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Methylation and demethylation of mercury under controlled redox, pH and salinity conditions.

In estuarine sediments, the microbially mediated processes of methylation, demethylation, and volatilization determine the state and overall toxicity of mercury pollutants. The effects of redox potential (Eh) and salinity on the above microbial processes were investigated in reactors constructed to allow for continuous monitoring and adjustment of the pH (6.8) and Eh of freshly collected estuarine sediments. For measurements of methylation and demethylation activity, sediment slurries adjusted to appropriate salinity were spiked with HgCl2 or CH3HgCl, respectively, and were incubated in the reactors. Methylmercury was measured by gas chromatography. Volatilized elemental mercury (Hg0) was trapped and determined by cold vapor atomic absorption spectrometry. Volatilization of Hg0 and CH3HgCH3 were found to be minimal. Methylation of Hg2+ was favored at Eh-220 mV as compared to +110 mV. At -220 mV, high salinity (2.5%) inhibited methylation, and low salinity (0.4%) favored it. At +110 mV, the salinity effect was less pronounced. Demethylation of CH3HgCl was favored at +110 mV regardless of the salinity level. Low redox potential under low salinity conditions inhibited demethylation, but high salinity reversed this inhibition. These findings are helpful for interpreting and predicting the behavior of mercury pollutants in estuarine sediments.

Dealkylation↗

Assessment of salinity-related mortality of freshwater bacteria in the saint lawrence estuary.

The growth response of freshwater bacteria from the St. Lawrence River, exposed to brackish waters (salinity of 0 to 20(permil)) from the upper estuary, was assessed by a methodology requiring the combined use of dilution cultures and diffusion chambers. The longitudinal distribution of bacterial abundance in waters within this salinity range was also examined. Growth of the freshwater bacteria was reduced by 15 and 50% after exposure to salinities of 10 and 20(permil), respectively. At lower salinities, no growth reduction was observed, and at a salinity of 2(permil), growth was even stimulated. Longitudinal distribution data showed that bacterial abundance also peaked at this salinity. In contrast with an earlier hypothesis, this study shows that the decline of bacterial abundance in the low-salinity waters of the estuary is not caused by salinity-related mortality of freshwater bacteria, because the mixing time between fresh and marine (>20(permil)) waters is relatively long (days). However, results suggest that mortality of freshwater bacteria can be an important process in estuaries with shorter mixing times (hours). The combined use of diffusion chambers and dilution cultures proved to be a valuable methodology for assessing growth (or mortality) of bacteria exposed to environmental gradients.

Journal Article↗

Minimizing central bile duct injury during radiofrequency ablation: use of intraductal chilled saline perfusion--initial observations from a study in pigs.

PURPOSE: To determine whether intraductal perfusion with chilled saline reduces thermal injury to bile ducts during radiofrequency (RF) ablation. MATERIALS AND METHODS: In swine, anesthesia was induced and the common bile duct was surgically cannulated with a pediatric feeding tube. RF thermal lesions were created adjacent to bile ducts by using an expandable-hook 2-cm RF electrode and 90-W generator. In three pigs, chilled saline was perfused through the ducts at 1.5 L/h (26 mL/min), and in another pig, room-temperature saline was perfused at the same rate. In three pigs (control group), RF lesions were created without perfusion. After 48 hours, animals were sacrificed. Periductal sections from all animals were reviewed by a liver pathologist. The degree of injury to biliary epithelium and subepithelial glands was assessed on a scale of 0%-100%. Significance of differences between degrees of injury was assessed with the Mann-Whitney test. RESULTS: In the control group, there was a mean of 100% injury to biliary ductal epithelium and 99.3% to subepithelial ductal glands. In the room-temperature saline group, there was a mean of 100% biliary epithelial injury and 84.4% glandular injury. In the chilled saline group, there was a mean of 52.9% ductal epithelial injury and 12.1% subepithelial glandular injury. In comparison with the control group, there was significantly less (P <.05) thermal injury to biliary epithelium in the chilled saline group and to subepithelial glands in both the room-temperature and chilled saline perfusion groups. CONCLUSION: RF-induced bile duct injury may be decreased significantly with an intraductal infusion of chilled saline.

Animals↗

Saline-enhanced radio-frequency tissue ablation in the treatment of liver metastases.

PURPOSE: To assess the effect of intraparenchymal saline injection on the results of radio-frequency (RF) tissue ablation. MATERIALS AND METHODS: Ex vivo and in vivo animal RF ablation was performed with and without intraparenchymal saline injection. Initially, saline was injected as a bolus (1-20 mL) before RF application. For subsequent in vivo studies, saline was injected as a bolus before RF application or continuously (1 mL/min) during RF application. Finally, 14 patients with liver metastases and one patient with primary cholangiocarcinoma were treated with the continuous infusion technique. A single RF electrode (tip exposure, 1-3 cm) was used with various ablation parameters. RESULTS: With pretreatment bolus injection of saline, lesions measured 1.4 cm +/- 0.1, 1.6 cm +/- 0.2, and 1.2 cm +/- 0.1 in ex vivo liver, in vivo animal muscle, and in vivo animal liver, respectively. Without saline enhancement, lesion sizes were 1.0 +/- 0.2, 1.2 +/- 0.2, and 0.8 +/- 0.1 cm, respectively. With continuous saline injection in in vivo pig liver, lesion size was 1.8 - 4.1 cm in diameter. In human tumors, necrosis volume was variable, but complete necrosis was seen in 13 of 25 lesions (diameter, 1.2-3.9 cm). Partial necrosis greater than 50% was seen in 12 lesions (diameter, 1.5-4.5 cm). CONCLUSION: Saline-enhanced RF ablation might permit percutaneous destruction of large liver lesions.

Adult↗

Time course of saline-induced recovery of the gustatory system in sodium-restricted rats.

Placing pregnant rats on a Na(+)-restricted diet (0.03% NaCl) results in greatly reduced chorda tympani nerve responses to Na+ stimuli in the offspring. Normal responses can be permanently restored by providing offspring one-time access to saline. We tested whether saline-induced recovery occurs in taste receptor cells present at the time of saline intake. Chorda tympani responses were recorded 2 h, 6 h, 24 h, 10 days, and 20 days after saline ingestion. Chorda tympani Na+ responses from Na(+)-restricted rats at 2 h, 6 h, 24 h, and 10 days after saline intake were comparable to responses from control Na(+)-restricted rats. Twenty days after saline consumption, responses to Na+ were significantly elevated compared with control Na(+)-restricted rats. The results indicate that extant taste receptor cells are not substantially influenced by the saline ingestion. Instead, the delayed recovery suggests that taste receptor stem cells exclusively are influenced by saline intake.

Animals↗

Effects of saline and albumin on plasma and urinary catecholamines in dogs.

Volume expansion by infusion of saline and 25% albumin has been compared in dogs to differentiate volume- and salt-induced catecholamine changes previously observed in humans. Plasma and urinary norepinephrine (NE) and epinephrine (E) decreased following both saline (urinary) NE+E, from 17.3 +/- 3.4 to 6.8 +/- 1.5 ng/min; P less than 0.005) and albumin (from 29.9 +/- 3.4 to 12.5 +/- 2; P less than 0.001) infusion. Urinary dopamine increased in saline-expanded dogs (from 3.4 +/- 0.6 to 4.4 +/- 0.8 ng/min, P less than 0.05), but did not significantly change in control and albumin-expanded dogs; whereas plasma free dopamine remained uninfluenced by saline or albumin. The mean renal clearance of dopamine more than doubled (from 110 +/- 37 to 272 +/- 96 ml/min; P less than 0.05) in response to saline expansion, but did not significantly change in response to albumin expansion or in control animals. A significant correlation between the increase of urinary dopamine and the tubular rejection fraction of sodium was found in saline-expanded dogs (P less than 0.05), or when all experiments (saline, albumin expansion, and control dogs) were considered together (P less than 0.001). The data indicate that : 1) the increase in urinary dopamine excretion (concomitant with sodium excretion) is related to the saline infusion rather than to the suppression of the sympathetic nervous system induced by plasma volume expansion; 2) this increased urinary dopamine originates probably in the kidney. Dopamine may thus be somehow related to regulation of urinary sodium excretion, either as an endogenous natriuretic factor or a response reflecting natriuresis.

Albumins↗

Comparison of water immersion and saline infusion as a means of inducing volume expansion in man.

Although previous studies have demonstrated that water immersion to the neck (NI) results in both central hypervolemia and a significant natriuresis, it is unclear whether the magnitude of the "volume stimulus" of NI is comparable to that induced by the extracellular fluid volume expansion (ECVE) induced by acute saline administration. The present study was undertaken therefore to compare the natriuresis induced by these two different stimuli. All subjects were studied on four occasions while in balance on a diet containing 150 meq of sodium and 80 meq of potassium daily: seated control; seated immersion; and saline administration in both the seated and recumbent posture. The increment in UNaV during NI was indistinguishable from that of seated saline. Similarly, the kaliuretic response during NI was similar to that induced by seated saline infusion. In contrast, supine saline infusion resulted in a greater increment in UNaV than either NI or seated saline. The present data indicate that the "volume stimulus" of immersion is identical with that of standard saline-induced ECVE in normal seated subjects. Furthermore, the ability of NI to induce a natriuresis without a concomitant increase in total blood volume and with a decrease in body weight, rather than the increase which attends saline infusion, suggests that NI may be a preferred investigative tool for assessing the effects of ECVE in man.

Adolescent↗

Salt level in weaning diet affects saline preference and fluid intake in Dahl rats.

Weanling Dahl salt-sensitive (DS) and salt-resistant (DR) rats were used to compare effects of feeding high or low NaCl diets on taste preference for, and intake of, a wide range of saline concentrations. The DS and DR were fed either 8.0 or 0.4% dietary NaCl for 4 weeks. Then, with all animals fed the 0.4% NaCl diet, their taste preferences for 0.0001 to 0.56 M saline were assessed using three 24-hour two-bottle preference tests of each solution versus distilled deionized water. Saline preference and intake were influenced by concentration and its interaction with genotype, with DS exhibiting higher preferences than DR for hypotonic saline. The DS preexposed to 8.0% dietary NaCl showed elevated consumption levels of water and total fluid (saline + water) that persisted throughout the 5-week test period, despite transfer to the 0.4% NaCl diet before the initiation of preference testing. Findings indicate that genotype, dietary NaCl levels in weaning diet, and saline concentration of preference test solutions interact to influence saline preference and saline and water intake in Dahl rats.

Animals↗

Central and peripheral adrenergic mechanisms in the development of deoxycorticosterone-saline hypertension in rats.

The role of the sympathetic nervous system in the development of deoxycorticosterone-sodium chloride (DOCA-saline) hypertension was investigated by measuring plasma levels of norepinephrine, total catecholamines, and dopamine-beta-hydroxylase activity at intervals after the initiation of the DOCA-saline regimen. Plasma norepinephrine was significantly higher in DOCA-saline-treated rats at 4 and 7 weeks and in rats treated with saline alone at 4 weeks compared with that in untreated controls. Total plasma catecholamine levels (epinephrine and norepinephrine) and dopamine-beta-hydroxylase activity were similar in hypertensive rats, untreated controls, and rats that received either DOCA or saline alone. The increases in plasma norepinephrine levels may have resulted from centrally mediated increases in peripheral sympathetic neuronal activity, since the destruction of central catecholaminergic neurons with intracerebroventricularly administered 6-hydroxydopamine (6-OHDA) prevented both the DOCA-saline-induced rise in blood pressure and the increases in plasma norepinephrine. Rats treated with 6-OHDA consistently drank less water or saline than did vehicle-treated controls. The actions of centrally administered 6-OHDA on blood pressure and plasma norepinephrine levels were not secondary to a reduction in salt intake, however, since intact rats given a similar reduced saline intake became hypertensive and demonstrated elevated plasma norepinephrine concentrations. Chronic salt loading may cause a centrally mediated increase in peripheral sympathetic neuronal activity with raised plasma concentrations of norepinephrine. The increased adrenergic activity in the presence of mineralocorticoid-induced sodium retention leads to the development of hypertension.

Adrenalectomy↗

Mechanisms of changes in nitrogen washout and lung volumes after saline infusion in humans.

This study was performed to determine the roles of increased intrathoracic blood volume and increased vagal tone in the changes in lung volume and nitrogen washout produced by saline infusion. In the first study, measurements of TLC, VC, FRC, ERV, and slope of phase III nitrogen washout (delta N2) were made on 8 subjects before, during, and after inflation of the leg compartments of medical anti-shock trousers (MAST). In the second study, 13 volunteers were infused intravenously with warm saline (30 ml/kg) for 30 min. Repeat measurements were made approximately 20 and 40 min after infusion. Each subject then received intravenously 0.03 mg/kg atropine, and measurements were repeated. In 7 of these subjects, a third study was performed in which the atropine was injected before saline infusion. Inflation of the MAST (see figures 5 and 6) caused a 1.9% decrease in VC, 5.3% decrease in FRC, and no change in delta N2. Saline infusion caused decreases in TLC, VC, and FRC (4.0, 3.1, and 10.1%, respectively) and a 15.0% increase in delta N2. Atropine reversed the change in delta N2 after saline infusion and prevented these changes when given prior to saline. Atropine had no effect on lung volumes whether given before or after saline infusion. We speculate from our data that saline infusion has 2 effects on the lung. One is a simple displacement of air by increased intravascular volume producing the reduction in lung volumes. The second is an increase in small airways resistance that is mediated by vagal reflex and blocked with atropine.

Adult↗

The mechanism of suppression of proximal tubular reabsorption by saline infusions.

The mechanism by which expansion of extracellular fluid volume with isotonic saline suppresses reabsorption in the proximal tubule was studied in rats by examining the relations among glomerular filtration rate (GFR), absolute and fractional reabsorption of filtrate, intrinsic reabsorptive capacity (rate of reabsorption per unit tubular volume), transit time, and tubular volume. Saline infusions reduced the per cent of the glomerular filtrate reabsorbed in the proximal tubule from 50% during antidiuresis to 25% during saline diuresis. The suppression of proximal reabsorption was the result of two factors: 1) a 30% reduction of intrinsic reabsorptive capacity, and 2) a 26% reduction of tubular volume per unit GFR.GFR invariably rose during saline diuresis. However, prevention of the rise in GFR by aortic clamping had no effect on either the inhibition of intrinsic reabsorptive capacity or the reduction in tubular volume per unit GFR produced by saline infusions. Expansion of extracellular fluid volume with isotonic saline, therefore, depressed intrinsic reabsorptive capacity and tubular volume per unit GFR by some mechanism completely independent of GFR. The effects of furosemide administration were contrasted with those of saline infusions. Furosemide inhibited intrinsic reabsorptive capacity by 40% but had no significant effect on proximal fractional reabsorption. The failure to suppress fractional reabsorption was the consequence of a disproportionate rise in tubular volume (relative to GFR) that was sufficient to completely overcome the inhibition of intrinsic reabsorptive capacity. Inhibition of intrinsic reabsorptive capacity alone, therefore, will not result in a net suppression of reabsorption of filtrate in the proximal tubule. We concluded that, although intrinsic reabsorptive capacity was inhibited during saline diuresis, the critical factor responsible for translating this inhibition into effective net suppression of proximal reabsorption was the observed reduction in tubular volume per unit GFR.

Absorption↗

Effect of changes in renal perfusion pressure on the suppression of proximal tubular sodium reabsorption due to saline loading.

Rapid intravenous infusion of saline is known to suppress reabsorption of sodium and water in the proximal tubule. It has previously been shown that this suppression is accompanied by two changes which in combination might account for the over-all decrease in reabsorption: a reduction in the intrinsic reabsorptive capacity of the tubular epithelium (C/pir(2)) and a reduction in the ratio between tubular volume and GFR (pir(2)d/V(o)). The present micropuncture experiments were carried out in order to study the possible role of altered peritubular physical forces (hydrostatic and colloid oncotic pressure) in mediating these two changes. Proximal tubular reabsorptive capacity, transit time, fractional reabsorption of sodium and water, pir(2)d/V(o), and intratubular hydrostatic pressure were measured in saline-loaded rats during acute changes in renal perfusion pressure induced by intermittent constriction of the abdominal aorta. We found that when renal perfusion pressure was lowered to 70-90 mm Hg, the usual effects of saline loading on C/pir(2), pir(2)d/V(o), and fractional reabsorption in the proximal tubule were greatly minimized. When the aortic clamp was released and renal perfusion pressure allowed to rise, C/pir(2), pir(2)d/V(o), and fractional reabsorption fell markedly to levels characteristically seen in saline diuresis. Reclamping of the aorta reversed all of these changes. In order to determine whether the changes in C/pir(2) accompanying changes in renal perfusion pressure were mediated by a circulating natriuretic hormone, we assayed in hydopenic rats the dialysate of plasma collected from saline-loaded rats during and after release of aortic constriction by the split oil drop method. No significant difference in reabsorptive half-time (t(1/2)) was found between the two dialysates, and t(1/2) with both dialysates was approximately the same as was found when isotonic saline was injected in the tubules of hydropenic control animals. These observations suggest that the large changes in C/pir(2) which occurred with changes in renal perfusion pressure in saline-loaded rats were not mediated by a circulating hormone. We suggest that the reduction in C/pir(2), pir(2)d/V(o), and fractional reabsorption which occurs in the proximal tubule during a saline diuresis is related to the rise in hydrostatic pressure within the kidney.

Animals↗

Saline activation of pseudoepileptic seizures: clinical EEG and neuropsychiatric observations.

Twenty patients with suspected pseudoseizures underwent saline infusion during prolonged sleep deprived EEG with video monitoring and nasopharyngeal electrodes. No patients had definite clinical evidence of epilepsy, but 35% had abnormal EEGs, 10% with epileptiform activity. Patients with epileptiform discharges did not experience pseudoseizures with saline infusion. Patients with generalized EEG slowing responded to saline infusion with characteristic seizures. Three groups of patients were differentiated. Eight patients had characteristic attacks with saline infusion, and in these patients females predominated, mean age was lower, and somatoform disorder was common. Six patients each either failed to respond to saline or had episodes different from their characteristic spells. These patients were more often male and more often had diagnoses of personality disorders. The findings suggest that, although saline infusion may identify pseudoseizures and confirm their non-epileptic nature, some patients may not be sufficiently suggestible to respond to saline infusion, while others may have non-epileptic attacks which are different from the spells under evaluation. Psychiatric and neuropsychological features suggestive of pseudoseizures may be more readily identified by psychiatric interview or psychometric testing. Ethical issues regarding saline infusion in the guise of a potent convulsant should also be considered.

Adult↗

Physiology and behaviour of free-swimming Atlantic cod (Gadus morhua) facing fluctuating salinity and oxygenation conditions

1. Atlantic cod (Gadus morhua L.) acclimated to a temperature of 5 &deg;C and 30 salinity were equipped with ultrasonic transmitters which allowed continuous monitoring of their heart rate and their position in the water column. Fish were placed in a 125 m3 tower tank which permitted various environmentally relevant modifications of the salinity and oxygenation conditions. Cod physiological and behavioural responses were followed in parallel to the environmental manipulations. Some of the experimental conditions studied in the tower tank were also reproduced in a swimming respirometer where fish oxygen consumption and heart rate were monitored at various levels of activity. 2. Lowering salinity from 30 to 26 did not change resting oxygen consumption, but increased active oxygen consumption. 3. Lowering salinity from 30 to 26 increased heart rate over the whole range of swimming speeds except at maximum speed. 4. Lowering oxygen tension to 9 kPa decreased oxygen consumption over the whole range of swimming speeds and decreased resting heart rate. 5. Low salinity did not significantly affect the relationship between heart rate and oxygen consumption. 6. Low oxygen levels decreased the oxygen transported per heart beat. 7. In the tower tank, bursts of activity were associated with tachycardias. 8. In uniform conditions, fish swam more deeply during the day than at night. 9. After an exploratory period of approximately 6 h, fish chose to remain in a low-salinity upper layer of the tank. Thereafter, high salinities were avoided. Fish tended to select low salinities if a choice was provided. 10. Fish generally avoided zones of low oxygen (<9 kPa) but continued voluntarily to enter regions with values as low as 3.0 kPa for short excursions or if food was offered.

Journal Article↗

Changes in plasma atrial natriuretic polypeptide concentration during head-out water immersion and saline infusion in normal men.

The physiological mechanism regulating secretion of human atrial natriuretic polypeptide (hANP) was examined by measuring plasma hANP by a specific radioimmunoassay during head-out total body water immersion (WI) and saline infusion in normal men. Seven healthy men were immersed in water for 1 hour, 6 normal men and women were given an infusion of 1 liter of normal saline over 1 hour and 8 normal men were given a similar infusion over 2 hours. During WI, the urinary volume (UV) and urinary Na excretion (UNaV) increased significantly, and the plasma hANP level increased significantly from 246 +/- 12 (mean +/- SE) pg/ml to 392 +/- 32 pg/ml after 35 +/- 5 min, but returned to the basal level after 90 min. The increase in hANP level was correlated with an increased UNaV between 30 to 60 min during WI. The plasma norepinephrine, renin activity, aldosterone and cortisol levels also decreased during WI. Saline infusion caused variable increases in the hANP level: the mean peak values of hANP and times of the peaks from the start of saline infusion were respectively 305 +/- 30 pg/ml after 30 +/- 3 min of infusion at a rate of 1L/1 hr and 285 +/- 25 pg/ml after 69 +/- 15 min of infusion at a rate of 1L/2 hrs. The time of the peak of plasma hANP during infusion at 1L/2 hrs was significantly longer than the peaks for WI or an infusion of saline at 1L/1 hr. Moreover, the peak hANP level was significantly smaller during either condition of saline infusion than during water immersion. These results indicate that i) acute central hypervolemia caused by WI increases hANP secretion, and this increase may participate in natriuresis during WI, and ii) saline infusion causes an increase in plasma hANP of variable magnitude, the increase being more rapid for a more rapid infusion of saline. This suggests that hANP is released into the circulation by acute volume expansion and plays a physiologically important role in maintaining blood volume homeostasis in man.

Adult↗

Effect of intravenous saline, albumin, or hydroxyethylstarch on blood volume during combined ultrafiltration and hemodialysis.

It is generally advocated to use saline or albumin infusions during symptomatic hypotension during dialysis. However, because of their side effects and/or costs, they are of limited use. Hydroxyethylstarch (HES), a synthetic colloid with a long-standing volume effect, is used in the management of hypovolemia. In this study, the efficacy of three fluids (isotonic saline [0.9%], albumin [20%], and HES [10%]) was assessed during three treatment sessions with combined ultrafiltration and hemodialysis, which differed in the type of fluid given intravenously. Changes in relative blood volume (BV), systolic BP (SBP), and vascular reactivity (venous tone [VT]) were compared. An intravenous infusion of 100 ml of fluid was given when the decrease in BV versus baseline was more than 10% as measured by a continuous optical reflection method. The ultrafiltration was continued. BV decreased significantly versus baseline independent of the intravenous fluid administration in all three treatment sessions. However, when we compared BV values at the end of the dialysis session with those at the time of infusion, BV continued to decrease significantly with saline (change in BV -4.56 +/- 2.75%; P < 0.05) and albumin (change in BV -2.13 +/- 2.51%; P < 0.05), but not with HES (change in BV -0.15 +/- 2.17%; NS). Between albumin and HES there were no significant differences in changes in BV (NS), whereas between HES and saline (P < 0.05) and between albumin and saline (P < 0.05) the differences in BV changes were significant. SBP remained unchanged within each session. Although SBP tended to decrease more with saline compared to albumin and HES, the difference was not significant. The higher decrease in BV and SBP with saline was counterbalanced by a significantly higher increase in VT, while VT remained unchanged in the other two sessions. It is concluded that HES is a promising fluid in preserving blood volume, comparable to albumin, but superior to saline.

Adult↗

Physiological saline is not a biocompatible peritoneal dialysis solution.

UNLABELLED: We have previously demonstrated that daily exposure to dialysis fluid results in significantly increased peritoneal lymphatic flow. In this study, we investigated if daily intraperitoneal infusion of saline (isotonic, glucose free) could cause similar changes. METHODS: Sixteen male SD rats received daily infusion (i.p.) of 20 ml saline for ten days (Saline group). Twenty-four hours after the last infusion, a 4 hour dwell study using 25 ml 3.86% glucose dialysis solution with frequent dialysate and blood sampling was done in each rat as well as in rats which did not receive daily infusion (Control, n=8). Radiolabeled human albumin (RISA) was added to the solution as an intraperitoneal volume marker. Radioactivity, glucose, urea, sodium, and potassium were measured for each sample. In a separate study, the RISA absorption to peritoneal tissue was also determined. RESULTS: The net ultrafiltration was significantly decreased in the daily infusion group (p<0.05). However, the apparent volume at 3 minutes of the dwell was markedly increased; this was due to a significant increase in the RISA binding (1.5-12.0% in the Saline group vs. 0.45-1.12% in the Control group) to peritoneal tissues as assessed by measurement of RISA recovery at 3 min of the dwell. This resulted in a significant overestimation both of the intraperitoneal volume (IPV) at 3 min and the (apparent) fluid absorption rate (as estimated by the transport of RISA out of peritoneal cavity): 0.087+/-0.026 ml/min in the Saline group vs. 0.052+/-0.007 ml/min in the Control group, p<0.001. The direct lymphatic flow as estimated by the clearance of RISA to plasma (which should not be affected by the RISA binding) also increased markedly (0.021+/-0.005 ml/min in the Saline group vs. 0.008+/-0.001 ml/min in the control group). There was no significant difference in the D/P values for small solutes (urea, sodium, potassium, urate) and D/D0 for glucose between the two groups. CONCLUSIONS: 1) Daily infusion of physiological saline into peritoneal cavity may increase the peritoneal lymphatic flow; 2) The significant (apparent) increase in IPV shortly after infusion may suggest increased RISA binding to peritoneal tissues (which may be related to the damage of the tissues, and results in overestimation of the peritoneal fluid absorption rate); 3) Saline is not a biocompatible peritoneal dialysis solution, and should therefore not be used as a control or flush solution.

Absorption↗

Instillation of normal saline during endotracheal suctioning: effects on mixed venous oxygen saturation.

BACKGROUND: Instillation of normal saline before endotracheal suctioning is thought to facilitate removal of secretions and ultimately to improve the patient's oxygenation status. To date, no studies have used an in vivo measure of oxygenation such as mixed venous oxygen saturation to characterize the effects of instillation of normal saline. OBJECTIVES: To describe the effects of instillation of normal saline into an endotracheal tube before suctioning on mixed venous oxygen saturation in critically ill adult patients. METHODS: In a descriptive, observational study, 35 patients were assigned to either of 2 groups after coronary artery bypass grafting. One group had 5 mL of normal saline instilled at the start of endotracheal tube suctioning; the other group had the same endotracheal tube suctioning procedure without the use of saline. Data on mixed venous oxygen saturation were recorded at 1-minute intervals for a 5-minute baseline period and then throughout the suctioning procedure until mixed venous oxygen saturation returned to baseline levels. RESULTS: The time required for mixed venous oxygen saturation to return to baseline values after suctioning was an average of 3.78 minutes longer when saline was used. CONCLUSIONS: Instillation of normal saline before endotracheal suctioning has an adverse effect on oxygenation as indicated by mixed venous oxygen saturation. This finding contradicts the assumption that instillation of normal saline improves oxygenation status.

Adult↗