikingly positive fluid balance persisting throughout the study. Thus, the synthetic colloids were superior to RA in expansion of the plasma volume, maintenance of the COP and prevention of fluid accumulation. The effect of the two colloids was similar except that COP was slightly better maintained during the follow-up period in animals which received HES 120.
Rats with bladder and venous cannulas were deprived of water from midnight (00:00) to 10:00. Water deprivation reduced food intake within 2 h, reducing the amount of water sequestered in the gut and the solute load to the tissues. There was little change in either urinary water loss or osmolality, but water-deprived rats excreted more Na+, K+, and Cl- than food-matched controls. The change in solute balance helped preserve osmolality and cell volume at the expense of extracellular fluid volume. When water was returned, rats quickly drank enough to restore the intracellular but not the extracellular fluid deficit. Plasma osmolality and sodium concentration fell below predeprivation values. Urine osmolality and excretion of Na+, K+, and Cl- fell rapidly after drinking. Drinking continued at a slower rate for at least 4 h, but urine flow also increased so water balance stabilized. The changes in intake and electrolyte excretion during water deprivation and rehydration illustrate the important role of changes in solute balance in fluid homeostasis.
If fetal drinking activity is prevented and it is assumed that in the latter third of gestation the fetus is capable of maintaining itself in fluid balance, then the net amount of fluid gained across the placenta by the fetus is equal to the amount of fluid lost from the fetus, by routes other than the placenta, plus fluid deposited in growing tissues minus the amount of water produced as a result of oxidative metabolism. Net transplacental transfer of fluid to the fetus over a 3 h period was measured in eight chronically catheterized fetal sheep in which drinking activity was prevented by ligating the oesophagus. Urine and lung liquid flow rates were measured. In the latter third of gestation, these are the only significant sources of fluid loss from these fetuses during the 3 h experimental period. Water produced as a result of oxidative metabolism was calculated, as was the amount of fluid deposited in growing tissues during the course of the experiment. The weight of the fetus at the beginning of the experiment and the change in weight that occurred during the experiment was calculated by measuring the weight of the fetus at death (within 30 h) and applying an equation which describes the body weight-gestation age relationship for merino sheep. Net transplacental fluid transfer was 0.40 +/- 0.09 ml min-1 kg-1 (range 0.30-0.54 ml min-1 kg-1). Fetal urine flow rate averaged 0.30 +/- 0.11 ml min-1 kg-1. It was 72.8 +/- 10.0% of the volumes used to calculate net transplacental fluid transfer to the fetus. Lung liquid flow rate was 0.079 +/- 0.039 ml min-1 kg-1. It was 20.2 +/- 9.2% of the volumes used to calculate net fluid intake. The amount of fluid deposited as a result of tissue growth was 0.023 +/- 0.001 ml min-1 kg-1; it was 5.94 +/- 1.1% of the volumes used in the equation, while the production of water as a result of metabolism was 3.9 X 10(-3) ml min-1 kg-1 (Conrad & Faber, 1977) and constituted 1.01 +/- 0.22% of the volumes used in the equation. This method of measuring net transplacental fluid transfer to the fetus can be used to measure fetal fluid intake over relatively short periods of time. It also means that the effects of disturbances in maternal fluid and electrolyte balance on fluid transfer to the fetus can be studied and quantitated.
The liquid ethanol diet is a widely used method of ethanol administration. The purpose of this study was to evaluate fluid balance using a multitude of physiological parameters (electrolytes, osmolality, total serum proteins, fluid intake/output and body weight), during and after the introduction of liquid ethanol diet. Animals were randomized into four different dietary protocols (two control and two ethanol groups) and were placed in metabolic cages for 16 days. Serum electrolytes, as well as the above parameters, were measured before, during and 1 week after the introduction of 9% (v/v) ethanol-containing diet (Lieber-DeCarli: LD). After the first night on 9% (v/v) ethanol LD, animals had significantly decreased diet consumption, urine output and body weight. However, a major finding of this study was that, during the habituation phase, the electrolyte values remained within the normal range for rats and, in particular, serum sodium was not altered at any time point measured in this study. Based upon the findings from this study, it is recommended that body weight be carefully monitored as a measure of the animal's equilibration and physiological adaptation during the initiation of a liquid ethanol diet, since neither the serum sodium nor calculated osmolality values were changed. Our results also highlight the need to offer water to animals during the habituation phase of ethanol consumption. This is because ethanol rats that were offered water ad libitum lost less weight than groups that did not receive water ad libitum, despite consuming the same amount of LD diet.
A patient who developed hyperosmolar, hyperglycemic, nonketotic coma (HHNC) while receiving home total parenteral nutrient (TPN) therapy is described, and the etiology, clinical features, and treatment of HHNC are reviewed. A 51-year-old black man diagnosed as having Dukes' stage D signet-cell carcinoma of the rectum was discharged on home TPN therapy after a prolonged hospital course and the persistence of a gastrointestinal fistula. Seventeen days after discharge, the patient developed polyuria, became febrile, and lost mental acuity. Upon hospitalization, the patient's physical condition and laboratory values were consistent with the diagnosis of HHNC. The patient was treated with intravenous fluids and small quantities of insulin. The patient's home records indicated that he had lost large volumes of fluid through his fistula, resulting in a net negative fluid balance. The patient's records also indicated that he had had mild glycosuria with a normal urine output at home. This normal urine output despite a body-fluid deficit could be explained by osmotic diuresis related to either glucose or urea. Hypotonic fluid loss resulting from fistula output and osmotic diuresis may have led to this patient's hypertonic state and critical illness. The patient died on hospital day 11 as a result of widely disseminated cancer. HHNC arises most often as a complication of non-insulin-dependent diabetes. It is also a major complication resulting from hypertonicity related to glucose intolerance or other conditions that can occur in patients receiving TPN therapy. The underlying cause of the hyperosmolar state appears to be dehydration.(ABSTRACT TRUNCATED AT 250 WORDS)
Fluctuations in estrogen and progesterone during the menstrual cycle can cause changes in body systems other than the reproductive system. For example, progesterone is involved in the regulation of fluid balance in the renal tubules and innervation of the diaphragm via the phrenic nerve. However, few significant changes in the responses of the cardiovascular and respiratory systems, blood lactate, bodyweight, performance and ratings of perceived exertion are evident across the cycle. Nevertheless, substantial evidence exists to suggest that increased progesterone levels during the luteal phase cause increases in both core and skin temperatures and alter the temperature at which sweating begins during exposure to both ambient and hot environments. As heat illness is characterised by a significant increase in body temperature, it is feasible that an additional increase in core temperature during the luteal phase could place females at an increased risk of developing heat illness during this time. In addition, it is often argued that physiological gender differences such as oxygen consumption, percentage body fat and surface area-to-mass ratio place females at a higher risk of heat illness than males. This review examines various physiological responses to heat exposure during the menstrual cycle at rest and during exercise, and considers whether such changes increase the risk of heat illness in female athletes during a particular phase of the menstrual cycle.
Sodium and water balance was determined in two strains of Wistar rats selectively bred for high (hypernatriophilic, HR) or low salt preference (hyponatriophilic, HO) under basal conditions and during sodium deprivation. Male rats from each stain were selected for an average ingestion of 1.5% NaCl solution of more than (HR) or less than (HO) 4 ml 100 g body weight (-1) day (-1), during a 10-day period. HR rats (N = 17) presented markedly higher sodium intake under basal conditions (2.983 +/- 0.316 mEq 100 g body weight (-1) day (-1)) than HO rats (N = 12; 0.406 +/- 0.076 mEq 100 g body weight (-1) day (-1); Mann-Whitney test, P < 0.01). Water (HR: 8.6 +/- 0.57; HO: 7.7 +/- 0.32 ml 100 g body weight (-1) day (-1)) and sodium balances (HR: 0.936 +/- 0.153; HO: 0.873 +/- 0.078 mEq 100 g body weight (-1) day (-1)) were similar in both strains, despite a higher sodium and total fluid (HR: 16.3 +/- 1.06; HO: 10.8 +/- 0.49 ml 100 g body weight (-1) day (-1); P < 0.01) ingestion in HR rats. During sodium deprivation HR rats (N = 13) exhibited a sodium balance similar to that of HO rats (N = 13) (HR: -0.159 +/- 0.011; HO: -0.129 +/- 0.019 mEq 100 g body weight (-1) day (-1)), and, in addition, an adequate suppression of natriuresis (HR: 0.049 +/- 0.011; HO: 0.026 +/- 0.004 mEq 100 g body weight (-1) day (-1)). These data show that HR rats present hypernatriophilia as a primary trait, since their sodium-conserving mechanisms are intact. Therefore, these rats provide an adequate model to study factors that determine innate sodium preference.
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OBJECTIVES: Perioperative fluid accumulation determination is a challenge for the clinician. Bioelectrical impedance analysis (BIA) is a noninvasive method based on the electrical properties of tissues, which can assess body fluid compartments. The study aimed at assessing their changes in three types of surgery (thoracic, abdominal, and intracranial) requiring various regimens of fluid administration. DESIGN: Prospective descriptive trial. PATIENTS: A total of 26 patients scheduled for elective surgery were separated into three groups according to site of surgery: thoracic (n = 8), abdominal aortic (n = 8), and brain surgery (n = 10). SETTING: University teaching hospital. INTERVENTION: None. MEASUREMENTS: Whole body, segmental (arm, trunk, and legs) BIA at multiple frequency (0.5, 50, 100 kHz) was used to assess perioperative fluid accumulation after surgery. The fluid balances were calculated from the charts. RESULTS: The patients were aged 62+/-4 yrs. Fluid balances were 4.8+/-1.0 L, 4.1+/-0.5 L, and 1.9+/-0.3 L, respectively, in the three groups. In trunk surgery patients, fluid accumulation was detected as a drop in impedance in the operated area at all frequencies. In the operated area, there was an expansion of both intra- and extracellular compartments. A reduction in high frequencies' impedance in the legs was only detected after aortic surgery. Fluid accumulation and trunk impedance changes were strongly correlated. Neurosurgery only induced minor body fluid changes. CONCLUSIONS: Segmental BIA is able to detect and localize perioperative fluid accumulation. It may become a bedside tool to quantify and to localize fluid accumulation.
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1. There were few changes in the water balance of gerbils drinking 0.25 and 0.50 M NaCl solutions for 5 days. 2. Imbibition of 0.75 and 1.0 M saline resulted in some dehydration of the body fluids and considerable depletion of the neural lobe vasopressin store. 3. Although large amounts of NaCl were excreted, the maximum urine osmolality was considerably less than that found following water deprivation. 4. The imbibition of 1.0 M saline caused similar changes in water balance to water deprivation showing that little, if any, water was gained from this solution.
The fluid and electrolyte management of the surgical neonate must take into account the acute transition to extrauterine life superimposed on the gradual changes associated with fetal and neonatal maturation and growth. With this transition, there are acute changes in body water distribution, and a striking increase in evaporative losses from the skin and respiratory tract. These changes, as well as those in renal function and sodium balance in the preterm and full-term infant are discussed.
Despite the physiologic rationale of their use in hypertension, traditional vasodilators such as hydralazine and minoxidil are often relegated to the second and, more often, to the third and fourth steps of step-care programs. Although they are powerful blood pressure-lowering agents, they cause tachycardia, excessive renin stimulation and sodium retention, and cannot be used as the only antihypertensive agent. The characteristics of the antihypertensive action of calcium antagonists make them suitable for monotherapy. Indeed, all calcium antagonists, while effectively lowering blood pressure through vasodilation, either do not affect heart rate (verapamil and its analogs) or cause a moderate and transient heart rate increase (dihydropyridine compounds). Dihydropyridines also possess a natriuretic effect, probably due to inhibition of tubular sodium transport. The natriuretic effect is evident during the first 2 days of administration, but a small negative sodium balance persists for at least 1 week. There is no increase in body weight or fluid volumes with long-term administration of calcium antagonists with a marked acute natriuretic response, such as dihydropyridines, and those antagonists with a very moderate immediate natriuretic response, such as verapamil. All calcium antagonists, therefore, appear capable of preventing the sodium and water retention that vasodilatation would otherwise entail. More liberal step-care guidelines are now possible to find the agent most suitable for the individual patient. In these guidelines, calcium antagonists, as well as angiotensin converting enzyme inhibitors, are considered as possible first-choice agents along with diuretics and beta blockers.
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