Effective Circulating Blood Volume Research Articles

Effect of different shock conditions on mesenteric hemodynamics

Background: Reduced effective circulating blood volume and impaired peripheral tissue perfusion play an important role in the pathophysiology of shock. However, there have been no studies examining the relationship between Doppler ultrasound of the superior mesenteric artery (SMA) under different shock conditions.Methods: We evaluated a total of 85 patients, including 63 patients with different types of shock and 22 in the control group. we included patients who were diagnosed with shock upon admission or developed shock during their hospital stay. At the same time, patients with stable hemodynamics, no use of vasoactive drugs and normal lactate levels were used as a control group. We collected SMA Doppler ultrasound parameters, including Peak Systolic Velocity (PSV), End Diastolic Velocity (EDV), Resistance Index (RI), pulsatility index (PI), Time-Averaged Mean Velocity (TAMV), and Blood Flow (BF).Results: In the cardiac shock group, SMA PSV, TAMV, and BF were lower compared to the other groups. There was no significant difference in SMA RI and PI between the different types of shock groups, but both were significantly lower than the control group. Cardiac index (CI) is correlated with SMA PSV (r = 0.487, P = 0.000) and TAMV (r = 0.538, P = 0.000), whereas SVRI is not correlated with SMA RI and PI. Lactate levels was correlation with SMA RI (r = -0.307, P = 0.000) and PI (r = -0.287, P = 0.000). The area under the ROC curve of SMA RI and PI to predict hyperlactatemia was 0.85[0.78-0.91] and 0.83[0.76–0.90].Conclusions: The velocity parameters of SMA Doppler ultrasound such as TAMV and PSV can reflect cardiac function. The measurements of SMA RI and PI are correlated with lactate levels, having a positive predictive value for hyperlactatemia and provide guidance for fluid resuscitation in patients with shock in the future.

Levosimendan and Dobutamin Attenuate LPS-Induced Inflammation in Microglia by Inhibiting the NF-κB Pathway and NLRP3 Inflammasome Activation via Nrf2/HO-1 Signalling.

Hypovolemic shock is a circulatory failure, due to a loss in the effective circulating blood volume, that causes tissue hypoperfusion and hypoxia. This condition stimulates reactive oxygen species (ROS) and pro-inflammatory cytokine production in different organs and also in the central nervous system (CNS). Levosimendan, a cardioprotective inodilator, and dobutamine, a β1-adrenergic agonist, are commonly used for the treatment of hypovolemic shock, thanks to their anti-inflammatory and antioxidant effects. For this reason, we aimed at investigating levosimendan and dobutamine's neuroprotective effects in an "in vitro" model of lipopolysaccharide (LPS)-induced neuroinflammation. Human microglial cells (HMC3) were challenged with LPS (0.1 µg/mL) to induce an inflammatory phenotype and then treated with levosimendan (10 µM) or dobutamine (50 µM) for 24 h. Levosimendan and dobutamine significantly reduced the ROS levels and markedly increased Nrf2 and HO-1 protein expression in LPS-challenged cells. Levosimendan and dobutamine also decreased p-NF-κB expression and turned off the NLRP3 inflammasome together with its downstream signals, caspase-1 and IL-1β. Moreover, a reduction in TNF-α and IL-6 expression and an increase in IL-10 levels in LPS-stimulated HMC3 cells was observed following treatment. In conclusion, levosimendan and dobutamine attenuated LPS-induced neuroinflammation through NF-κB pathway inhibition and NLRP3 inflammasome activation via Nrf2/HO-1 signalling, suggesting that these drugs could represent a promising therapeutic approach for the treatment of neuroinflammation consequent to hypovolemic shock.

Hypovolemic shock Hypovolemic Shock: How Does Lactic Acid Affect the Heart?

Hypovolemic shock is due to a critical loss in the effective circulating blood volume with systemic hypoperfusion. If left untreated, hypovolemic shock can lead to ischemic injury of vital organs, leading to multi-system organ failure and death. Hypovolemic shock is a potentially life-threatening condition (1,2). There are five causes of hypovolemic shock: hemorrhage, trauma, surgical intervention, burns, and fluid loss caused by vomiting or diarrhea. This woman was involved in a motor vehicle accident, which resulted in a traumatic crash (2,3). This was caused by blood loss to the abdomen, as the physical examination suggested (3). Early recognition and appropriate management are essential. Hypovolemic shock results from depletion of intravascular volume, whether by extracellular fluid loss or blood loss (1,2). The pre-shock stage is characterized by compensatory mechanisms with increased sympathetic tone resulting in increased heart rate, increased cardiac contractility, and peripheral vasoconstriction (2,3).

Cardio–Splenic Relationship in Patients Receiving Trans-Catheter Aortic Valve Replacement

Background: The spleen seems to be a significant buffer of the effective circulating blood volume by changing its size dramatically according to hemodynamics. The cardio–splenic relationship has been recently proposed in the literature regarding heart failure cohorts, and the splenic size has been proposed as a prognostic factor in these cohorts. However, the clinical implication of the splenic size in patients receiving trans-catheter aortic valve replacement (TAVR) remains unknown. Methods: Patients who underwent TAVR at our institute between 2015 and 2022 were eligible. Of these, the patients whose abdominal computed tomography imaging was obtained before TAVR were included. The volume of the spleen was measured in all the participants. The prognostic impact of the indexed splenic volume (SVI) on the 2-year cardiac death or heart failure readmissions was evaluated. Results: A total of 343 patients (86 years, 98 males) were included. The median value of the peak velocity at the aortic valve was 4.4 (4.0, 4.8) m/s and the median SVI was 65.5 (48.9, 86.9) mL/m2. A lower SVI tended to be associated with a lower cardiac output, whereas a higher SVI was associated with a higher plasma volume. The SVI was independently associated with the 2-year cardiac death or heart failure readmission after TAVR with a hazard ratio of 1.09 (95% confidence interval 1.01–1.18, p = 0.041), adjusted for potential confounders. A calculated cutoff of SVI was 70.2 mL/m2, which significantly stratified the cumulative incidence of the primary outcome (10% versus 4%, p = 0.033). Conclusion: A high baseline SVI, which was associated with systemic congestion, was associated with a higher incidence of cardiac death or heart failure readmission after TAVR. Further studies are warranted to clarify the detailed cardio–splenic relationship and implication of measuring the SVI in this cohort.

Perioperative Fluid Management and Volume Assessment

Fluid therapy is an integral component of perioperative care and helps maintain or restore effective circulating blood volume. The principal goal of fluid management is to optimize cardiac preload, maximize stroke volume, and maintain adequate organ perfusion. Accurate assessment of volume status and volume responsiveness is necessary for appropriate and judicious utilization of fluid therapy. To accomplish this, static and dynamic indicators of fluid responsiveness have been widely studied. This review discusses the overarching goals of perioperative fluid management, reviews the physiology and parameters used to assess fluid responsiveness, and provides evidence-based recommendations on intraoperative fluid management.

Aquaporins in Edema.

One of the most prevalent indications of water-electrolyte imbalance is edema. Aquaporins (AQPs) are a protein family that can function as water channels. Osmoregulation and body water homeostasis are dependent on the regulation of AQPs. Human kidneys contain nine AQPs, five of which have been demonstrated to have a role in body water balance: AQP1, AQP2, AQP3, AQP4, and AQP7. Water imbalance is connected with AQP dysfunction. Hyponatremia with elevated AQP levels can accompany edema, which can be caused by disorders with low effective circulating blood volume and systemic vasodilation, such as congestive heart failure (CHF), hepatic cirrhosis, or the syndrome of incorrect antidiuretic hormone secretion (SIADH). In CHF, upregulation of AQP2 expression and targeting is critical for water retention. AQP2 is also involved in aberrant water retention and the formation of ascites in cirrhosis of the liver. Furthermore, water retention and hyponatremia in SIADH are caused by increased expression of AQP2 in the collecting duct. Fluid restriction, demeclocycline, and vasopressin type-2 receptor antagonists are widely utilized to treat edema. The relationship between AQPs and edema is discussed in this chapter.

Effects and Mechanisms of Peritoneal Resuscitation on Acute Kidney Injury After Severe Burns in Rats.

Acute kidney injury (AKI) is a common complication in severe burn patients with poor prognosis and high mortality. Reduced kidney perfusion induced by the decreased effective circulating blood volume after severe burn is a common cause of AKI. Routine intravenous resuscitation (IR) is difficult or delayed in extreme conditions such as war and disaster sites. Peritoneal resuscitation (PR) is a simple, rapid resuscitation strategy via a puncture in the abdominal wall. This study investigated whether PR is a validated resuscitation strategy for AKI after severe burns in rats and explored its mechanisms. Eighty Sprague-Dawley rats were randomized into four groups: (1) sham group; (2) IR group, which was characterized by the full thickness burn of 50% of the total body surface area received IR immediately post-injury; (3) early PR group, in which rats with the same burn model received PR immediately post-injury; and (4) delayed resuscitation (DR) group, in which rats with the same burn model received no resuscitation within 3-hour post-injury. PR and DR groups animals received IR after 3-hour post-injury. The survival rate, mean arterial pressure, renal histopathology, renal function, indicators of renal injury, and renal hypoxia-inducible factor-1α and NADPH oxidase 4 (NOX4) proteins of rats were measured at 3 h, 12 h, and 24 h post-injury. Compared with rats in the DR group, rats in the PR group had a significantly improved survival rate (100% vs. 58.3% at 24 h, P = 0.0087), an increased mean arterial pressure (92.6 ± 6.6 vs. 65.3 ± 10.7, 85.1 ± 5.7 vs. 61.1 ± 6.9, 90.1 ± 8.7 vs. 74.9 ± 7.4 mmHg, at 3 h, 12 h, and 24 h, P < 0.01), a reduced renal water content rate (51.6% ± 5.0% vs. 70.1% ± 6.8%, 57.6% ± 7.7% vs. 69.5% ± 8.7%, at 12 h and 24 h, P < 0.01), attenuated histopathological damage, reduced serum creatinine expression (36.36 ± 4.27 vs. 49.98 ± 2.42, 52.29 ± 4.31 vs. 71.32 ± 5.2, 45.25 ± 2.55 vs. 81.15 ± 6.44 μmol/L, at 3 h, 12 h, and 24 h, P < 0.01) and BUN expression (7.62 ± 0.30 vs. 10.80 ± 0.58, 8.61 ± 0.32 vs. 28.58 ± 1.99, 8.09 ± 0.99 vs. 20.95 ± 1.02 mmol/L, at 3 h, 12 h, and 24 h, P < 0.01), increased kidney injury markers neutrophil gelatinase-associated lipocalin expression (95.09 ± 7.02 vs. 101.75 ± 6.23, 146.77 ± 11.54 vs. 190.03 ± 9.87, 112.79 ± 15.8 vs. 194.43 ± 11.47 ng/mL, at 3 h, 12 h, and 24 h, P < 0.01) and cystatin C expression (0.185 ± 0.006 vs. 0.197 ± 0.006, 0.345 ± 0.036 vs. 0.382 ± 0.013, 0.297 ± 0.012 vs. 0.371 ± 0.028 ng/mL, at 3 h, 12 h, and 24 h, P < 0.01), and reduced renal hypoxia-inducible factor-1α and NADPH oxidase 4 protein expression (P < 0.01). There was no significant difference between rats in the PR group and the IR group in the above indicators. Early PR could protect severe burn injury rats from AKI. It may be an alternative resuscitation strategy in severe burn injury when IR cannot be achieved.

Targeting Preload in Heart Failure: Splanchnic Nerve Blockade and Beyond.

Preload augmentation represents a critical mechanism for the cardiovascular system to increase effective circulating blood volume to increase cardiac filling pressures and, subsequently, for the heart to increase cardiac output. The splanchnic vascular compartment is the primary source of vascular capacity and thus the primary target for preload recruitment in humans. Under normal conditions, sympathetic stimulation of these primary venous vessels promotes the shift of blood from the splanchnic to the thoracic compartment and elevates preload and cardiac output. However, in heart failure, since filling pressures may be elevated at rest due to decreased venous capacitance, incremental recruitment of preload to enhance cardiac output may exacerbate congestion and limit exercise capacity. Accordingly, recent attention has focused on therapies designed to regulate splanchnic vascular redistribution to improve cardiac filling pressures and patient-centered outcomes such as quality of life and exercise capacity in patients with heart failure. In this review, we discuss the relevance of splanchnic circulation as a venous reservoir, the contribution of stressed blood volume to heart failure pathogenesis, and the implications for pharmacological therapeutic interventions to prevent heart failure decompensation. Further, we review emerging device-based approaches for cardiac preload reduction such as partial/complete occlusion of the superior vena cava or the inferior vena cava.

Application value of bedside ultrasound for assessing volume responsiveness in patients with septic shock

Background/Aim. Septic shock is a serious complication that can occur as consequence of infection. As the effective circulating blood volume is of vital importance in these cases, it is very important to keep track of this parameter constantly. The aim of this study was to explore the application value of bedside ultrasound for assessing volume responsiveness in patients with septic shock. Methods. A total of 102 patients with septic shock were selected. The volume load (VL) test was performed, and based on the results of the test, the patients were divided into the response group that had an increase in stroke volume (?SV ) ? 15% and non-response group (?SV &lt; 15%). Hemodynamic parameters were compared before and after the test. The correlation between ?SV and each hemodynamic index was explored by Pearson?s analysis. The receiver operating characteristic (ROC) curve was plotted. Results. There were 54 patients in response group and 48 patients in non-response group. Before VL test, retro-hepatic inferior vena cava (IVC) distensibility index (?IVC1), respiratory variation in IVC index (?IVC2), respiratory variation in aortic blood flow peak velocity index (?VpeakAO), respiratory variation in brachial artery blood flow peak velocity index (?VpeakBA) and respiratory variation in common femoral artery blood flow peak velocity index (?VpeakCFA) were all higher in response group than those in non-response group (p &lt; 0.05), while heart rate (HR), mean arterial pressure (MAP) and central venous pressure (CVP) were similar (p &gt; 0.05). After VL test, response group had significantly decreased HR, ?IVC1, ?IVC2, ?VpeakAO, ?VpeakBA and ?VpeakCFA, and increased MAP and CVP (p &lt; 0.05), while non-response group had significantly decreased CVP (p &lt; 0.05) and no significant changes in other indices. ?IVC1, ?IVC2, ?VpeakAO, ?VpeakBA and ?VpeakCFA significantly correlated with ?SV ( r= 0.589, r = 0.647, r = 0.697, r = 0.621, r = 0.766, p &lt; 0.05), but there was no correlation between CVP and ?SV (r = -0.345, p &gt; 0.05). The areas under the curves of ?IVC1, ?IVC2, ?VpeakAO, ?VpeakBA and ?VpeakCFA for predicting volume responsiveness were 0.839, 0.858, 0.878, 0.916 and 0.921, respectively, which were significantly larger than that of CVP (0.691), indicating higher sensitivity and specificity. Conclusion. Bedside ultrasound monitoring of ?IVC, ?VpeakAO, ?VpeakBA and ?VpeakCFA can better assess the volume responsiveness in patients with septic shock.

Coronavirus diseases 2019 and kidney injury: a brief review based on current evidence.

Coronavirus diseases 2019 and kidney injury: a brief review based on current evidence.

Evaluation of Hypervolemia in Children.

Hypervolemia is a condition with an excess of total body water and when sodium (Na) intake exceeds output. It can have different causes, such as hypervolemic hyponatremia (often associated with decreased, effective circulating blood volume), hypervolemia associated with metabolic alkalosis, and end-stage renal disease. The degree of hypervolemia in critically ill children is a risk factor for mortality, regardless of disease severity. A child (under 18 years of age) with hypervolemia requires fluid removal and fluid restriction. Diuretics are able to increase or maintain urine output and thus improve fluid and nutrition management, but their benefit in preventing or treating acute kidney injury is questionable.

Approach to haemoabdomen in small animal patients

Background: Haemoabdomen (also sometimes called haemoperitoneum) is the pathological accumulation of blood within the peritoneal cavity and can present a challenging clinical scenario. It frequently combines an emergency presentation with...

4. Midodrine for diuretic intractable ascites with hyponatremia

Background and Aims: Midodrine hydrochloride is an orally available, α-adrenergic agonist that increases effective circulating blood volume and renal perfusion by increasing systemic and splanchnic blood pressure. There is scanty data besides the study from North India, on use of midodrine in patients with cirrhosis and ascites with an additional component persistent hyponatremia and hypotension. Methods: In this single center observational study patients with diuretic intractable ascites (EASL criteria) with persistent hyponatremia (Serum Sodium <130 mEq/L) even after withholding the diuretics and albumin replacement (100 ml 20% per day) for 3 consecutive days were started on Midodrine 5 mg three times a day. The dose was increased to 7.5 mg three times a day at the end of 7 days if mean arterial pressure (MAP) remained less than 80. Tolvaptan 15 mg once a day was added at 15 days if serum sodium remained <125 mEq/L at 2 weeks. We excluded patients if there was proven sepsis or renal dysfunction (serum creatinine 1 mg/dl). Serum sodium was measured every week. Results: Ten patients were included (7 NASH, 3 ALD). The Mean age was 49 ± 2.1 years, with pretreatment MAP 73 mm of Hg (Range 70–78) serum sodium of 127 mEq/L (Range 118–130). At the end of six weeks, 6 patients were on 5 mg dose while 4 patients were on 7.5 mg dose. Only one patient required tolvaptan for 14 days (stopped once serum sodium reached 140). The mean arterial pressure was 86 mg of Hg (P < 0.05) and mean serum sodium levels were 136 mEq/L (Range 132–139) (p < 0.05). We were able to reintroduce low dose diuretics in 4 patients. Conclusions: Midodrine use can successfully reverse hyponatremia related diuretic intractable refractory ascites in 40% cases besides significantly improving serum sodium levels and mean arterial blood pressures. The author has none to declare.

Hyponatremia in children with acute respiratory infections: A reappraisal.

Hyponatremia (<135 mmol/L), typically associated with an elevated anti-diuretic hormone level, is common among children admitted with bronchiolitis, pneumonia, or pulmonary exacerbation of cystic fibrosis. The main consequences of acute hyponatremia include cerebral edema and Ayus-Arieff pulmonary edema. A widespread belief is that, in children with pneumonia or bronchiolitis, hyponatremia results from inappropriate anti-diuresis. By contrast, the pathogenic role of extracellular fluid volume depletion or decreased effective circulating blood volume is underscored. Considering the prevalence of hyponatremia, sodium determination is advised on admission in children diagnosed with bronchiolitis, pneumonia, or pulmonary exacerbation of cystic fibrosis. There is no necessity to do anything beyond reassessing the appropriateness of fluid therapy in cases with mild (130-134 mmol/L) hyponatremia. In children with sodium <130 mmol/L, the underlying etiology is sometimes evident from history and physical findings. Given that clinical assessment of fluid volume status is difficult in hyponatremia, further laboratory evaluation is often required in these patients. An increase in sodium level ≤6 mmol/L per day is currently considered the therapeutic goal in all cases. Emergency correction with a 2 mL/kg body weight bolus of 3.0% saline over 10-15 min intravenously is advised in cases with severe symptoms due to hyponatremia and in cases with symptoms, even if mild, due to a rapid-onset (<48 h) of hyponatremia (two additional doses are administered if the patient's condition does not improve).

A Study on Acute Kidney Injury in Intensive Care Setting

A Study on Acute Kidney Injury in Intensive Care Setting

Reliability of mannitol for fluid responsiveness test in patients undergoing intracranial surgery

Objective To evaluate the reliability of mannitol for fluid responsiveness test in the patients undergoing intracranial surgery. Methods Sixty-two ASA physical status Ⅰ or Ⅱ patients, aged 18-64 yr, with body mass index of 18-25 kg/m2, scheduled for elective intracranial surgery, were enrolled in the study.The patients were mechanically ventilated after induction of anesthesia.The radial artery and central vein were cannulated, and FloTrac™/Vigileo™ system was connected for stroke volume variation monitoring.Before infusion of mannitol, effective circulating blood volume was confirmed according to stroke volume variation.20% mannitol 250 ml was infused over 20 min starting from onset of craniotomy.The fluid responsiveness test was recorded at the end of mannitol infusion. Results The sensitivity of fluid responsiveness test was 43%, and the specificity of fluid responsiveness test was 44%. Conclusion Mannitol can not be used for fluid responsiveness test in the patients undergoing intracranial surgery. Key words: Mannitol; Diagnostic tests, routine; Fluid therapy; Neurosurgical procedures

Perioperative fluid therapy: a statement from the international Fluid Optimization Group.

BackgroundPerioperative fluid therapy remains a highly debated topic. Its purpose is to maintain or restore effective circulating blood volume during the immediate perioperative period. Maintaining effective circulating blood volume and pressure are key components of assuring adequate organ perfusion while avoiding the risks associated with either organ hypo- or hyperperfusion. Relative to perioperative fluid therapy, three inescapable conclusions exist: overhydration is bad, underhydration is bad, and what we assume about the fluid status of our patients may be incorrect. There is wide variability of practice, both between individuals and institutions. The aims of this paper are to clearly define the risks and benefits of fluid choices within the perioperative space, to describe current evidence-based methodologies for their administration, and ultimately to reduce the variability with which perioperative fluids are administered.MethodsBased on the abovementioned acknowledgements, a group of 72 researchers, well known within the field of fluid resuscitation, were invited, via email, to attend a meeting that was held in Chicago in 2011 to discuss perioperative fluid therapy. From the 72 invitees, 14 researchers representing 7 countries attended, and thus, the international Fluid Optimization Group (FOG) came into existence. These researches, working collaboratively, have reviewed the data from 162 different fluid resuscitation papers including both operative and intensive care unit populations. This manuscript is the result of 3 years of evidence-based, discussions, analysis, and synthesis of the currently known risks and benefits of individual fluids and the best methods for administering them.ResultsThe results of this review paper provide an overview of the components of an effective perioperative fluid administration plan and address both the physiologic principles and outcomes of fluid administration.ConclusionsWe recommend that both perioperative fluid choice and therapy be individualized. Patients should receive fluid therapy guided by predefined physiologic targets. Specifically, fluids should be administered when patients require augmentation of their perfusion and are also volume responsive. This paper provides a general approach to fluid therapy and practical recommendations.

The Current Opinions of Capillary Leak Syndrome

Capillary Leak Syndrome (CLS) in patients with severe course of disease is more and more common, and the clinical manifestations of CLS include systemic edema, hypoproteinemia, effective circulating blood volume reduction and hemoconcentration. The common pathogenies are sepsis, severe trauma, cardiopulmonary bypass and so on. Clinically, CLS is usually divided into leakage period and recovery period, with different pathophysiologic process, clinical manifestation and treatment in different period respectively. Although there are more treatments, they are not effective treatment measures. There have been so many studies about improvement of endothelial function, macromolecular colloid liquid applications, and continuous blood purification treatment. Systematic understanding of the pathological mechanism, clinical manifestations and staging, diagnosis and treatment of the CLS has a guiding value.

Contemporary management of arrhythmias during pregnancy.

Cardiac arrhythmias are among the most common cardiac complications encountered during pregnancy.1 In some, pregnancy may trigger exacerbations of pre-existing arrhythmias, whereas in others arrhythmias may manifest for the first time.2 Fortunately, severe arrhythmias requiring aggressive or invasive therapies are rare. There are unfortunately few randomized studies, little data on the efficacy or safety of antiarrhythmic drugs (AADs), or even explicit guidelines to support decision making on pregnant women with arrhythmias. Thus, much of the clinical care is guided by knowledge of the physiology of pregnancy and educated risk/benefit decisions made in collaboration with high-risk obstetric colleagues in Maternal-Fetal Medicine, as well as with the patient. The precise mechanism of increased arrhythmia burden during pregnancy is unclear, but it is likely because of a combination of hemodynamic, hormonal, and autonomic changes. Increases in effective circulating blood volume of 30% to 50% are seen beginning at 8 weeks of gestation and peaking at ≈34 weeks. Cardiac output is increased as well, with an average of 6.7 L/min in the first trimester and ≤8.7 L/min in the third trimester. This is the result of a 35% increase in stroke volume and a 15% increase in heart rate. The increase in plasma volume causes stretching of atrial and ventricular myocytes, and this may result in early after depolarizations, shortened refractoriness, slowed conduction, and spatial dispersion through activation of stretch-activated ion channels.3,4 A larger heart can also potentially sustain re-entry more easily because of an increase in path length of potential reentrant circuits. The increase in heart rate during pregnancy, seen predominantly in the third trimester, may also predispose to arrhythmia, as a high resting heart rate has been associated with markers of arrhythmogenesis.5 Hormonal and autonomic changes may also contribute to arrhythmogenesis. Estradiol and progesterone have been …

Therapeutic effects of compound hypertonic saline on rats with sepsis

Sepsis is one of the major causes of death and is the biggest obstacle preventing improvement of the success rate in curing critical illnesses. Currently, isotonic solutions are used in fluid resuscitation technique. Several studies have shown that hypertonic saline applied in hemorrhagic shock can rapidly increase the plasma osmotic pressure, facilitate the rapid return of interstitial fluid into the blood vessels, and restore the effective circulating blood volume. Here, we established a rat model of sepsis by using the cecal ligation and puncture approach. We found that intravenous injection of hypertonic saline dextran (7.5% NaCl/6% dextran) after cecal ligation and puncture can improve circulatory failure at the onset of sepsis. We found that the levels of tumor necrosis factor-α, interleukin-1β, interleukin-6 and intracellular adhesion molecule 1 levels in the lung tissue of cecal ligation and puncture rats treated with hypertonic saline dextran were significantly lower than the corresponding levels in the control group. We inferred that hypertonic saline dextran has a positive immunoregulatory effect and inhibits the overexpression of the inflammatory response in the treatment of sepsis. The percentage of neutrophils, lung myeloperoxidase activity, wet to dry weight ratio of lung tissues, histopathological changes in lung tissues, and indicators of arterial blood gas analysis was significantly better in the hypertonic saline dextran-treated group than in the other groups in this study. Hypertonic saline dextran-treated rats had significantly improved survival rates at 9 and 18h compared to the control group. Our results suggest that hypertonic saline dextran plays a protective role in acute lung injury caused after cecal ligation and puncture. In conclusion, hypertonic/hyperoncotic solutions have beneficial therapeutic effects in the treatment of an animal model of sepsis.