Resuscitation Of Hemorrhagic Shock Research Articles

Resuscitation of haemorrhagic shock with normal saline vs. lactated Ringer's: effects on oxygenation, extravascular lung water and haemodynamics

IntroductionPulmonary oedema and impairment of oxygenation are reported as common consequences of haemorrhagic shock and resuscitation (HSR). Surprisingly, there is little information in the literature examining differences in crystalloid type during the early phase of HSR regarding the development of pulmonary oedema, the impact on oxygenation and the haemodynamic response. These experiments were designed to determine if differences exist because of crystalloid fluid type in the development of oedema, the impact on oxygenation and the haemodynamic response to fluid administration in early HSR.MethodsTwenty anaesthetised swine underwent a grade V liver injury and bled without resuscitation for 30 minutes. The animals were randomised to receive, in a blinded fashion, either normal saline (NS; n = 10) or lactated Ringer's solution (LR; n = 10). They were then resuscitated with study fluid to, and maintained at, the preinjury mean arterial pressure (MAP) for 90 minutes.ResultsExtravascular lung water index (EVLWI) began to increase immediately with resuscitation with both fluid types, increasing earlier and to a greater degree with NS. A 1 ml/kg increase in EVLWI from baseline occurred after administartion of (mean ± standard error of the mean) 68.6 ± 5.2 ml/kg of normal saline and 81.3 ± 8.7 ml/kg of LR (P = 0.027). After 150 ml/kg of fluid, EVLWI increased from 9.5 ± 0.3 ml/kg to 11.4 ± 0.3 ml/kg NS and from 9.3 ± 0.2 ml/kg to 10.8 ± 0.3 ml/kg LR (P = 0.035). Despite this, oxygenation was not significantly impacted (Delta partial pressure of arterial oxygen (PaO2)/fraction of inspired oxygen (FiO2) ≤ 100) until approximately 250 ml/kg of either fluid had been administered. Animals resuscitated with NS were more acidaemic (with lower lactates), pH 7.17 ± 0.03 NS vs. 7.41 ± 0.02 LR (P < 0.001).ConclusionsThis study suggests that early resuscitation of haemorrhagic shock with NS or LR has little impact on oxygenation when resuscitation volume is less than 250 ml/kg. LR has more favourable effects than NS on EVLWI, pH and blood pressure but not on oxygenation.

Resuscitation of hemorrhagic shock with normal saline versus lactated Ringer's: effects on oxygenation, extravascular lung water, and hemodynamics

Which type of fluid to use in the resuscitation from hemorrhagic shock, within and between crystalloids or colloids, is still a matter of debate. In this context, with respect to organ dysfunction, early detection of lung injury is widely considered of particular clinical importance. For these purposes, the transpulmonary thermodilution technique that enables one to assess extravascular lung water as a marker of pulmonary edema is applied in the clinical setting. In this issue of Critical Care, Phillips and colleagues describe that early resuscitation of hemorrhagic shock in pigs with two different crystalloid solutions – normal saline or Ringer's lactate – had little impact on oxygenation when the resuscitation volume was <250 ml/kg. Ringer's lactate had more favorable effects than normal saline, however, on extravascular lung water, pH, and blood pressure but not on oxygenation. Although several pathophysiological aspects remain unanswered, these data are interesting in so far as they indicate that clinically applied amounts of crystalloids per se do not negatively influence pulmonary function, while with larger amounts the type of fluid has different effects on the extent of fluid extravasation in the lungs.

Relationship between mean arterial pressure and end-tidal partial pressure of carbon dioxide during hemorrhagic shock andvolume resuscitation

Objectives. We examined the relationship between partial end-tidal CO2 (pet) and mean arterial pressure in patients with traumatic hemorrhagic shock, who were receiving constant minute ventilation.Methods. In 61 patients we continuously measured pet CO2 with a capnograph, direct arterial pressure via a cannula, oxygen levels via pulse oximetry and body temperature.Results. We observed significant changes in pet CO2 (increase) after volume resuscitation and a quantitative linear relati-onship between pet CO2 and mean arterial pressure.Conclusions. Partial end-tidal CO2 can be used as a reliable non-invasive monitoring device in patients with hemorrhagic shock when minute ventilation is relatively constant. The monitoring of pet CO2 might also be a useful guide for volume resuscitation in hemorrhagic shock, especially in the pre-hospital setting.

Microvascular benefits of increasing plasma viscosity and maintaining blood viscosity: Counterintuitive experimental findings

The circulation is adapted to specific levels of blood viscosity resulting in a balance that simultaneously sets peripheral vascular resistance, blood pressure and cardiac output, factors in part mediated by the production of nitric oxide by the endothelium. Although it is generally perceived that decreasing blood viscosity is beneficial for cardiovascular function, small increases of blood viscosity in normal healthy experimental subjects significantly improve cardiovascular function. These changes are within the normal variations of viscosity due to the variations of hematocrit in the healthy population. Hemodilution reduces blood viscosity, which is proposed to be physiologically beneficial. However, in extreme hemodilution, increased plasma viscosity via the use of viscogenic plasma expanders sustains microvascular and tissue function at significantly reduced levels of oxygen delivery. Studies in hemorrhagic shock resuscitation using oxygen carrying and non-carrying red blood cells show that restoration of blood viscosity is as important as restoration of oxygen carrying capacity. It is concluded that although hemodilution is indicated for reducing abnormally high blood viscosities, it is beneficial to increase plasma viscosity when hematocrit is reduced. Furthermore small increases in hematocrit may be beneficial due to the related increase in blood viscosity, independently of the increase of oxygen delivery capacity.

Monitoring trauma and intensive care unit resuscitation with tissue hemoglobin oxygen saturation

IntroductionThe purpose of the present review is to review our experience with near-infrared spectroscopy (NIRS) monitoring in shock resuscitation and predicting clinical outcomes.MethodsThe management of critically ill patients with goal-oriented intensive care unit (ICU) resuscitation continues to evolve as our understanding of the appropriate physiologic targets improves. It is now recognized that resuscitation to achieve supranormal indices is not beneficial in all patients and may precipitate abdominal compartment syndrome.ResultsOver the years, ICU technology has provided physicians with specific physiologic parameters to guide shock resuscitation. Throughout this time, the tissue hemoglobin oxygen saturation (StO2) monitor has emerged as a non-invasive means to obtain reliable physiologic parameters to guide clinicians' resuscitative efforts. StO2 monitors have been shown to aid in early identification of nonresponders and to predict outcomes in hemorrhagic shock and ICU resuscitation. These data have also been used to better understand and refine existing resuscitation protocols. More recently, use of NIRS technology to guide resuscitation in septic shock has been shown to predict outcomes in high-risk patients.ConclusionsStO2 is an important tool in identifying high-risk patients in septic and hemorrhagic shock. It is a non-invasive means of obtaining vital information regarding outcome and adequacy of resuscitation.

Apoptosis and haemorrhagic shock

Abstract This is a review paper that provides an overview of current information on programmed cell death in haemorrhagic shock, including the identification of different molecular receptor signals. A PubMed search for all dates was undertaken using the search terms apoptosis, trauma and haemorrhagic shock. Original research, sentinel and review papers from peer-reviewed journals were included for identification of key concepts. Haemorrhagic shock remains a primary cause of death in civilian and military trauma. Apoptosis is accelerated following haemorrhagic shock. Many methods are used to detect and quantify apoptosis. Fluid resuscitation regimens vary in their effect on the extent of apoptosis. Investigators are examining the effects of haemorrhagic shock and fluid resuscitation on apoptotic signalling pathways. Molecular information is becoming available and being applied to the care of patients experiencing haemorrhagic shock, making it essential for nurses and other health care providers to consider the mechanisms and consequences of apoptosis.

Florida Emergency Physicians 9 th Annual Symposium on Emergency Medicine, April 8-11 2009

At the Florida Emergency Physicians Annual Symposium on Emergency Medicine, several important updates that could have a direct impact on patient care were presented by nationally recognized leaders in emergency medicine, critical care and trauma. All the topics presented were relevant to more than one specialty and included detailed discussions on optimal ventilator tidal volume, tissue oxygen saturation, ideal blood sugar levels, timing of intubation, appropriate blood transfusions and vasopressor use in the critical care patient. This article will focus on three aspects: Optimal ventilator tidal volume in the critical care patient, the use of a new hemostatic agent for hemorrhage control and vasopressor use in the early resuscitation of hemorrhagic shock.

Interacting Neuroendocrine and Innate and Acquired Immune Pathways Regulate Neutrophil Mobilization from Bone Marrow following Hemorrhagic Shock

Polymorphonuclear neutrophils (PMN) are critical innate immune effector cells that either protect the host or exacerbate organ dysfunction by migrating to injured or inflamed tissues. Resuscitated hemorrhagic shock following major trauma promotes the development of organ inflammation by priming PMN migration and activation in response to a second, often trivial, stimulus (a so-called "two hit" phenomenon). PMN mobilization from bone marrow supports a sustained, hemorrhagic shock/resuscitation (HS/R)-primed migration of PMN. We addressed the role and mechanism of HS/R in regulating PMN egress from bone marrow. We demonstrate that HS/R through the alarmin HMGB1 induces IL-23 secretion from macrophages in an autocrine and TLR4 signaling-dependent manner. In turn IL-23, through an IL-17 G-CSF-mediated mechanism, induces PMN egress from bone marrow. We also show that beta-adrenergic receptor activation by catecholamine of macrophages mediates the HS/R-induced release of HMGB1. These data indicate that HS/R, a global ischemia/reperfusion stimulus, regulates PMN mobilization through a series of interacting pathways that include neuroendocrine and innate and acquired immune systems. Blocking this novel signaling axis may present a novel therapeutic target for posttrauma inflammation.

Effects of different resuscitation fluids on the rheologic behavior of red blood cells, blood viscosity and plasma viscosity in experimental hemorrhagic shock

Background Hemorrhagic shock is associated with severe rheological abnormalities. We hypothesized that in the setting of hemorrhagic shock, resuscitation can alter hemorheological characteristics dramatically, and different fluids cause different effects. The aim of this study was to investigate whether the type of fluid administered has an impact on hemorheological characteristics at the early stage of resuscitation in a rodent model of hemorrhagic shock. Methods Animals were randomized into five groups: (1) sham hemorrhage (SHAM); (2) shock and sham resuscitation (SHOCK); (3) shock and resuscitation with normal saline 32 ml/kg (NS); (4) shock and resuscitation with 7.5% hypertonic saline 4 ml/kg (HS); (5) shock and resuscitation with 7.5% hypertonic saline/6% Dextran 70 4 ml/kg (HSD). Hemorheological characteristics were measured at 60 min after resuscitation. Results Results showed that NS resuscitation deteriorated red blood cell (RBC) deformability compared with the SHOCK group. The HS group showed improved RBC deformability compared with the NS group, although the differences were not statistically significant. There were significant improvements of RBC deformability at all shear rates in the HSD group compared with the NS group. Whole blood and plasma viscosities decreased significantly in the SHOCK group compared with the SHAM group. At shear rates of 60 and 150 s −1, the NS group decreased whole blood viscosity compared with the SHOCK group. The HSD group showed elevated plasma viscosity compared with the SHOCK, NS and HS groups. Conclusion These results suggested that at the early stage of hemorrhagic shock resuscitation, hypertonic–hyperoncotic resuscitation could improve RBC deformability compared with isotonic crystalloid resuscitation. Dextran 70 could elevate plasma viscosity to nearly baseline level. These effects of hypertonic–hyperoncotic resuscitation could be beneficial to maintain microcirculation.

Abstract P29: Impaired Systemic but Preserved Cerebral Microcirculation Following Hemorrhagic Shock and Fluid Resuscitation

Background: Decreases in buccal microcirculation are associated with severity and outcomes of circulatory shock. However, there is evidence that cerebral function is unimpaired after even severe states of hemorrhagic shock. We therefore hypothesized that in severe states of hemorrhagic shock with profound decreases in buccal microcirculation, the cerebral microcirculation may be preserved. Method: Craniotomies were performed in 15 male Sprague-Dawley rats, weighing 450–550g, to expose the parietal cortex for visualization of microcirculation. Animals were then bled via a catheter advanced into the descending aorta. An estimated 35% or 25% of blood volume was bled over 60 minutes and measurements were compared with unbled control. Sixty minutes after onset of hypotension, bled animals received normal saline infused over 30 minutes in amounts equivalent to two times the volume of shed blood. Cerebral and buccal microcirculations were visualized with orthogonal polarization spectral imaging. Result: Reductions in mean arterial pressure (MAP) were partially reversed after fluid infusion (Figure 1 ). Buccal microcirculation was restored to baseline level after the 25% blood loss and partially restored after the 35% loss. The cerebral microcirculation, however, was unchanged during both hemorrhagic hypotension and following volume repletion. Conclusion: In contrast to the striking reduction in arterial pressure and systemic microcirculation, the cerebral microcirculatory blood flow was preserved during hemorrhagic shock of moderate and severe degrees. These findings confirm a dissociation between the macrocirculation and the cerebral microcirculation.

INHIBITION OF CYTOCHALASIN-PRIMED NEUTROPHILS BY HYPEROSMOLARITY

Experimental and clinical investigations using hyperosmotic solutions for resuscitation of hemorrhagic shock demonstrated modulation of the inflammatory response. Decreased postinjury hyperinflammation has been attributed to a reduction in neutrophil-mediated tissue damage. This study shows that cytoskeletal disruption with cytochalasinB did not reverse or prevent the inhibitory effect of an osmolarity increase on the neutrophil cytotoxic response to a formyl peptide. In cytochalasin-primed neutrophils, the hyperosmolarity-dependent inhibition promptly reversed after returning to iso-osmotic levels. Paradoxically, an increase in osmolarity after stimulation produced an increase in the release of reactive oxygen species to the extracellular medium. The inhibitory effect of hyperosmotic NaCl can be reproduced by solutions of similar osmolarity containing N-methyl glucamine or sucrose, but solutions containing mannitol allowed an almost complete response to N-formyl methionyl leucyl phenylalanine. The effects on the release of reactive oxygen species to the extracellular media found with the OxyBURST-bovine serum albumin assay correlated with the changes of the intracellular calcium signal, indicating that the inhibition by hyperosmolarity occurs near the receptor level.

Successful resuscitation of unexpected neonatal hemorrhagic shock due to massive feto‐maternal hemorrhage

Successful resuscitation of unexpected neonatal hemorrhagic shock due to massive feto‐maternal hemorrhage

Methemoglobin Effects on Coagulation: A Dose-Response Study With HBOC-200 (Oxyglobin) in a Thrombelastogram Model

Because oxidation affects platelet and coagulation factors, hemoglobin auto-oxidation in HBOCs results in the transformation to methemoglobin, which may have additive adverse effects on coagulation. The risk of coagulopathy after different dilutions of HBOC-200 with low and high methemoglobin concentrations was studied. A laboratory study on donor blood using thromboelastography (TEG; Haemoscope, Niles, IL). A university laboratory. Volunteer donor blood. Blood samples simulated hemodilution during clinical resuscitation of hemorrhagic shock with varying doses of HBOC-200 (Oxyglobin; Biopure Corp, Cambridge, MA). Coagulopathy related to 1:11, 1:5, 1:2, and 1:1 dilution of whole blood with HBOC-200 high methemoglobin concentrations (65%) and HBOC-200 low methemoglobin concentrations (1%) were analyzed. Analysis of fixed effects of dilution on coagulation showed that the progressive dilution of HBOC-200 (low methemoglobin) and HBOC-200 (high methemoglobin) produced significant prolongation in reaction time (R) and clot propagation (K) and significant decreases in clot kinetics (alpha) and clot strength (MA and G). Analysis of fixed effects of treatment group on coagulation showed that clot propagation (K, alpha) and clot strength (MA and G) are significantly different in HBOC-200 (high methemoglobin) compared with HBOC-200 (low methemoglobin). High methemoglobin concentrations in HBOC-200 cause additive coagulation impairment that likely results from the effects of oxidative substances on platelet function and coagulation proteins. Oxidative products adversely react with coagulation factors and modify redox-sensitive sites in the platelets. Therefore, if methemoglobinemia occurs as a result of HBOC administration and if the levels are significantly elevated (greater than 10%), impairment of coagulation is possible.

Effect of Immediate Enteral Feeding on Trauma Patients with an Open Abdomen: Protection from Nosocomial Infections

Damage-control laparotomy has become increasingly common after operative resuscitation of severe hemorrhagic shock after injury. Despite increased use, uncertainty exists about the safety and timing of enteral nutrition. The purpose of this study was to determine the safety and effect of immediate enteral nutrition. Data were obtained from a multicenter prospective cohort study evaluating clinical outcomes in adults with hemorrhagic shock after injury and were limited to patients with an open abdomen and no hollow viscus injury. The immediate enteral nutrition cohort was defined as initiation of enteral feeds within 36 hours after acute resuscitation completion. Multivariate stepwise logistic regression was used to evaluate factors associated with immediate enteral nutrition. One hundred subjects met inclusion criteria; 32 immediate enteral nutrition and 68 nonimmediate enteral nutrition. Nearly all patients underwent fascial closure (93.8% immediate enteral nutrition versus 94.1% nonimmediate enteral nutrition), with an average closure day of 6.47 +/- 0.83 with immediate enteral nutrition and 8.55 +/- 0.85 with nonimmediate enteral nutrition (p = 0.129). No significant difference in multiorgan dyfunction syndrome, length of ventilator days, ICU days, hospital days, or mortality was seen between groups. The rate of pneumonia was significantly different: 14 (43.8%) in immediate enteral nutrition and 49 (72.1%) in nonimmediate enteral nutrition (p = 0.008). Immediate enteral nutrition remained independently associated with a reduction in pneumonia within our stepwise regression (odds ratio = 0.32; 95% CI, 0.13 to 0.79). Immediate enteral nutrition after damage control appears safe, with no effect on abdominal closure rate. In addition, the reduction in pneumonia associated with immediate enteral nutrition suggests a tangible benefit. Immediate enteral nutrition should be considered in patients with open abdomens after severe trauma.

Volume resuscitation from hemorrhagic shock with albumin and hexaPEGylated human serum albumin

The effect of restoring intravascular volume with polyethylene glycol (PEG) conjugated to human serum albumin (PEG-Alb) on systemic parameters and microvascular hemodynamics after hemorrhagic shock resuscitation was studied in the hamster window chamber model. Moderate hemorrhagic shock was induced by controlled arterial bleeding of 50% of blood volume, and hypovolemia was maintained for 1h. Fluid resuscitation was accomplished by infusion of 25% of blood volume and recovery was followed over 90 min. The PEG-Alb (six chains of maleimide phenyl PEG conjugated human serum albumin at 4%) resuscitation group was compared human serum albumin (HSA) at 5% (HSA5) and 10% (HSA10) protein concentrations. Systemic parameters, microvascular perfusion and capillary perfusion (functional capillary density, FCD) were measured by noninvasive methods. Hyperoncotic solutions provided rapid restoration of blood pressure, blood gas parameters and microvascular perfusion. Systemic and microvascular recovery was best and most rapid with PEG-Alb and followed by HSA10 and HSA5. Only recovery with PEG-Alb was sustained beyond 90 min. Hemodynamic functional benefits of PEG-Alb and the potential disadvantages associated with HSA, suggest PEG-Alb as better resuscitation solution.

Hypertonic saline dextran versus ringer lactate in the resuscitation of haemorrhagic shock in polytraumatized patients

Clinic of Anesthesiology and Intensive Therapy, Military Medical Academy, Belgrade, Serbia, Yugoslavia

Hemorrhagic shock-resuscitation does not exacerbate ventilator associated lung injury in pigs

Wang, H.; Bodenstein, M.; Duenges, B.; Ghanaati, S.; Markstaller, K. Author Information

Does Hextend Impair Coagulation Compared to 6% Hetastarch? An Ex Vivo Thromboelastography Study

The objective of this study was to determine if coagulation is different between 6% hetastarch in normal saline (NS) and 6% hetastarch in lactated Ringer's solution (LR), with use of an ex vivo thromboelastography (TEG) model with healthy donated volunteer blood. We simulated hemodilution that occurs during clinical resuscitation of hemorrhagic or hypovolemic shock, using healthy human donor whole blood (WB) ex vivo. Coagulopathy related to low, medium, high, or very high dilution of WB with NS or a high-molecular-weight hetastarch-based plasma expander, 6% hetastarch in NS (HSNS) or 6% hetastarch in lactated Ringer's [Hextend (HSLR)], was analyzed by thromboelastography (TEG). No changes were noted in the TEG profile of undiluted WB controls during the 6-hour period of use (P > 0.95). Dilution with HSNS and HSLR significantly impaired coagulation compared to both WB control and NS. Progressive dilution with NS impaired coagulation but to a lesser extent than colloids (P < 0.01). Low dilution of blood with NS increased clot strength by 12% (not significant; P = 0.097). We conclude that WB containing citrate obtained from healthy donors for TEG analysis yields reproducible data over a minimum of 6 hours. Either hetastarch, when present at concentrations comparable to the manufacturer's maximum recommended dose of 20 mL/kg (equivalent to the high dilution used in these experiments), decreases clot tensile strength to levels associated with an increased risk of bleeding. Substitution of lactated Ringer's for NS in 6% hetastarch appears to offer no advantage in avoiding hemostatic compromise in an in vitro model.

Relationship between P-selectin and cardiac function in hemorrhagic shock resuscitation: experiment with rats

To investigate the relationship between the left ventricular function and the expression of P-selectin in the serum and cardiac muscle in hemorrhagic shock resuscitation, and to evaluate the effects of L-arginine (L-Arg) against the harmful effect of P-selectin. Thirty SD rats were randomly divided into 3 equal groups: hemorrhagic shock resuscitation (HS) group (undergoing bloodletting until the mean arterial pressure of 40 mm Hg and then re-infusion of the lost blood), L-Arg treatment group (undergoing bloodletting and then re-infusion with L-Arg simultaneously), and normal control (NC) group (undergoing infusion of normal saline). Cannulation was conducted via left carotid artery into the left ventricular to record left ventricular systolic pressure (LVSP), left ventricular end diastolic pressure (LVEDP), and left ventricular +/- dp/dtmax. Serum creatine kinase (CK) was detected by colorimetry. Three hours after the HS the rats were killed with samples of blood and apex of heart collected to detect the P-selectin expression by ELISA and immunohistochemistry. Microscopy was used to observe the expression of P-selectin in the vascular endothelial cells and cardiac muscle cells. The LVSP, maximal rate of LV pressure elevation (+ dp/dtmax), and maximal rate of LV pressure depression (- dp/dtmax) of the HS and L-Arg groups were all significantly lower than those of the NC group (all P < 0.01). The LVEDP of the HS and L-Arg groups were all higher than that of the NC group (both P < 0.01). Three hours after resuscitation, the CK levels of the HS and L-Arg groups were significantly higher than that of the NC group (both P < 0.01), and that of the L-Arg groups was significantly lower than that of the HS group (P < 0.05), the P-selectin levels of the serum and cardiac muscle cells of the HS and L-Arg groups were all significantly higher than those of the NC group (both P < 0.01), and those of the L-Arg group were significantly lower than those of the HS group (both P < 0.05). After hemorrhagic shock and resuscitation P-selectin may play an important role in cardiac injury, L-Arg can inhibit the expression of P-selectin, thus protecting the cardiac function against the harmful effect of P-selectin.

Increased plasma viscosity prolongs microhemodynamic conditions during small volume resuscitation from hemorrhagic shock

Systemic and microvascular hemodynamic responses to hemorrhagic shock resuscitation with hypertonic saline (HTS, 7.5% NaCl) followed with a small volume of plasma expander were studied in the hamster window chamber model to determine the role of plasma expander viscosity in the acute resuscitation outcome. Moderate hemorrhagic shock was induced by arterial controlled bleeding of 50% of blood volume (BV) and the hypovolemic state was maintained for 1 h. Volume restitution was performed by infusion of HTS, 3.5% of BV followed by 10% of BV plasma expanders. Resuscitation was followed for 90 min. The experimental groups were named based on the plasma expanders infused after the HTS, namely: [Hextend], Hextend (6% Hetastarch 670 kDa in lactated electrolyte solution, 4 cp), [Hextend+V], Hextend with viscosity enhanced by the addition of 0.4% alginate, 8 cp, and [NVR] no volume resuscitation as control group. Measurement of systemic parameters, microvascular hemodynamics and capillary perfusion were performed during hemorrhage, shock and resuscitation. Restitution with Hextend yielded the higher mean arterial pressure (MAP), followed by Hextend+V and NVR. Increasing plasma viscosity did not increase peripheral vascular resistance. Functional capillary density (FCD) was higher for Hextend+V than Hextend and NVR. The level of restoration of acid-base balance correlated with microvascular perfusion and was significantly improved with Hextend+V when compared to Hextend and NVR. These results suggest the importance of restoration of blood rheological properties through enhancing plasma viscosity, influencing the re-establishment of microvascular perfusion during small volume resuscitation from hemorrhagic shock.