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At least 307 records · Page 17Linked to original sources
PubMed1988

Effects of crystalloid on lung fluid balance after smoke inhalation.

Inhalation injury occurs in 21% of flame burn victims who require large fluid volumes for resuscitation and have a mortality rate greater than 30%. This study was done to determine how vulnerable the smoke-injured lung is to fluid accumulation when crystalloids are infused rapidly. Mongrel dogs were exposed to smoke and 10% body-weight Ringer's lactate in three groups: (I) fluid only, (II) smoke only, and (III) smoke and fluid. The increase in wet-dry lung weight ratio was 2% in Group I, 28% in Group II, and 42% in Group III, consistent with pulmonary edema present only in Group III. The decrease in colloid oncotic pressure was similar in both of the groups that were given fluid, and the rise in the surface tension minimum of lung extracts was similar in both of the groups that were exposed to smoke. The smoke-injured lung loses the ability to protect itself when challenged with fluid. Reduced oncotic pressure is not responsible. Changes in microvascular pressure, endothelial and epithelial damage, and surfactant inactivation interact to cause this increase in extravascular lung water.

Animals↗
PubMed1950

Some experiences and problems in treating renal insufficiency: I. Extracorporeal dialysis of the blood in vivo in cases of uremia; 22 treatments on 18 cases. II. Fluid balance problems in cases of acute oliguria; anuria due to acute nephritis, incompatible blood transfusions lower-nephron nephrosis and so on i. a. illustrating the risks of excessive electrolyte-fluid supply and the i. a. illustrating the risks of the modern electrolyte; fluid therapy and the importance of continual weight control.

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Anuria↗
PubMed2002

Effects of dehydration on endocrine regulation of the electrolyte and fluid balance and atrial natriuretic peptide-binding sites in perinatally malnourished adult male rats.

OBJECTIVE: The first aim of this work was to investigate, under basal conditions in adult male rats, the long-term consequences of perinatal maternal food restriction on the plasma concentrations of vasopressin (VP), aldosterone and atrial natriuretic peptide (ANP) and on plasma renin activity (PRA). Furthermore, under these same conditions, the hypothalamic VP gene expression as well as the density (B(max)), affinity (K(d)) and gene expression of ANP receptors were determined in kidneys and adrenals. The second aim of this work was to examine the responsiveness to dehydration in perinatally malnourished rats. Thus, the latter parameters were studied in these rats after 72 h water deprivation. METHODS: This study was conducted on 4-Month-old male rats from mothers exposed to 50% food restriction (FR50) during the last week of gestation and lactation and on age-matched control animals (C). At this stage, both C and FR50 rats were killed by decapitation between 0900 h and 1000 h in order to determine parameters under basal conditions or after 72 h water deprivation. Plasma VP, ANP and aldosterone levels and PRA were determined by radioimmunoassay. Hypothalamic VP gene expression was determined in the paraventricular nucleus (PVN) and supraoptic nucleus (SON) by in situ hybridization. The B(max) and K(d) values of ANP receptors were evaluated from Scatchard plots. ANP receptor gene expression was determined by Northern blot analysis. RESULTS: Under basal conditions, perinatal malnutrition reduced body weight, absolute weight of kidneys and adrenals, and haematocrit. Compared with control rats, FR50 rats had significantly greater plasma VP and aldosterone levels but PRA, plasma ANP levels, plasma osmolality and hypothalamic VP gene expression were not significantly different. Perinatal malnutrition did not significantly affect glomerular ANP receptor density, but in adrenals it decreased both B(max) and K(d) values of ANP-B receptors (biological receptors) and increased B(max) of ANP-C receptors (clearance receptors). ANP-B(A) (receptor subtype A of ANP-B receptors) receptor gene expression was not significantly affected, whereas ANP-C receptor gene expression was enhanced in both adrenals and kidneys in FR50 rats. After 72 h dehydration, control rats showed a significant rise in haematocrit, plasma osmolality, PRA, circulating levels of VP and aldosterone and VP gene expression in both PVN and SON but showed a decrease in plasma ANP levels. B(max) of ANP-B receptors was decreased whereas B(max) of ANP-C receptors was enhanced in both adrenals and kidneys. ANP-B(A) receptor gene expression was not significantly affected in either kidneys or adrenals in dehydrated control rats. Similarly, ANP-C receptor gene expression was unaffected in kidneys whereas it was significantly enhanced in adrenals. In FR50 rats, the effects of water deprivation were qualitatively similar to those reported in controls concerning plasma parameters except for plasma VP levels which tended to rise (not significant) but this increase was only very slight compared with controls. Moreover, unlike controls, VP gene expression in both PVN and SON was not enhanced after dehydration in FR50 rats. In kidneys, dehydrated FR50 rats, like controls, upregulated ANP-C receptors, but they were unable to downregulate ANP-B receptors. In adrenals, unlike controls, FR50 rats enhanced ANP-B receptor density whereas they decreased both ANP-C receptor density and expression after 72 h dehydration. Similar to controls, the expression of ANP-B(A) receptors in both kidneys and adrenals as well as the expression of ANP-C receptors in kidneys, were unaffected in dehydrated FR50 rats. CONCLUSION: Perinatal malnutrition had long-lasting effects on regulation of the fluid and electrolyte balance under basal conditions. The main effects were a significant rise in circulating levels of VP and aldosterone, and changes in density of adrenal ANP-binding sites and ANP-C receptor gene expression in both adrenals and kidneys. Perinatal malnutrition also affects the responsiveness to water deprivation with alterations in both hypothalamic VP gene expression and regulation of ANP-binding sites.

Adrenal Glands↗
PubMed1981

Prolactin, fluid balance and lactation.

The hypothesis that prolactin may play a part in osmoregulation was investigated by given a hypotonic fluid load to two groups of normal lactating women. No changes in serum prolactin, milk yield, serum or breast milk osmolality were noted, suggesting that encouraging women to drink excessively has no effect upon lactation, either in terms of yield or composition of milk.

Female↗
PubMed1994

Effects of alteration in fluid balance on angiotensinogen gene expression in the rat.

The renin-angiotensin system (RAS) functions in circulatory and fluid homeostasis. There is evidence that genes encoding the protein elements of this system (renin and angiotensinogen) are expressed in a variety of tissues and that interaction of the products of these genes within tissues may represent part of the physiological function of this system. Using a solution hybridization assay for rat angiotensinogen (Ao) gene which incorporates a quantitative sense RNA standard we have measured angiotensinogen gene expression (AGE) in rat liver, brain (basal forebrain and brain stem), kidney and heart (atrium and ventricle) from individual animals. The effect of a 48hr period of dehydration on gene expression was compared with age and sex-matched animals which had water available ad libitum. Dehydration lead to a significant increase in plasma osmolality (pOsm) and plasma angiotensin II immunoreactivity (pAII). AGE was unaffected by dehydration in liver, brain stem, kidney, atrium and ventricle. However, significant increases AGE were observed in basal forebrain. In individual animals there was a significant positive correlation between pOsm and basal forebrain gene expression regardless of hydration state. This selective activation of the Ao gene in the forebrain during dehydration supports other observations which suggest that an intra-cranial RAS may participate in hypothalamic mechanisms of fluid homeostasis.

Angiotensin II↗
PubMed1983

Thromboxane generation after thrombin. Protective effect of thromboxane synthetase inhibition on lung fluid balance.

We examined the role of thromboxane in mediating the alterations in pulmonary hemodynamics and in lung fluid and protein exchange after thrombin. Studies were made in control sheep and in sheep pretreated with the thromboxane synthetase inhibitor, Dazoxiben (injection of 10 mg/kg followed by infusion of 4 mg/kg per hr). Thrombin infusion caused an increase in mixed venous and aortic concentrations of thromboxane B2, a stable degradation product of thromboxane A2, whereas the concentrations of 6-keto-PGF1 alpha, a degradation product of prostacyclin, did not change significantly. In sheep pretreated with Dazoxiben, thromboxane B2 concentrations did not increase, indicating effectiveness of the thromboxane synthetase inhibitor. The blood concentrations of 6-keto-PGF1 alpha after thrombin increased in the thromboxane synthetase-inhibited group, indicating shunting towards prostacyclin synthesis. Thrombin in untreated sheep increased pulmonary lymph flow (Qlym) and the lymph protein clearance (Qlym X lymph-to-plasma protein concentration ratio). The increases in lymph parameters were due to an increase in pulmonary vascular permeability to proteins because raising left atrial pressure further increased Qlym but did not change lymph-to-plasma ratio. Dazoxiben prevented the thrombin-induced increase in pulmonary vascular permeability because the increase in left atrial pressure resulted in an increase in Qlym and a decrease in lymph-to-plasma ratio, as was the case after left atrial hypertension in normal animals. Therefore, thrombin results in selective release of thromboxane A2 which precedes the increase in pulmonary vascular permeability. Thromboxane A2 may contribute to the increased permeability after thrombin, since inhibition of thromboxane synthesis prevents the permeability change.

Animals↗
PubMed1992

Fluid balance in elderly patients following acute stroke.

We studied the relationship between plasma osmolality, arginine vasopressin (AVP), and fluid input in patients during the acute phase of a first stroke. Fifteen consecutive patients were studied (median age 79) and their blood sampled on days 0, 1, 2, 3, 7 and 14. Plasma osmolality was related to fluid input over days 0-3 (p = 0.0013) and AVP over 14 days (p less than 0.001). Patients with a poor outcome had higher AVP concentrations (p = 0.02). Those on intravenous fluids received a higher volume (p less than 0.01) and had a lower plasma osmolality (p = 0.04). The results of this preliminary study indicate that a standard regime for fluid input is inappropriate.

Aged↗
PubMed1983

Effects of cyclooxygenase and lipoxygenase inhibition on lung fluid balance after thrombin.

We examined the roles of the cyclooxygenase and lipoxygenase pathways in the alterations in lung fluid and protein exchange after pulmonary microembolism. Infusion of alpha-thrombin (T) (55 +/- 13 U/kg) immediately increased mean pulmonary arterial pressure (Ppa) and mean pulmonary vascular resistance (PVR), but both Ppa and PVR waned with time after T. Cyclooxygenase inhibition with either indomethacin or ketoprofen produced sustained increases in Ppa and PVR. The initial increases in Ppa in the cyclooxygenase-inhibited groups (CI) were matched to the control group by administering greater amounts of T. In the control group, T rapidly increased pulmonary lymph flow (Qlym) by two- to threefold, and this was associated with a steady increase in lymph-to-plasma protein concentration ratio (L/P). In contrast, in cyclooxygenase-inhibited (CI) groups, Qlym increased gradually to greater levels than in the control group, and L/P did not change. The effect on lung vascular permeability was determined by inflating a left atrial balloon catheter to raise pulmonary capillary pressure (Pc). An increase in Pc after T in the control group further increased Qlym and did not change L/P, whereas the increase in Pc after T in CI groups further increased Qlym and decreased L/P, indicating that cyclooxygenase inhibition prevented the increase in permeability. We determined whether lipoxygenase activation contributed to the increase in Qlym in CI groups by examining the effects of BW755C, an inhibitor of both cyclooxygenase and lipoxygenase pathways. BW755C resulted in the same increase in Qlym after T as in the control group, but the increase in Qlym was associated with a decrease in L/P. Therefore, inhibition of both pathways prevented the permeability increase and the greater increase in Qlym. The results indicate that cyclooxygenase and lipoxygenase pathways contribute to the increases in pulmonary transvascular fluid and protein fluxes after thrombin.

4,5-Dihydro-1-(3-(trifluoromethyl)phenyl)-1H-pyraz↗
PubMed1995

The influence of vascular pressure and different primes on the fluid balance of, and oxygen supply to, the patient during CABG.

Detrimental changes of blood and erythrocyte rheology, and fluid exchange between the vascular and interstitial spaces, which influence the rate that oxygen is supplied to the patient, occur during cardiac bypass surgery. Venous flow is subject to a pulsatile and uncertain variation, because the vena cava is more than 30 mmHg below atmospheric pressure. This occurs because the patient is about 1 m above the air-blood surface of the bypass reservoir. Before any reliable study of fluid exchange can be undertaken this effect must be controlled. It was then established that optimum oxygen exchange occurs when equilibration of the plasma oncotic pressure and the capillary hydrostatic pressure is achieved without alteration of the interstitial fluid volume. At the lower arterial blood pressures used during bypass, it is necessary to reduce the plasma oncotic pressure by using an appropriate volume of crystalloid prime.

Coronary Artery Bypass↗
PubMed2000

Randomized trial of two levels of fluid input in the perinatal period--effect on fluid balance, electrolyte and metabolic disturbances in ventilated VLBW infants.

The aim of this study was to determine whether fluid restriction does indeed significantly increase acute adverse effects. One-hundred-and-sixty-eight ventilated infants, median gestational age 27 wk (range 23-33) and birthweight 953 g (range 486-1500), entered into a randomized controlled trial of two fluid regimes. Infants on regime A were to be prescribed 60 ml/kg of fluids on day 1 which was gradually increased over the first week to 150 ml/kg, infants on fluid regime B were to be prescribed approximately 20% less fluid over the first week. Daily fluid input and output were recorded. Serum electrolytes, bilirubin, creatinine and urine osmolalities were measured daily. Arginine vasopressin levels were assessed on days 1, 3 and 5. Episodes of jaundice, hypoglycaemia and hypotension requiring treatment were noted. Infants on regime B actually received overall 11% and, in the first 4 days, 19% less fluid than those on regime A (p < 0.001). There were no statistically significant differences in the occurrence of episodes of jaundice, hypotension, hypoglycaemia, hypernatraemia or hyponatraemia between infants on the two regimes. Although the infants on regime B had significantly higher urine osmolalities and lower urine output for most of the perinatal period, their median creatinine and arginine vasopressin levels did not differ significantly from those on regime A. We conclude that fluid restriction to less than 90% of usual maintenance fluids is not associated with an excess of acute adverse effects.

Dehydration↗