Plasma-like Electrolyte Solution Research Articles

Fluid administration: Which direction?

Introduction: Although fluid administration for intravenous hydration is a common practice in pediatric age, it is not devoid of risks. Methods: This was a retrospective cohort study including all children admitted to surgical recovery and receiving intravenous hydration at a Pediatric Intensive Care Unit between January and December 2015. Sodium, chloride, and base excess values were registered on two occasions: after surgery and during Unit’s hospitalization. Results: Two hundred and seven children were included in the study, 66% of which, male, with a median age of 6.7 years. Fluids used consisted of 0.9% saline solution, 0.45% saline solution, and polyelectrolyte solution. The most frequently used fluids were polyelectrolyte (62%) and 0.9% saline solution (48%) at the operating room, and 0.9% saline (63%) and 0.45% saline (44%) solutions at the Pediatric Intensive Care Unit. At the operating room, 0.9% saline solution led to higher chloride median values and more negative base excess (metabolic acidosis) values compared with polyelectrolyte solution. At the Pediatric Intensive Care Unit, 0.9% saline solution administration resulted in hyperchloremia (p=0.002) and more metabolic acidosis (p=0.019) compared with 0.45% saline solution. There was no statistically significant association between type of solution used and sodium values. Discussion: This study shows that the use of 0.9% saline solution is associated with development of hyperchloremic acidosis. This suggests that replacement of 0.9% saline solution with a plasma-like electrolyte solution may improve patient outcomes.

Intraluminal capsaicin does not affect fluid and electrolyte absorption in the human jejunum but does cause pain

Background—Stimulation of sensory nerves with capsaicin regulates ion transport in the small intestine in animal experiments.Aim—To investigate whether sensory nerves that are stimulated by capsaicin administration influence fluid and electrolyte...

Effects of serotonin on rat ileocolonic transit and fluid transfer in vivo: possible mechanisms of action.

The aim was to investigate the action of serotonin (5HT) on function of the ileocolonic junction (ICJ) in vivo. In anaesthetised rats, models were developed to study the effects of intra-aortic (ia) serotonin on ileocolonic and colonic transit, and the effects on transit of a number of 5HT receptor antagonists. In the first series of experiments, a bolus of saline labelled with 99mTc DTPA was instilled 20 cm proximal to the ICJ and transit was assessed three hours later by the geometric centre of the spread of isotope. In the second series, similar techniques were used on the postcaecal colon and transit assessed two hours later. In the third series of experiments, the effects of ia 5HT on ileal net fluid flux was evaluated by standard perfusion experiments with 14C polyethylene glycol (PEG) 4000 as a non-absorbable marker in rat plasma-like electrolyte solution. Compared with ia saline, 5HT accelerated ICJ transit significantly (p < 0.05). This acceleration was comparable with the effect of ia bethanechol. The effects of 5HT on ICJ transit were inhibited by the intraperitoneal (ip) infusion of atropine, the 5HT receptor antagonists, methysergide, ketanserin, zacopride, and the 5HT4 agonist, SC53116. Methysergide, zacopride, and SC53116 given with ia 5HT slowed ICJ transit to rates below those of ia saline alone. When these same agents were given together with ia saline, the ICJ transit was not significantly altered. Serotonin, at the dose that accelerated ICJ transit, did not significantly alter colonic transit or ileal fluid transport. In conclusion, 5HT is a potent pharmacological stimulant of transit across the rat ICJ in vivo; the action of 5HT is mediated partly through muscarinic neurones and several 5HT receptor subtypes.

Effects of acute respiratory acidosis on water and electrolyte transport in the human ileum.

Animal experiments have shown that acute respiratory acidosis stimulates water, Na and Cl absorption and HCO3 secretion in the ileum. The aim of this study was to investigate whether the human ileum also responds to changes in systemic acid-base balance. Seven healthy volunteers (mean age 24, range 21-29 years) underwent segmental ileal perfusion using a multi-lumen tube assembly with a proximal occluding balloon. A 30 cm test segment was perfused under steady state conditions with a plasma-like electrolyte solution containing PEG as a non-absorbable volume marker. After a control period, respiratory acidosis (blood pCO2 56.2 mmHg, pH 7.29 and [HCO3] 26.4 mmol l-1) was induced by CO2-breathing over a period of 50 min. Acute respiratory acidosis stimulated net HCO3 secretion in patients secreting HCO3 and reduced absorption in patients exhibiting net HCO3 absorption. These changes were immediate and appeared to be at least partly reversible. Net water, Na, K and Cl movement were not affected. The data suggest that HCO3 transport in the human ileum responds to acute respiratory acidosis.

Effect of neuropeptide Y on jejunal water and ion transport in humans

Neuropeptide Y is a neurotransmitter in enteric and postganglionic sympathetic neurons. In animal models of intestinal water and ion transport, neuropeptide Y decreases stimulated secretion but has no consistent effect on basal transport. In the present study, the effect of neuropeptide Y on jejunal water and electrolyte transport in healthy volunteers was investigated under basal conditions and during intestinal secretion induced by intraluminal administration of prostaglandin E2. The triple-lumen tube technique was used for perfusion of the small intestine with a plasmalike electrolyte solution containing polyethylene glycol as a nonabsorbable volume marker. After an initial control period (saline IV) neuropeptide Y was administered IV at a dose of 400 pmol · kg−1 · h−1. Neuropeptide Y significantly increased net absorption of water, sodium, potassium, and chloride under basal conditions. The peptide significantly reduced the secretion of these electrolytes induced by an intraluminal prostaglandin E2 concentration of 5 μmol/L and reduced net water secretion by 36%. The results of the current study suggest that neuropeptide Y can change intestinal water and ion transport from secretion toward absorption.

Intravenous atrial natriuretic peptide does not affect water and ion transport in the human small intestine

Atrial natriuretic peptide (ANP) increases renal sodium and water excretion in several species including man. In rats ANP was also found to influence water and electrolyte transport in the small intestine. In the present study we investigated whether ANP can alter transport in the jejunum and ileum of healthy volunteers using a triple-lumen perfusion technique. The small intestine was perfused under steady-state conditions with a plasma-like electrolyte solution using polyethylene glycol as a nonabsorbable volume marker. After an initial control period with intravenous saline infusion ANP was administered intravenously at a dose of 400 pmol kg-1 h-1. This dose led to a significant (P less than 0.05) increase in the plasma levels of ANP (up to 22-fold) and cGMP (up to 15-fold), and of urine volume. Intestinal water and electrolyte transport were, however, not affected by ANP. Our results suggest that circulating ANP does not play a role in the regulation of mucosal water and ion transport in the human small intestine.

Jejunal Secretory Effect of Intraduodenal Food in Humans: A Comparison of Mixed Nutrients, Proteins, Lipids, and Carbohydrates

The effect of the presence of food in the intestinal lumen on fluid transport by an intestinal loop isolated from nutrients is debatable and seems to be species dependent. The aim of the present study was to investigate this effect in humans. Fluid and ion transport by a 30-cm-long jejunal loop was measured by the perfusion of a plasmalike electrolyte solution below an occlusive balloon inflated at the angle of Treitz. At the same time, the duodenum was infused at the papilla by saline (control period) or one of the following solutions (test period): protein hydrolysate, starch hydrolysate, lipids, or mixed nutrients. The four solutions (pH 7; 300 mosmol/L; 540 kcal/L) were infused in 6 normal subjects in a randomized order. In 6 further subjects, two other loads of intraduodenal lipids (120 and 1080 kcal/L) were tested according to a similar protocol. Blood samples were taken serially for radioimmunoassays of gastrin, secretin, cholecystokinin, pancreatic polypeptide, gastric inhibitory polypeptide, vasoactive intestinal polypeptide, motilin, and somatostatin. Intraduodenal mixed nutrients, proteins, and lipids significantly reduced water and ion jejunal net absorption or induced a net secretion (without dose-effect relationship for lipids) and stimulated plasma cholecystokinin, pancreatic polypeptide, and gastric inhibitory polypeptide. Intraduodenal lipids also stimulated circulating levels of gastrin and vasoactive intestinal polypeptide. Intraduodenal sugars did not change jejunal fluid and ion transport and significantly increased plasma gastric inhibitory polypeptide. Covariance analysis showed transjejunal fluid movements to be linked with plasma levels of cholecystokinin. We conclude that an intraduodenal mixed meal exerts a secretory effect on a jejunal loop isolated from the nutrients and that this effect is due to the lipid and protein content of the meal; our data are compatible with a mediation of this phenomenon by cholecystokinin.

Effect of 13-norleucin motilin on water and ion transport in the human jejunum

Passage of the interdigestive migrating myoelectric complex through the proximal small bowel is associated with elevated plasma motilin levels and an increase in transmucosal potential difference suggesting altered ion transport. The aim of the present study was to investigate whether motilin may have an effect on intestinal water and ion transport. Steady state jejunal perfusion studies were carried out in healthy volunteers while either saline (control) or synthetic motilin (256 pmol/kg · h) was infused via peripheral vein. Plasma motilin levels rose from a mean of 31 to a plateau of 832 pmol/L. Motilin infusion significantly reduced absorption of water, sodium, potassium, and chloride when a plasmalike electrolyte solution was perfused. During perfusion with a bicarbonate-free salt solution, motilin significantly enhanced secretion of water, potassium, and chloride. Chloride secretion was active inasmuch as it occurred against both an electrical and chemical gradient. Motilin infusion had no effect on transit time during perfusion of the 30-cm jejunal test segments. We conclude that motilin can act as an intestinal secretagogue in the human jejunum.

Effect of somatostatin infusion on VIP-induced transport changes in the human jejunum

This study was designed to elucidate the mechanism by which somatostatin administration ameliorates or abolishes diarrhea in pancreatic cholera syndrome (PCS). Absorption (or secretion) of water and electrolytes was measured in 30-cm segments of jejunum of 18 healthy volunteers in whom PCS was mimicked by intravenous infusion of VIP. Using the triple-lumen tube technique, the intestine was perfused with a plasma-like electrolyte solution while administering intravenous saline (control), VIP (400 pmol/kg/hr), somatostatin (5000 pmol/kg/hr), or VIP plus somatostatin. VIP infusion abolished water and electrolyte absorption and somtostatin had no effect on these VIP-induced transport changes regardless of whether somatostatin infusion was started before or after VIP infusion. Somatostatin infusion had no effect on VIP plasma concentration when elevated by intravenous VIP infusion (control: 10±1 pmol/l ; during VIP infusion: 108±6). In a patient with pancreatic cholera syndrome identical perfusion experiments showed jejunal water secretion (93 ml/30 cm/hr) which changed to absorption (65 ml/30 cm/hr) when somatostatin was infused (5000 pmol/kg/hr). Plasma VIP concentration fell from 145 to 74 pmol/l (normal<50) during somatostatin infusion. Stool weight fell from 3722 g to 819 g per 24 hours when somatostatin was given at a dose of 2500 pmol/kg/hr for two days. Our observations in healthy subjects show that somatostatin has no effect on intestinal transport at the mucosal level when circulating VIP concentration is elevated. The findings in the patient with pancreatic cholera syndrome indicate that the effect of somatostatin on secretion (and diarrhea) is due to a decrease in circulating levels of VIP presumably due to reduced release of VIP from a tumor.

Water and electrolyte movement and mucosal morphology in the jejunum of patients with portal hypertension

Intestinal secretion and intercellular space dilatation can be induced in animal models by acute elevation of intravascular volume or portal pressure. We examined whether patients with increased portal venous pressure might represent a clinical counterpart to these animal models. Portal venous pressure, determined by hepatic wedge pressure measurement, was elevated to 10–55 mmHg (mean 29 mmHg) in 8 patients with chronic liver disease without diarrhea. Intestinal transport studies utilizing a steady-state perfusion technique revealed normal absorption of a plasmalike electrolyte solution. A solution designed to unmask intestinal secretion demonstrated no difference from control subjects in the movement of water, electrolytes, or protein into the intestinal lumen. There was no correlation of absorption or secretion with hepatic wedge pressure. Jejunal biopsy revealed a significant increase in dilatation of intercellular spaces in patients compared to controls; this increase was not correlated with hepatic wedge pressure, but was significantly inversely correlated to plasma renin and aldosterone concentration. We conclude that patients with chronic liver disease and portal hypertension absorb water and electrolytes normally, but have mild morphologic alterations in the intestinal mucosa, possibly related to intravascular volume status.

Effect of VIP infusion on water and ion transport in the human jejunum

Infusion of vasoactive intestinal polypeptide (VIP) is known to cause intestinal secretion in animal models. The present study was designed to answer the question whether VIP has a similar effect on the human intestine. Pure porcine VIP was administered by constant i.v. infusion to healthy subjects while their jejunum was perfused with a plasma-like electrolyte solution. At the lowest VIP infusion rate (100 pmol/kg/hr), plasma VIP levels rose two- to fourfold, and there was an increase in the transmucosal potential difference but no change in sodium chloride absorption. At higher VIP infusion rates (200 and 400 pmol/kg/hr), VIP plasma concentrations rose to levels commonly observed in patients with pancreatic cholera syndrome. At these levels VIP caused a dose-dependent decrease of water and sodium absorption. Chloride absorption changed to secretion, while bicarbonate movement remained completely unaffected. Chloride secretion was active, since it occurred against an electrical and chemical gradient. All changes induced by VIP were reversible after discontinuance of VIP infusion. Our observations suggest that elevated levels of circulating VIP are capable of affecting water and ion movement in the human jejunum. They lend support to the hypothesis that high levels of circulating VIP may be a mediator of secretory diarrhea in some patients with pancreatic cholera syndrome.

Effect of intravenous somatostatin on jejunal absorption of glucose, amino acids, water, and electrolytes

Somatostatin has previously been reported to reduce plasma levels of sugars and triglycerides following oral test meals. This study was designed to answer the question as to whether or not somatostatin affects transport directly by inhibiting absorption across the mucosa of the small bowel. Steady-state perfusion experiments with either glucose- and amino acid-containing test solutions or a plasmalike electrolyte solution were carried out in the jejunum of healthy subjects. During the intestinal perfusion either saline (control) or somatostatin (8 μg/ kg/h) was infused for 90 min through a peripheral vein. Somatostatin infusion significantly reduced glucose absorption, and kinetic analysis revealed that this effect was mainly due to a reduction of Vmax of glucose transport. Amino acid absorption (l-glycine and l-lysine) was also reduced by somatostatin infusion. Despite a significant decrease in undirectional water fluxes and calculated rate of water and urea diffusion, somatostatin did not affect net water or electrolyte absorption when the plasma-like electrolyte solution was perfused. These studies suggest that somatostatin inhibits glucose and amino acid absorption by a direct effect on the intestinal mucosa. Although the mechanism is unknown, we think that somatostatin most likely causes its effect by a selective reduction of functional mucosal surface area of the intestine.