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Objectives: To evaluate the efficacy of the simultaneous hypertonic saline solution and IV furosemide (HSS+Fx) for patients with fluid overload compared with IV furosemide alone (Fx).Data Sources: Electronic databases (MEDLINE, EMBASE, CENTRAL, Cochrane Database of Systematic Reviews, PsycINFO, Scopus, and WOS) were searched from inception to March 2020.Study Selection: Randomized controlled trials on the use of HSS+Fx in adult patients with fluid overload versus Fx were included.Data Extraction: Data were collected on all-cause mortality, hospital length of stay, heart failure-related readmission, along with inpatient weight loss, change of daily diuresis, serum creatinine, and 24-hour urine sodium excretion from prior to post intervention. Pooled analysis with random effects models yielded relative risk or mean difference with 95% CIs.Data Synthesis: Eleven randomized controlled trials comprising 2,987 acute decompensated heart failure patients were included. Meta-analysis demonstrated that HSS+Fx was associated with lower all-cause mortality (relative risk, 0.55; 95% CI, 0.46-0.67; p < 0.05; I2 = 12%) and heart failure-related readmissions (relative risk, 0.50; 95% CI, 0.33-0.76; p < 0.05; I2 = 61%), shorter hospital length of stay (mean difference, -3.28 d; 95% CI, -4.14 to -2.43; p < 0.05; I2 = 93%), increased daily diuresis (mean difference, 583.87 mL; 95% CI, 504.92-662.81; p < 0.05; I2 = 76%), weight loss (mean difference, -1.76 kg; 95% CI, -2.52 to -1.00; p < 0.05; I2 = 57%), serum sodium change (mean difference, 6.89 mEq/L; 95% CI, 4.98-8.79; p < 0.05; I2 = 95%), and higher 24-hour urine sodium excretion (mean difference, 61.10 mEq; 95% CI, 51.47-70.73; p < 0.05; I2 = 95%), along with decreased serum creatinine (mean difference, -0.46 mg/dL; 95% CI, -0.51 to -0.41; p < 0.05; I2 = 89%) when compared with Fx. The Grading of Recommendation, Assessment, Development, and Evaluation certainty of evidence ranged from low to moderate.Conclusions: Benefits of the HSS+Fx over Fx were observed across all examined outcomes in acute decompensated heart failure patients with fluid overload. There is at least moderate certainty that HSS+Fx is associated with a reduction in mortality in patients with acute decompensated heart failure. Factors associated with a successful HSS+Fx utilization are still unknown. Current evidence cannot be extrapolated to other than fluid overload states in acute decompensated heart failure. [ABSTRACT FROM AUTHOR]

Objectives: Mannitol and hypertonic saline are used to treat raised intracerebral pressure in patients with traumatic brain injury, but their possible effects on kidney function and mortality are unknown.Design: A post hoc analysis of the erythropoietin trial in traumatic brain injury (ClinicalTrials.gov NCT00987454) including daily data on mannitol and hypertonic saline use.Setting: Twenty-nine university-affiliated teaching hospitals in seven countries.Patients: A total of 568 patients treated in the ICU for 48 hours without acute kidney injury of whom 43 (7%) received mannitol and 170 (29%) hypertonic saline.Interventions: None.Measurements and Main Results: We categorized acute kidney injury stage according to the Kidney Disease Improving Global Outcome classification and defined acute kidney injury as any Kidney Disease Improving Global Outcome stage-based changes from the admission creatinine. We tested associations between early (first 2 d) mannitol and hypertonic saline and time to acute kidney injury up to ICU discharge and death up to 180 days with Cox regression analysis. Subsequently, acute kidney injury developed more often in patients receiving mannitol (35% vs 10%; p < 0.001) and hypertonic saline (23% vs 10%; p < 0.001). On competing risk analysis including factors associated with acute kidney injury, mannitol (hazard ratio, 2.3; 95% CI, 1.2-4.3; p = 0.01), but not hypertonic saline (hazard ratio, 1.6; 95% CI, 0.9-2.8; p = 0.08), was independently associated with time to acute kidney injury. In a Cox model for predicting time to death, both the use of mannitol (hazard ratio, 2.1; 95% CI, 1.1-4.1; p = 0.03) and hypertonic saline (hazard ratio, 1.8; 95% CI, 1.02-3.2; p = 0.04) were associated with time to death.Conclusions: In this post hoc analysis of a randomized controlled trial, the early use of mannitol, but not hypertonic saline, was independently associated with an increase in acute kidney injury. Our findings suggest the need to further evaluate the use and choice of osmotherapy in traumatic brain injury. [ABSTRACT FROM AUTHOR]

Objectives: Traumatic brain injury is a leading cause of hospital visits for children. Hyperosmolar therapy is often used to treat severe traumatic brain injury. Hypertonic saline is used predominantly, yet there remains disagreement about whether hypertonic saline or mannitol is more effective.Data Sources: Literature search was conducted using Pubmed, Cochrane, and Embase. Systematic review followed Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines.Study Selection: Retrospective and prospective studies assessing use of hyperosmolar therapy in pediatric patients with severe traumatic brain injury were included.Data Extraction: Two independent authors performed article review. Two-thousand two-hundred thirty unique articles were initially evaluated, 11 were included in the final analysis, with a total of 358 patients. Study quality was assessed using Modified Newcastle-Ottawa Scale and Jadad score.Data Synthesis: Of the 11 studies, all evaluated hypertonic saline and four evaluated both hypertonic saline and mannitol. Nine reported that hypertonic saline lowered intracranial pressure and two reported that mannitol lowered intracranial pressure. The studies varied significantly in dose, concentration, and administrations schedule for both hypertonic saline and mannitol. Five studies were prospective, but only one directly compared mannitol to hypertonic saline. The prospective comparison study found no difference in physiologic outcomes. Clinical outcomes were reported using different measures across studies. For hypertonic saline-treated patients, mechanical ventilation was required for 6.9-9 days, decompressive craniectomy was required for 6.25-29.3% of patients, ICU length of stay was 8.0-10.6 days, in-hospital mortality was 10-48%, and 6-month mortality was 7-17%. In mannitol-treated patients, ICU length of stay was 9.5 days, in-hospital mortality was 56%, and 6-month mortality was 19%.Conclusions: Both hypertonic saline and mannitol appear to lower intracranial pressure and improve clinical outcomes in pediatric severe traumatic brain injury, but the evidence is extremely fractured both in the method of treatment and in the evaluation of outcomes. Given the paucity of high-quality data, it is difficult to definitively conclude which agent is better or what treatment protocol to follow. [ABSTRACT FROM AUTHOR]

Objectives: Hyponatremic encephalopathy, symptomatic cerebral edema due to a low osmolar state, is a medical emergency and often encountered in the ICU setting. This article provides a critical appraisal and review of the literature on identification of high-risk patients and the treatment of this life-threatening disorder.Data Sources, Study Selection, and Data Extraction: Online search of the PubMed database and manual review of articles involving risk factors for hyponatremic encephalopathy and treatment of hyponatremic encephalopathy in critical illness.Data Synthesis: Hyponatremic encephalopathy is a frequently encountered problem in the ICU. Prompt recognition of hyponatremic encephalopathy and early treatment with hypertonic saline are critical for successful outcomes. Manifestations are varied, depending on the extent of CNS's adaptation to the hypoosmolar state. The absolute change in serum sodium alone is a poor predictor of clinical symptoms. However, certain patient specific risks factors are predictive of a poor outcome and are important to identify. Gender (premenopausal and postmenopausal females), age (prepubertal children), and the presence of hypoxia are the three main clinical risk factors and are more predictive of poor outcomes than the rate of development of hyponatremia or the absolute decrease in the serum sodium.Conclusions: In patients with hyponatremic encephalopathy exhibiting neurologic manifestations, a bolus of 100 mL of 3% saline, given over 10 minutes, should be promptly administered. The goal of this initial bolus is to quickly treat cerebral edema. If signs persist, the bolus should be repeated in order to achieve clinical remission. However, the total change in serum sodium should not exceed 5 mEq/L in the initial 1-2 hours and 15-20 mEq/L in the first 48 hours of treatment. It has recently been demonstrated in a prospective fashion that 500 mL of 3% saline at an infusion rate of 100 mL per hour can be given safely. It is critical to recognize the early signs of cerebral edema (nausea, vomiting, and headache) and intervene with IV 3% sodium chloride as this is the time to intervene rather than waiting until more severe symptoms develop. Cerebral demyelination is a rare complication of overly rapid correction of hyponatremia. The principal risk factors for cerebral demyelination are correction of the serum sodium more than 25 mEq/L in the first 48 hours of therapy, correction past the point of 140 mEq/L, chronic liver disease, and hypoxic/anoxic episode. [ABSTRACT FROM AUTHOR]

Objectives: Hyperchloremia has been associated with increased morbidity and mortality in critically ill patients. While previous research has demonstrated an association between hypertonic saline and hyperchloremia, limited data exist in neurocritical care patients. The objective of this study is to determine the impact of moderate hyperchloremia (chloride ≥ 115 mmol/L) on clinical outcomes in intracerebral hemorrhage patients treated with continuous IV infusion 3% hypertonic saline.Design: Multicenter, retrospective, propensity-matched cohort study.Setting: Neurocritical care units at two academic medical centers with dedicated neurocritical care teams and comprehensive stroke center designation.Patients: Intracerebral hemorrhage patients discharged between September 2011 and September 2015 were evaluated and matched 1:1 based on propensity scoring.Interventions: Continuous IV infusion 3% hypertonic saline.Measurements and Main Results: A total of 219 patients were included in the unmatched cohort (143 moderate hyperchloremia and 76 nonhyperchloremia) and 100 patients in the propensity-matched cohort. In-hospital mortality was significantly higher in those who developed moderate hyperchloremia in a propensity-matched cohort (34% vs 14%; p = 0.02). Moderate hyperchloremia independently predicted in-hospital mortality in multivariable logistic regression analysis (odds ratio, 4.4 [95% CI, 1.4-13.5]; p = 0.01).Conclusions: We observed higher rates of in-hospital mortality in patients who developed moderate hyperchloremia during treatment with continuous IV infusion 3% hypertonic saline, with moderate hyperchloremia independently predicting in-hospital mortality. These results suggest that chloride values should be monitored closely during hypertonic saline treatment as moderate elevations may impact outcomes in intracerebral hemorrhage patients. [ABSTRACT FROM AUTHOR]

SP 1 sp Division of Pulmonary and Critical Care Medicine, Department of Medicine, Mayo Clinic, Rochester, MN SP 2 sp Division of Nephrology and Hypertension, Department of Medicine, Mayo Clinic, Rochester, MN SP 3 sp Unidad de Conocimiento y Evidencia, CONEVID, Universidad Peruana Cayetano Heredia, Lima, Peru SP 4 sp Division of Critical Care, Department of Medicine, Mayo Clinic Health System, Mankato, MN SP 5 sp Department of Critical Care Medicine, Zhongnan Hospital of Wuhan University, Wuhan, China The authors have disclosed that they do not have any potential conflicts of interest. Kitajima et al ([1]) point out some concerns about how to categorize the evidence certainty. BMJ Evid Based Med 2018; 23:84 5 Sterne JAC, Sutton AJ, Ioannidis JPA, et al: Recommendations for examining and interpreting funnel plot asymmetry in meta-analyses of randomised controlled trials. [Extracted from the article]

Am Heart J 2012; 164:351-357 4 Parrinello G, Paterna S, Di Pasquale P, et al: Changes in estimating echocardiography pulmonary capillary wedge pressure after hypersaline plus furosemide versus furosemide alone in decompensated heart failure. SP 1 sp Department of Primary Care and Emergency Medicine, Graduate School of Medicine, Kyoto University, Kyoto, Japan SP 2 sp Department of Nephrology, Graduate School of Medicine, Kyoto University, Kyoto, Japan SP 3 sp Department of Respiratory Medicine, Graduate School of Medicine, Kyoto University, Kyoto, Japan Drs. Am Heart J 2003; 145:459-466 3 Parrinello G, Di Pasquale P, Torres D, et al: Troponin I release after intravenous treatment with high furosemide doses plus hypertonic saline solution in decompensated heart failure trial (Tra-HSS-Fur). [Extracted from the article]

Baseline characteristics collected include HTS dose, rate and site of administration, indication for use and patient demographics. The primary safety outcome was incidence of extravasation and phlebitis within 1 hour of HTS administration. B Introduction: b Hypertonic sodium chloride (HTS) is used for emergent treatment of acute cerebral edema and other neurologic emergencies. [Extracted from the article]

Each bolus administered during invasive ICP monitoring contributed to the outcomes data, separated into normonatremic and hypernatremic cohorts based on serum sodium prior to bolus administration. Patients > 18 years were included if they had any type of intracranial hemorrhage or traumatic brain injury (TBI), invasive ICP monitoring (external ventricular drain or subdural bolt), and received > 1 HTS bolus during ICP monitoring. Bolus characteristics collected included time from bolus to ICP measurement, bolus concentration and volume, and percentage of boluses given when ICPs were less than 20 mmHg. [Extracted from the article]

B Conclusions: b Chloride level, rather than chloride load, may be associated with the development of AKI in TBI patients treated with HTS. B Introduction: b Hypertonic saline (HTS) is the mainstay of pharmacologic treatment for severe traumatic brain injury (TBI) to mitigate secondary injury. [Extracted from the article]

Objectives: We tested the hypothesis that osmotherapy with hypertonic saline attenuates cerebral edema following experimental cardiac arrest and cardiopulmonary resuscitation by exerting its effect via the perivascular pool of aquaporin-4. We used mice with targeted disruption of the gene encoding α-syntrophin (α-Syn) that demonstrate diminished perivascular aquaporin-4 pool but retain the non-endfoot and ependymal pools.Design: Laboratory animal study.Setting: University animal research laboratory.Interventions: Isoflurane-anesthetized adult male wild-type C57B/6 or α-Syn mice were subjected to cardiac arrest/cardiopulmonary resuscitation and treated with either a continuous IV infusion of 0.9% saline or various concentrations of hypertonic saline. Serum osmolality, regional brain water content, blood-brain barrier disruption, and aquaporin-4 protein expression were determined at 24 hours after cardiac arrest/cardiopulmonary resuscitation.Measurements and Main Results: Hypertonic saline (7.5%) treatment significantly attenuated water content in the caudoputamen complex and cortex compared with 0.9% saline treatment in wild-type mice subjected to cardiac arrest/cardiopulmonary resuscitation. In contrast, in α-Syn mice subjected to cardiac arrest/cardiopulmonary resuscitation, 7.5% hypertonic saline treatment did not attenuate water content. Treatment with 7.5% hypertonic saline attenuated blood-brain barrier disruption at 24 hours following cardiac arrest/cardiopulmonary resuscitation in wild-type mice but not in α-Syn mice. Total aquaporin-4 protein expression was not different between 0.9% saline and hypertonic saline-treated wild-type mice.Conclusions: Following experimental cardiac arrest/cardiopulmonary resuscitation: 1) continuous hypertonic saline therapy maintained to achieve serum osmolality of ≈ 350 mOsm/L is beneficial for the treatment of cerebral edema; 2) perivascular pool of aquaporin-4 plays a critical role in water egress from brain; and 3) hypertonic saline attenuates blood-brain barrier disruption via perivascular aquaporin-4 pool. [ABSTRACT FROM AUTHOR]

Objective: Cerebral edema is common in severe hepatic encephalopathy and may be life threatening. Bolus 23.4% hypertonic saline improves surveillance neuromonitoring scores, although its mechanism of action is not clearly established. We investigated the hypothesis that bolus hypertonic saline decreases cerebral edema in severe hepatic encephalopathy utilizing a quantitative technique to measure brain and cerebrospinal fluid volume changes.Design: Retrospective analysis of serial CT scans, and clinical data for a case-control series were performed.Setting: ICUs of a tertiary care hospital.Patients: Patients with severe hepatic encephalopathy treated with 23.4% hypertonic saline and control patients who did not receive 23.4% hypertonic saline.Interventions: 23.4% hypertonic saline bolus administration.Measurements and Main Results: We used clinically obtained CT scans to measure volumes of the ventricles, intracranial cerebrospinal fluid, and brain using a previously validated semiautomated technique (Analyze Direct, Overland Park, KS). Volumes before and after 23.4% hypertonic saline were compared with Wilcoxon signed rank test. Associations among total cerebrospinal fluid volume, ventricular volume, serum sodium, and Glasgow Coma Scale scores were assessed using Spearman rank correlation test. Eleven patients with 18 administrations of 23.4% hypertonic saline met inclusion criteria. Total cerebrospinal fluid (median, 47.6 mL [35.1-69.4 mL] to 61.9 mL [47.7-87.0 mL]; p < 0.001) and ventricular volumes (median, 8.0 mL [6.9-9.5 mL] to 9.2 mL [7.8-11.9 mL]; p = 0.002) increased and Glasgow Coma Scale scores improved (median, 4 [3-6] to 7 [6-9]; p = 0.008) after 23.4% hypertonic saline. In contrast, total cerebrospinal fluid and ventricular volumes decreased in untreated control patients. Serum sodium increase was associated with increase in total cerebrospinal fluid volume (r = 0.83, p < 0.001), and change in total cerebrospinal fluid volume was associated with ventricular volume change (r = 0.86; p < 0.001).Conclusions: Total cerebrospinal fluid and ventricular volumes increased after 23.4% hypertonic saline, consistent with a reduction in brain tissue volume. Total cerebrospinal fluid and ventricular volume change may be useful quantitative measures to assess cerebral edema in severe hepatic encephalopathy. [ABSTRACT FROM AUTHOR]

Patients were excluded if they were missing >=2 daily nephrology notes specifying flow rates, received MARS/CRRT for <=24 hours, received 23.4% NaCl for any non-ALF indication, or died within 24 hours of admission to ICU. B Conclusions: b Acute liver failure patients on CRRT/MARS therapy had a higher percentage of time within goal sodium range and trended toward a decreased mortality with the addition of a 3% sodium chloride continuous infusion to 23.4% sodium chloride boluses. B Methods: b A retrospective chart review of medical records from January 1, 2014 to September 30, 2018 was performed on patients that received MARS/CRRT and concurrent 23.4% NaCl in the surgical intensive care unit (ICU) at Emory University Hospital. [Extracted from the article]

The article explores the hypothesis that aerosolized inhaled hypertonic saline given at the onset of resuscitation will reduce acute lung injury after hemorrhagic shock by preventing the release of epithelial derived proinflammatory mediators. Results reveal that inhaled hypertonic saline decreases postshock acute lung injury by exerting an anti-inflammatory effect on the pulmonary epithelium. This indicates a new clinical approach to treat acute lung injury/acute respiratory distress syndrome.

The article discusses research done on the effectiveness of hypertonic saline over mannitol in attenuating cerebral edema in a rabbit bacterial meningitis model. The researchers concluded that adjunctive three percent hypertonic saline treatment affected the elevation of mean arterial pressure. It also minimized cerebral edema, enhanced cerebral perfusion pressure, and decreased intracranial pressure.

The article presents a study which investigates the events that occur within eight hours after spinal cord injury (SCI) and the effect of hypertonic saline (HS) on cord swelling, edema and hemorrhage through magnetic resonance imaging (MRI). It notes that after the SCI, MRI revealed the swelling of the spinal cord and the presence of hypointense core. However, cord swelling easily attenuated and the volume of edema and hypointense core has decreased after HS was administered.

The article investigates whether the protective effects of hypertonic saline are associated with improved γδT cell-mediated neutrophil killing. Results indicate that hypertonic saline improves the elimination of inflammatory neutrophils by γδT cells by augmenting heat shock protein-72 expression on the cell surface of neutrophils. Hypertonic saline resuscitation may safeguard host tissues by improving neutrophil clearance from the lungs.

Objective: Recognition of the limitations of standard crystalloid resuscitation has led to exploration for alternative resuscitation strategies that might better prevent the development of trauma-hemorrhage-induced organ dysfunction and systemic inflammation. Thus, the goal of this study was to compare the effects of two resuscitation strategies alone and in combination with that of standard resuscitation with Ringer's lactate. These two strategies were intravenous injection of amiloride, an inhibitor of Na/H exchange and epithelial Na channels, and resuscitation with hypertonic saline.Design: Prospective animal study with concurrent control.Setting: Small animal laboratory.Subjects: Adult male Sprague-Dawley rats.Interventions: Rats injected with amiloride or its vehicle were subjected to trauma-hemorrhagic shock (T/HS) or trauma sham-shock (T/SS) and resuscitated with Ringer's lactate or hypertonic saline. The T/HS model consisted of a laparotomy plus 90 mins of shock (mean arterial pressure 30 mm Hg). Three hours after the end of the shock or sham-shock period, lung permeability, lung histology, pulmonary neutrophil sequestration, neutrophil CD11b expression, gut injury, and red blood cell rigidification were assessed.Measurements and Main Results: Both amiloride and hypertonic saline reduced T/HS-induced pulmonary permeability and neutrophil sequestration, and coadministration of these two agents was more efficacious than administration of the individual agents. In contrast, whereas gut injury was attenuated by both amiloride and hypertonic saline, combined administration of amiloride and hypertonic saline failed to further protect the gut. Additionally, hypertonic saline reduced both neutrophil CD11b expression and red blood cell rigidification, whereas amiloride was without effect.Conclusions: Combined administration of amiloride and small-volume resuscitation with hypertonic saline may be a strategy worthy of further evaluation in the therapy of shock-induced distant organ injury. [ABSTRACT FROM AUTHOR]

OBJECTIVE: Recognition of the limitations of standard crystalloid resuscitation has led to exploration for alternative resuscitation strategies that might better prevent the development of trauma-hemorrhage-induced organ dysfunction and systemic inflammation. Thus, the goal of this study was to compare the effects of two resuscitation strategies alone and in combination with that of standard resuscitation with Ringer’s lactate. These two strategies were intravenous injection of amiloride, an inhibitor of Na/H exchange and epithelial Na channels, and resuscitation with hypertonic saline. DESIGN: Prospective animal study with concurrent control. SETTING: Small animal laboratory. SUBJECTS: Adult male Sprague-Dawley rats. INTERVENTIONS: Rats injected with amiloride or its vehicle were subjected to trauma-hemorrhagic shock (T/HS) or trauma sham-shock (T/SS) and resuscitated with Ringer’s lactate or hypertonic saline. The T/HS model consisted of a laparotomy plus 90 mins of shock (mean arterial pressure 30 mm Hg). Three hours after the end of the shock or sham-shock period, lung permeability, lung histology, pulmonary neutrophil sequestration, neutrophil CD11b expression, gut injury, and red blood cell rigidification were assessed. MEASUREMENTS AND MAIN RESULTS: Both amiloride and hypertonic saline reduced T/HS-induced pulmonary permeability and neutrophil sequestration, and coadministration of these two agents was more efficacious than administration of the individual agents. In contrast, whereas gut injury was attenuated by both amiloride and hypertonic saline, combined administration of amiloride and hypertonic saline failed to further protect the gut. Additionally, hypertonic saline reduced both neutrophil CD11b expression and red blood cell rigidification, whereas amiloride was without effect. CONCLUSIONS: Combined administration of amiloride and small-volume resuscitation with hypertonic saline may be a strategy worthy of further evaluation in the therapy of shock-induced distant organ injury. [ABSTRACT FROM AUTHOR]

Objective: To compare the effectiveness of normal saline, dextran, hypertonic, and hypertonic-hyperoncotic solutions in hemorrhagic shock.Design: Laboratory investigation.Setting: University hospital, Emergency Surgery and Intensive Care staff.Subjects: Thirty-two large white female pigs.Interventions: Routine care included: anesthesia and sedation (ketamine 10 mg/kg, droperidol 0.25 mg/kg, diazepam 0.7 mg/kg, fentanyl 0.006 mg/kg, 2% enflurane, 20% nitrous oxide, pancuronium bromide 0.13 mg/kg); volume-controlled ventilation (Paco(2) 35-40 torr; 4.7-5.4 kPa); cannulation of right carotid artery and pulmonary artery. Three flow probes (subdiaphragmatic aorta, superior mesenteric artery, right renal artery) and regional venous catheters (superior mesenteric vein, right renal vein) were positioned. Animals were bled to 45 mm Hg for 1 hr and resuscitated with four different fluids and blood to normal aortic blood flow and hemoglobin.Measurements and Main Results: Mean arterial pressure and blood flow through abdominal aorta ([OV0312](aor)), mesenteric artery ([OV0312](mes)), and renal artery ([OV0312](ren)) were continuously monitored. Cardiac output, systemic and regional oxygen delivery ([U1E0A]o(2), [U1E0A]o(2mes), [U1E0A]o(2ren)), and consumption ([OV0312]o(2), [OV0312]o(2mes), [OV0312]o(2ren)) were recorded every 30 mins. Baseline [OV0312](aor) was restored with different amounts of fluids in the four groups: normal saline (91.35 +/- 22.18 mL/kg); dextran (16.24 +/- 4.42 mL/kg); hypertonic (13.70 +/- 1.44 mL/kg); and hypertonic-hyperoncotic (9.11 +/- 1.20 mL/kg). The amount of sodium load was less using dextran and hypertonic-hyperoncotic and sodium levels were only transiently increased after hypertonic infusion. Mean arterial pressure and cardiac output were normalized in all groups. Animals resuscitated with normal saline and dextran showed increased pulmonary artery pressures. [U1E0A]o(2) was significantly higher after hypertonic-hyperoncotic infusion, because of reduced hemodilution. Hypertonic and hypertonic-hyperoncotic normalized [OV0312](mes), [U1E0A]o(2mes), [OV0312]o(2mes), [OV0312](ren), and [U1E0A]o(2ren), whereas normal saline and dextran did not achieve this result. At the end of the experiment, hypertonic-hyperoncotic maintained mean arterial pressure, cardiac output, and [U1E0A]o(2) until the end of observation in contrast to normal saline, dextran, and hypertonic.Conclusions: Resuscitation with a small volume of hypertonic-hyperoncotic solution allows systemic and splanchnic hemodynamic and oxygen transport recovery, without an increase in pulmonary artery pressure. It only transiently increased sodium concentration. [ABSTRACT FROM AUTHOR]

B Learning Objectives: b The use of non-buffered 0.9% normal saline (NS) for resuscitation contributes to metabolic disturbances, kidney injury and increased mortality. In this study, a porcine model of controlled hemorrhage and volume overload resuscitation was used to characterize the effects of NS compared to a balanced buffered electrolyte solution [PlasmaLyte (PL)] on acid base status and endothelial function. [Extracted from the article]