Effect Of Hypertonic Saline Research Articles

Effect of hypertonic saline on rat hypothalamic paraventricular nucleus parvocellular neurons in vitro

The effects of hypertonic saline on hypothalamic paraventricular nucleus (PVN) parvocellular neurons were examined using whole-cell patch-clamp technique. Under current-clamp, 50% (41/82) of parvocellular neurons were depolarized than the predicted values by hypertonic saline, and associated with increasing action potential frequency. Under voltage-clamp, unless hypertonic saline induced a shift of reverse potential to more positive values, neither mannitol nor hypertonic saline obviously increased the conductance in parvocellular neurons. Moreover, spontaneous excitatory postsynaptic currents (sEPSCs) were increased by isotonic increases in [Na +] o in the parvocellular neurons. Bath application AMPA receptor antagonist CNQX or non-selective glutamate antagonist kynurenic acid almost completely blocked the sEPSCs. Extracellular application of gadolinium (Gd 3+) blocked the hypertonic saline-induced response. These results suggested that subpopulation of PVN parvocellular neurons are selectively sensitive to NaCl. Hypertonic saline excited the PVN parvocellular neurons through Na +-detection and the excitatory glutamatergic synaptic input.

Role of the mTOR Pathway in LPS-Activated Monocytes: Influence of Hypertonic Saline

As heightened protein synthesis is the hallmark of many inflammatory syndromes, we hypothesize that the mammalian target of rapamycin (mTOR) pathway, which control the cap-dependent translation initiation phase, was activated by lipopolysaccharide (LPS). In addition, we studied the effect of hypertonic saline solution (HTS) on the mTOR cascade in peripheral blood mononuclear cells (PBMCs). PBMCs were isolated from healthy volunteers and treated with LPS. Cells were pretreated with phosphatidylinositol 3-kinase (PI3K) and mTOR inhibitors, or with HTS. Supernatants were harvested 20 h following LPS treatment, and interleukin-10 (IL-10), interleukin-6 (IL-6) and tumor necrosis alpha (TNFα) were analyzed by ELISA. Immunoblot experiments were performed for components of the PI3K/Akt/mTOR pathway at various time points. RNA was extracted after 90 min for real-time RT-PCR quantification. The mTOR pathway is activated in PBMCs within 1 h of LPS stimulation. Pretreatment with rapamycin, a specific inhibitor of mTOR, resulted in a significant decrease of IL-10 and IL-6 translation and expression but did not affect the LPS-induced TNFα production. Both the mTOR pathway and the LPS-induced IL-6 production were down-regulated by HTS pretreatment. The PI3k/Akt/mTOR cascade modulates LPS-induced cytokines production differentially. IL-10 and IL-6 expression are both up-regulated by activation of the mTOR pathway in response to LPS in PBMCs, while TNFα is not controlled by the mTOR cascade. Meanwhile, pretreatment of PBMCs with a HTS solution suppresses mTOR activity as well as LPS-induced IL-6, suggesting a more central role for mTOR as a regulator of the immuno-inflammatory response.

Effect of hypertonic saline on electrocardiography QRS duration in rabbit model of bupivacaine toxicity resuscitated by intravenous lipid

Intravenous lipid emulsion is established therapy for bupivacaine induced cardiotoxicity. The benefit of combined hypertonic saline and lipid treatment is unexplored. In this experiment, sedated rabbits were resuscitated from bupivacaine-induced asystole with intravenous lipid according to the Association of Anaesthetists of Great Britain and Ireland's guideline, or by identical lipid dosing with hypertonic saline: 6 mEq x kg(-1) 21% sodium chloride. Early electrocardiography QRS prolongation was less with lipid plus hypertonic saline (mean (SD) QRS 0.19 (0.07) s lipid only vs 0.09 (0.01) s lipid plus hypertonic saline; p = 0.003) at 9 min though not different from the lipid only group at 20 min. No difference was observed in rates of circulatory return (7/10 lipid only and 9/10 lipid plus hypertonic saline; p = 0.58) or survival (5/10 lipid only and 6/10 lipid plus hypertonic saline; p = 1.00). Some benefit to cardiac conduction may be afforded by hypertonic saline co-administered with lipid emulsion in bupivacaine-induced cardiotoxicity.

T1948 Further Insights on the Mechanisms of the Beneficial Effect of Hypertonic Saline Solution in Acute Pancreatitis

lower esophageal sphincter length and pressure were collected using high-resolution manometry (Sierra Scientific Instruments, Los Angeles, CA). These parameters were recorded after complete dissection of the hiatus and after each of the individual components. Results: Between May and October 2009, 18 patients were enrolled and randomized. There was no difference between the groups in terms of demographics, size of the hernia, severity of GERD or presence of Barrett's esophagus. Overall, mean LES length was significantly increased by 1.3 cm (p 0.7). Although there is a trend toward a greater contribution by hiatal closure versus the fundal wrap on LES pressure, the difference is not significant (P=0.07) Conclusion: The aim of anti-reflux surgery is to restore the function of the LES. This is accomplished by increasing both LES length and pressure. In attempting to achieve these objectives, the laparoscopic Nissen fundoplication relies on two main components: the crural closure and the construction of a 360 degree fundal wrap. We have demonstrated that each of these components is equally important in establishing both increased LES length as well as increased LES pressure.

Effects of hypertonic saline solution in inflammatory response in sepsis

Sepsis is a systemic inflammatory response to infection and a major cause of mortality. The hypertonic saline solution (HSS) has been showed to improve hemodynamic and inflammatory response. We studied the hypertonic solution effects in sepsis through cecal ligation and puncture (CLP) in mice Balb‐C, divided in 3 groups: CLP without treatment (C); CLP treated with saline solution 0,9% ‐ 34mg/Kg (SS); CLP treated with HSS 7,5% ‐ 4ml/Kg (SH); and a 4° group to indicate the basal values without both CLP and treatment; both treatments (HSS and saline) were applied 30 min after CLP. The lung was collected after 6, 12 e 24 h to analyze cytokines levels by ELISA and nitric oxide (NO) by Griess method. The group SH showed higher survival rates (60%) when compared to SS (46,6%) and C (33,3%). The SS group (27,3 ± 3,05 pg/ml) presented increased TNF‐α level in 12 h when compared to group C (14,07 ± 1,68 pg/ml) and SH (19,66±3,19 pg/ml). After 24 h the SH (6,2 ± 3,5 pg/ml) decreased TNF‐α when compared to C (73,40± 49,52 pg/ml); IL‐10 level in 24 h was increased in C (CLP ‐ 3,12 ± 0,46 pg/ml) and SS (2,9 ± 0,9 pg/ml) in relation to SH (0,59 ± 0,34 pg/ml). NO concentration was lower in SH (2,26 ± 1,34 pg/ml) compared with C (10,96 ± 2,2 pg/ml) after 24 h. The HSS protects the animal against sepsis, but saline solution doesn't. Our results suggest that the volume replacement of both treatments modulate pro and anti‐inflammatory cytokines and NO. CAPES.FAPESP.

Effects of hypertonic saline on a pig model of acute lung injury induced by hydrochloric acid instillation

Controversy exists over the possible beneficial effects of hypertonic saline (HS) in pulmonary inflammatory response, particularly in neutrophil immunomodulation [1,2]. This study was designed to investigate possible benefits of HS in the treatment of pigs submitted to experimental acute lung injury.

Hypertonic saline reduces metalloproteinase expression in liver during pancreatitis

1. We recently demonstrated that hypertonic saline reduces inflammation and mortality in acute pancreatitis. The present study investigated the effects of hypertonic saline in metalloproteinase (MMP) regulation and pancreatitis-associated hepatic injury. 2. Wistar rats were divided into four groups: (i) control, not subjected to insult or treatment; (ii) no treatment (NT), induction of pancreatitis (retrograde infusion of 2.5% sodium taurocholate (1.0 mL/kg)), but no further treatment; (iii) normal saline (NS), induction of pancreatitis and treatment with normal saline (0.9% NaCl, 34 mL/kg, i.v. bolus, 1 h after the induction of pancreatitis); and (iv) hypertonic saline (HS), induction of pancreatitis and treatment with hypertonic saline (7.5% NaCl, 4 mL/kg administered over a period of 5 min, 1 h after the induction of pancreatitis). In all four groups, 4, 12 and 24 h after the induction of pancreatitis, liver tissue samples were assayed to determine levels of MMP-2, MMP-9, 47 kDa heat shock protein (HSP47) and collagen (Type I and III). 3. Compared with the control group, MMP-9 expression and activity was increased twofold in the NS and NT groups 4 and 12 h after the induction of pancreatitis, but remained at basal levels in the HS group. In contrast, MMP-2 expression was increased twofold 12 h after the induction of pancreatitis only in the NS group, whereas the expression of HSP47 was increased 4 h after the induction of pancreatitis in the NS and NT groups. Greater extracellular matrix remodelling occurred in the NS and NT groups compared with the HS group, probably as a result of the hepatic wound-healing response to repeated injury. However, the collagen content in hepatic tissue remained at basal levels in the HS group. 4. In conclusion, the results of the present study indicate that hypertonic saline is hepatoprotective and reduces hepatic remodelling, maintaining the integrity of the hepatic extracellular matrix during pancreatitis. Hypertonic saline-mediated regulation of MMP expression may have clinical relevance in pancreatitis-associated liver injury.

Timing-dependent protection of hypertonic saline solution administration in experimental liver ischemia/reperfusion injury

During liver ischemia, the decrease in mitochondrial energy causes cellular damage that is aggravated after reperfusion. This injury can trigger a systemic inflammatory syndrome, also producing remote organ damage. Several substances have been employed to decrease this inflammatory response during liver transplantation, liver resections, and hypovolemic shock. The aim of this study was to evaluate the effects of hypertonic saline solution and the best timing of administration to prevent organ injury during experimental liver ischemia/reperfusion. Rats underwent 1 hr of warm liver ischemia followed by reperfusion. Eighty-four rats were allocated into 6 groups: sham group, control of ischemia group (C), pre-ischemia treated NaCl 0.9% (ISS) and NaCl 7.5% (HTS) groups, pre-reperfusion ISS, and HTS groups. Blood and tissue samples were collected 4 hr after reperfusion. HTS showed beneficial effects in prevention of liver ischemia/reperfusion injury. HTS groups developed increases in AST and ALT levels that were significantly less than ISS groups; however, the HTS pre-reperfusion group showed levels significantly less than the HTS pre-ischemia group. No differences in IL-6 and IL-10 levels were observed. A significant decrease in mitochondrial dysfunction as well as hepatic edema was observed in the HTS pre-reperfusion group. Pulmonary vascular permeability was significantly less in the pre-reperfusion HTS group compared to the ISS group. No differences in myeloperoxidase activity were observed. The liver histologic score was significantly less in the pre-reperfusion HTS group compared to the pre-ischemia HTS group. HTS ameliorated local and systemic injuries in experimental liver ischemia/reperfusion. Infusion of HTS in the pre-reperfusion period may be an important adjunct to accomplish the best results.

The effects of hypertonic saline and nicotinamide on sensorimotor and cognitive function following cortical contusion injury in the rat

Hypertonic saline (HTS) is an accepted treatment for traumatic brain injury (TBI). However, the behavioral and cognitive consequences following HTS administration have not thoroughly been examined. Recent preclinical evidence has suggested that nicotinamide (NAM) is beneficial for recovery of function following TBI. The current study compared the behavioral and cognitive consequences of HTS and NAM as competitive therapeutic agents for the treatment of TBI. Following controlled cortical impact (CCI), bolus administrations of NAM (500 mg/kg), 7.5% HTS, or 0.9% saline Vehicle (1.0 mL/kg) were given at 2, 24, and 48 h post-CCI. Behavioral results revealed that animals treated with NAM and HTS showed significant improvements in beam walk and locomotor placing compared to the Vehicle group. The Morris water maze (MWM) retrograde amnesia test was conducted on day 12 post-CCI and showed that all groups had significant retention of memory compared to injured, Vehicle-treated animals. Working memory was also assessed on days 8–20 using the MWM. The NAM and Vehicle groups quickly acquired the task; however, HTS animals showed no acquisition of this task. Histological examinations revealed that the HTS-treated animals lost significantly more cortical tissue than either the NAM or Vehicle-treated animals. HTS-treated animals showed a greater loss of hippocampal tissue compared to the other groups. In general, NAM showed a faster rate of recovery than HTS without this associated tissue loss. The results of this study reiterate the strengths of NAM following injury and show concerns with bolus administrations of HTS due to the differential effects on cognitive performance and apparent tissue loss.

Antiedema effects of hypertonic saline after spinal cord injury*

Antiedema effects of hypertonic saline after spinal cord injury*

Effects of hypertonic saline on T-lymphocyte subpopulations in patients with traumatically hemorrhagic shock

Objective To investigate the potential and early effect of hypertonic saline resuscitation on Tlymphocyte subpopulations in patients with traumatically hemorrhagic shock.Method Eighty-two patients with acute traumatically hemorrhagic shock admitted from Department of Emergency，Beijing Tongren Hospital，from December 2006 to July 2008 were randomly divided into：hypotonic saline(HS)group(n=43)and Lactated Ringer's solution(LR)group(n=39).The criteria of eligible patients were systolic blood pressure＜90mm Hg at admission with definite evidence of blood loss.Patients with immune system diseases and those who died within 24 hours of admission were excluded.Patients in HS group received intravenous administration of 200 mL of 7.5% sodium chloride withhin 15～20 minutes，and LR group received routine therapy with Lactated Ringer's solution.Blood pressure and heart rate were recorded 10，20，and 60 minutes after the start of resuscitation and compared between two groups.Before and 24 hours after treatment，peripheral blood levels of T-lymphocyte subpopulationsincluding CD3+，CD4+，and CD8+ were measured by using direct immunofluorescence test and compared between two groups.The inter-group comparison was carried out by using independent sample t-lest and intragroup comparison using paired t-test.The numabers of operation，complication cases and death cases were conducted by using X2 test.SPAS version 11.0 software was used for statistical analysis.Results The volume of solution infused in HS group was(3820±623)mL and in LR group was(5430±1254)mL(P＜0.05).At 10 and 20 minutes after the sdministration of solution.the mean blood pressures in HS group were both significantly higher than those in LR group(P＜0.01).The levels of CD3+and CD4+lymphocytes in peripheral blood in HS group 24 hours after treatment were sinificantly higher than those in LR group(P＜0.01).Totally，63(76.8%)patients were cured and 19(23.2%)patients died.ARDS occurred in 10 patients and MODS occurred in 14 patiellts.The mortality，and the rates of ARDS and MODS in HS group were sinificantly higher than those in LP group(P＜0.05).Conclusiom In patients with acute traumatically hemorrhagic shock.HS can increase the effective circulating vol.ume，ameliorate the perfusion of tissues and organs，improve the immune fuction of T-lymphocytes，decrease the rats of ABDS and MODS，mad decrease the morality.HS is more effective than routine solution used for resuscitation. Key words: Hemorrhagic shock; Trauma; Hypertonic saline; T-lymphocyte subpopulations

73. The Effect of Hypertonic Saline and Phosphodiesterase Inhibition on the PI3K/Akt Pathway in Neutrophil Oxidative Burst

Background: Neutrophils play an important role in the innate immune response to invading microorganisms. An exaggerated inflammatory response leads to the generation of cytokines and toxic radicals that can be injurious to the host. In sepsis and hemorrhagic shock, hypertonic saline (HS) and Pentoxifylline (PTX), a phosphodiesterase inhibitor, have been shown to decrease neutrophil oxidative burst and proinflammatory mediator synthesis alone, and synergistically when given in combination (HSPTX).

Effects of hypertonic saline on the development of acute lung injury following traumatic shock

Hypertonic saline (HS) is a promising fluid resuscitation therapy with the potential to reduce lung injury caused by severe trauma. The experimental evidence that HS has hemodynamic, anti-inflammatory, immunological, and neuroprotective properties and that it attenuates post-traumatic lung injury and multiple organ dysfunction syndrome (MODS) is undeniable. Laboratory evidence continues to accumulate to suggest that administration of HS affects cells, organs, and the neuro-humoral response to trauma, which affects both the innate and adaptive immunity. In contrast to the experimental findings, no clinical study to date has demonstrated that resuscitation of trauma patients with HS significantly reduces lung injury and MODS. Two recent clinical trials have confirmed that HS exerts similar hemodynamic, anti-inflammatory, and immunological effects as in experimental models. While it is possible that in humans such effects do not result in attenuation of post-traumatic lung injury and MODS, another explanation could be that no clinical study to date was powered to identify such clinical outcomes. An ongoing large, multicenter, randomized clinical trial across the USA and Canada is the first that is powered to determine whether resuscitation with a single dose of HS reduces post-traumatic lung dysfunction and consequently should become part of the resuscitation of severely traumatized patients.

Instructions for Obtaining Journal CME Credit

Anesthesiology’s journal-based CME program is open to all readers. Members of the American Society of Anesthesiologists participate at a preferred rate, but you need not be an ASA member or a journal subscriber to take part in this CME activity. Please complete the following steps:The American Society of Anesthesiologists is approved by the Accreditation Council for Continuing Medical Education (ACCME) to sponsor continuing medical education programs for physicians.The American Society of Anesthesiologists designates this educational activity for a maximum of 1 AMA PRA Category 1 Credit™ . Physicians should only claim credit commensurate with the extent of their participation in the activity.Purpose: The focus of the journal-based CME program, and the articles chosen for the program, is to educate readers on current developments in the science and clinical practice of the specialty of Anesthesiology.Target Audience: Physicians and other medical professionals whose medical specialty is the practice of anesthesia.Learning Objectives: After reading this article, participants should have a better understanding of the physiology of hyperosmolar therapy and its effect on brain relaxation.Authors – Irene Rozet, M.D., Nuj Tontisirin, M.D., Saipin Muangman, M.D., Monica S. Vavilala, M.D., Michael J. Souter, M.B., Ch.B., F.R.C.A., Lorri A. Lee, M.D., M. Sean Kincaid, M.D., Gavin W. Britz, M.D., M.P.H., and Arthur M. Lam, M.D., F.R.C.P.C.Grants or research support: NoneConsultantships or honoraria: NoneThe article authored by Drs. Rozet, Tontisirin, Muangman, Vavilala, Souter, Lee, Kincaid, Britz, and Lam was supported solely from institutional and/or departmental sources.Authors – David L. McDonagh, M.D., and David S. Warner, M.D.Grants or research support: NoneConsultantships or honoraria: NoneThe article authored by Drs. McDonagh and Warner was supported solely from institutional and/or departmental sources.Question Writers – Peter L. Bailey, M.D., and Leslie C. Jameson, M.D.Drs. Bailey and Jameson have no grants, research support, or consultant positions, nor do they receive any honoraria from outside sources, which may create conflicts of interest concerning this CME program.Based on the article by Rozet et al . entitled “Effect of equiosmolar solutions of mannitol versus hypertonic saline on intraoperative brain relaxation and electrolyte balance”http://content.wkhealth.com/linkback/openurl/trusted?issn=0003-3022&volume=102&issue=1&spage=188&part=fulltextand its accompanying editorial by McDonagh and Warner entitled “Hypertonic saline for craniotomy?”http://content.wkhealth.com/linkback/openurl/trusted?issn=0003-3022&volume=102&issue=1&spage=3&part=fulltextin the November issue of Anesthesiology, choose the one correct answer for each question:1. Which of the following statements about the effects of hypertonic saline is most likely true?A. It crosses the normal blood–brain barrier.B. It causes a diuresis.C. It reduces brain bulk.D. It is recommended for treatment of increased intracranial pressure in traumatic brain injury.2. The shared physiologic effects of 20% mannitol and 3% hypertonic saline include all of the following except A. Reduction in blood cell sizeB. Increase in cerebrospinal fluid sodium concentrationC. Reduction in cerebrospinal fluid productionD. Increase in serum osmolality3. Which of the following statements about the reflection coefficient is most likely true?A. It measures the relative permeability of a solute through the blood–brain barrier.B. Hypertonic saline has a lower reflection coefficient than mannitol.C. Drugs that do not penetrate the blood–brain barrier have a reflection coefficient of 0.D. The reflection coefficient of sodium indicates it readily crosses the blood–brain barrier.4. When comparing the effect of administering equivolemic and equiosmolar solutions of 3% hypertonic saline or 20% mannitol on brain relaxation, which of the following statements is most likely true?A. They produce clinically equal degrees of brain relaxation.B. More patients with subarachnoid hemorrhage require an additional dose of hypertonic saline.C. More patients with subarachnoid hemorrhage require an additional dose of mannitol.D. Mannitol provides better brain relaxation.5. Which of the following statements about the administration of equivolemic and equiosmolar solutions of 3% hypertonic saline or 20% mannitol is most likely true?A. Arterial lactate concentrations are greater after hypertonic saline.B. Arteriovenous oxygen differences are greater with mannitol.C. A stepwise increase in serum potassium occurs with hypertonic saline.D. Acute hyponatremia occurs with mannitol.

Effects of hypertonic saline solution and mannitol in acute intracranial hypertension in rabbits

Review the current, extensive, litera-ture on this topic in order to analyze whether the ra-diographic criteria mentioned in several studies (ky-phosis, wegding of the vertebra, spinal canal com-pression, and ligament lesion) can be used to indicate instability of the burst fracture and the need for surgi-cal treatment in patients without neurological deficit.

The effect of hypertonic saline solution on vasodilatation of the superior sagittal sinus using magnetic resonance imaging in normovolemic dogs

Several animal studies have demonstrated the beneficial effects of hypertonic saline (HSS) on cerebral blood flow, intracranial pressure and brain water content. This study aimed to investigate, using magnetic resonance imaging, whether a small volume of HSS is superior to dextran in vasodilatation of cerebral vessels and reduction of cerebrospinal fluids in dogs. HSS induced a significant expansion of the cross-section of the superior sagittal sinus in the axial transverse section of the pituitary and a decrease in cerebrospinal fluid area in the axial transverse section of the epencephalon more than dextran 40 did ( p < 0.001, respectively). However, the relative plasma volume in the dog which received dextran 40 was significantly higher after t = 30 min than in the HSS group ( p < 0.001). Therefore, it is suggested that HSS might be superior to colloid solutions in improving cerebral circulation, whereas dextran 40 is superior to HSS in enhancing systemic circulation in dogs.

130 Effect of hypertonic saline on Exhaled Breath Condensate

130 Effect of hypertonic saline on Exhaled Breath Condensate

Treating Ischemic Left Ventricular Dysfunction With Hypertonic Saline Administered After Coronary Occlusion in Pigs

The effects of hypertonic saline on ventricular function are controversial, whether it is increasing contractility or preload. There are no data, however, on the influence of hypertonic saline in a stunned myocardium. This study was prospective and randomized in order to analyze the effects of hypertonic saline solution (7.5%) on myocardial function and systemic hemodynamics in a porcine model of ischemia and reperfusion. A university teaching hospital, animal research laboratory. Twelve adult domestic swine. Myocardial stunning was produced by the complete occlusion of the proximal left anterior descending artery for 15 minutes followed by reperfusion. Five minutes after reperfusion, the animals were assigned to receive 4 mL/kg of hypertonic saline (n = 7) or normal saline (n = 5) over 10 minutes. Pressure-tipped catheters were placed in the left ventricular cavity and aorta. The dimensions of the left ventricle were measured with ultrasonic microcrystals. Cardiac output was measured with transit time ultrasound. Data were recorded continuously and compared before the occlusion, 5 minutes after reperfusion, and at the end of the infusion. Compared with baseline, ventricular function was significantly depressed after left anterior descending artery occlusion. Left ventricular dP/dT and its end-systolic pressure-volume slope decreased (38% and 52%, respectively; p < 0.05), with a concomitant increase in systemic vascular resistance. The administration of hypertonic saline significantly improved left ventricular function (Emax 1,422 +/- 198 mmHg/mL, and dP/dT 3.2 +/- 0.4 mmHg/s v normal saline group values of 1,156 +/- 172 and 2.5 +/- 0.5, respectively; p < 0.05), cardiac output (2.5 +/- 0.5 v 1.84 +/- 0.4 L/min, p < 0.05), and lowered systemic vascular resistance (from 28.8 +/- 2.3 to 23.5 +/- 1.4, p < 0.05), with no significant changes with normal saline administration. After transient myocardial ischemia, hypertonic saline administered over a short period of time acts as an inodilator by increasing contractility while simultaneously lowering systemic vascular resistance.

207: The effects of hypertonic saline and phosphodiesterase inhibition on neutrophil MAPK signaling: The whole is greater than the sum of its parts

Background: Ringer’s lactate (RL), the current standard resuscitation fluid used in the treatment of hemorrhagic shock, has been shown to increase neutrophil (PMN) activation, superoxide radical production, and subsequent end-organ injury. Therefore, the ideal resuscitation fluid which has yet to be defined may potentially be a combination or cocktail of different solutions with unique mechanism of actions on the inflammatory cascade. Hypertonic saline (HS) and the nonspecific phosphodiesterase inhibitor pentoxifylline (PTX) are both capable of attenuating PMN function and activation after shock and sepsis.

Effects of hypertonic saline solution and pentoxifylline on rat mesenteric microcirculation after hemorrhagic shock/reperfusion followed by cecal ligation/puncture: an intravital microscopic study

Effects of hypertonic saline solution and pentoxifylline on rat mesenteric microcirculation after hemorrhagic shock/reperfusion followed by cecal ligation/puncture: an intravital microscopic study