Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “RESUSCITATION”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,765 records · Page 98Linked to original sources
PubMed1999

The effects of varying fluid volume and rate of resuscitation during uncontrolled hemorrhage.

BACKGROUND: The role of rate and volume of infusion in survival from experimental uncontrolled hemorrhage was evaluated. METHODS: Hemorrhage was initiated using tail resection in 43 female rats assigned to the following five groups: nonresuscitated; resuscitated with moderate volume, slower rate; resuscitated with moderate volume, faster rate; resuscitated with high volume, slower rate; and resuscitated with high volume, faster rate. RESULTS: A trend toward improved survival was noted with faster rate of infusion (60 vs. 33.3% survival rate with moderate volume and 28.6 vs. 12.5% with high volume, compared with 16.7% in the nonresuscitated animals). CONCLUSION: Rapid infusion of moderate volume of isotonic saline improved survival in uncontrolled hemorrhage. Extreme volumes, infused rapidly, also resulted in higher survival rates compared with those observed in nonresuscitated rats.

Animals↗
PubMed1999

Brain tissue oxygenation during hemorrhagic shock, resuscitation, and alterations in ventilation.

OBJECTIVES: Recently developed polarographic microelectrodes permit continuous, reliable monitoring of oxygen tension in brain tissue (PbrO2). The aim of this study was to investigate the feasibility and utility of directly monitoring PbrO2 in cerebral tissue during changes in oxygenation or ventilation and during hemorrhagic shock and resuscitation. We also sought to develop a model in which treatment protocols could be evaluated using PbrO2 as an end point. METHODS: Licox Clark-type polarographic probes were inserted in the brain tissue of 16 swine to monitor PbrO2. In eight swine, changes in PbrO2 were observed over a range of fractional concentrations of inspired O2 (FiO2) as well as during periods of hyperventilation and hypoventilation. In eight other swine, PbrO2 was monitored during a graded hemorrhage of up to 70% estimated blood volume and during the resuscitation period. RESULTS: When FiO2 was elevated to 100%, PbrO2 increased from a baseline of 15+/-2 mm Hg to 36+/-11 mm Hg. Hyperventilation while breathing 100% oxygen resulted in a 40% decrease in PbrO2 (p < 0.05), whereas hypoventilation increased PbrO2 to 88 mm Hg (p < 0.01). A graded hemorrhage to 50% estimated blood volume significantly reduced PbrO2, mean arterial pressure, and intracranial pressure (p < 0.01). Continued hemorrhage to 70% estimated blood volume resulted in a PbrO2 of 2.9+/-1.5 mm Hg. After resuscitation, PbrO2 was significantly elevated, reaching 65+/-13 mm Hg (p < 0.01), whereas mean arterial pressure and cerebral perfusion pressure simply returned to baseline. CONCLUSION: Directly measured PbrO2 was highly responsive to changes in FiO2, ventilatory rate, and blood volume in this experimental model. In particular, hypoventilation significantly increased PbrO2, whereas hyperventilation had the opposite effect. The postresuscitation increase in PbrO2 may reflect changes in both O2 delivery and O2 metabolism. These experiments set the stage for future investigations of a variety of resuscitation protocols in both normal and injured brain.

Animals↗
PubMed1999

Hypertonic saline dextran attenuates leukocyte accumulation in the liver after hemorrhagic shock and resuscitation.

BACKGROUND: Hemorrhagic shock and resuscitation triggers a global ischemia/reperfusion phenomenon, in which activated leukocytes are considered strong contributors to the ensuing tissue damage. METHODS: The aim of the study was to investigate the effects of hypertonic saline dextran (HSD) on the early leukocyte/endothelial interactions (intravital fluorescence microscopy) in a rat model of hemorrhagic shock (1 hour at mean arterial pressure of 40 mm Hg). The resuscitation was performed with lactated Ringer's solution (RL, four times shed blood/20 minutes, n = 6), 6% dextran 60 (DEX, 100% shed blood/5 minutes, n = 8), and 7.2% NaCl/10% dextran 60 (HSD, 10% shed blood/2 minutes, n = 8). RESULTS: After 1 hour of resuscitation, shock-induced stasis/adherence of leukocytes was further enhanced with RL (sinusoids 17.6+/-6.9%; venules 33.9+/-8.5%), whereas DEX and HSD attenuated leukocyte stagnation in sinusoids (DEX -7.4+/-6,1%; HSD -14.7+/-2.9%, p<0.01 vs. RL) and leukocyte adherence in postsinusoidal venules (DEX -12.2+/-8.6%, p<0.05 vs. RL; HSD -27+/-7.4%, p<0.01 vs. RL). CONCLUSION: HSD reduced significantly the number of leukocytes accumulated in the liver after resuscitation of hemorrhagic shock, probably due to a combination of mechanisms of both components.

Animals↗
PubMed1999

Comparison of standard and alternative prehospital resuscitation in uncontrolled hemorrhagic shock and head injury.

BACKGROUND: Recently acquired data suggest that prehospital fluid resuscitation may worsen outcome of patients with penetrating torso trauma. In patients with head injury, delayed resuscitation (DR) could lead to secondary cerebral ischemia. We hypothesized that standard prehospital resuscitation (SPR) with lactated Ringer's solution or diaspirin cross-linked hemoglobin would reduce secondary cerebral ischemia compared with DR. METHODS: Anesthetized swine were randomized to receive SPR, diaspirin cross-linked hemoglobin, or DR after cryogenic brain injury and uncontrolled hemorrhagic shock and studied for 70 minutes after the combined insults. RESULTS: Hemorrhage volume was lowest in the DR group (p<0.05). There were no significant differences between the groups in systemic or cerebral oxygen delivery. Intracranial pressure was lower and cerebral perfusion pressure higher in the diaspirin cross-linked hemoglobin group compared with SPR (p<0.05). Lesion size was greatest in the SPR group, but the difference was not significant. CONCLUSION: In this model, SPR leads to secondary cerebral ischemia. DR is no worse and may be superior to conventional prehospital resuscitation with lactated Ringer's solution.

Animals↗
PubMed1999

Limited resuscitation with hypertonic saline, hypertonic sodium acetate, and lactated Ringer's solutions in a model of uncontrolled hemorrhage from a vascular injury.

BACKGROUND: Hypertonic sodium acetate-dextran solution (HAD) causes vasodilatation and buffers metabolic acidosis. In controlled hemorrhage models, HAD in small volumes increases cardiac output without increasing blood pressure, thus creating a "high flow-low pressure" state. The objective of this study was to determine whether limited resuscitation of uncontrolled hemorrhage with HAD solution improves gut perfusion as measured by intestinal mucosal tonometry. METHODS: Three groups of 10 swine were bled 25 mL/kg by means of a femoral artery catheter to produce a mean blood pressure of 30 mm Hg. A 4-mm abdominal aortic laceration was then produced by pulling out a preimplanted wire loop. Groups were then randomly assigned to be resuscitated with either lactated Ringer's solution, a hypertonic saline-dextran solution or HAD solution sufficient to maintain a mean blood pressure of 45 mm Hg for 5 hours or until death. Outcomes were measured by survival, intraperitoneal blood loss, hemodynamic monitoring, and ileal mucosal tonometry. RESULTS: HAD infusions caused transient worsening of hypotension and were associated with increased mortality (p = 0.038). Blood loss and volumes required for resuscitation were significantly increased in the lactated Ringer's solution group. HAD showed significant buffering effect against metabolic acidosis in arterial blood only, but intestinal ileal mucosal tonometry was not different among the groups. CONCLUSION: HAD did not improve gut perfusion despite buffering the systemic acidosis of shock and caused increased mortality. Limited resuscitation with any of these solutions is associated with significant mucosal acidosis.

Acid-Base Equilibrium↗
PubMed2000

Fibrin sealant foam sprayed directly on liver injuries decreases blood loss in resuscitated rats.

OBJECTIVE: The majority of early trauma deaths are attributable to uncontrolled hemorrhage from truncal sites. A hemorrhage-control technique that reduced bleeding in the prehospital phase of treatment without requiring manual compression may improve the outcome of these patients. We conducted this preliminary study to determine whether an expanding fibrin sealant foam (FSF) would reduce bleeding from a severe liver injury even during resuscitation. METHODS: Rats (n = 31; 291 +/- 5 g; 37.4 +/- 0.3 degrees C; mean +/- SEM), underwent a 60 +/- 5% excision of the median hepatic lobe. The animals received one of three treatments: (1) FSF, (2) immunoglobulin G placebo foam (IgGF), or (3) no treatment. All animals were resuscitated with 40 degrees C lactated Ringer's solution at 3.3 mL/ min/kg to a mean arterial pressure of 100 mm Hg. Total blood loss, mean arterial pressure, and resuscitation volume were recorded for 30 minutes. A qualitative measure of foam coverage and adherence to the cut liver edge was recorded. RESULTS: The total blood loss was less (p < 0.01) in the FSF group (21.2 +/- 5.0 mL/kg) than in either IgGF (41.4 +/- 4.3 mL/kg) or the no treatment group (44.6 +/- 4.7 mL/kg), which did not differ. The resuscitation volume was not different. The amount of foam used in the treated groups, 9.1 +/- 1.0 g in the FSF group and 10.0 +/- 1.0 g in the IgGF group, did not differ. Survival for 30 minutes was not different among groups. There was no difference in the amount of cut liver covered by either foam, but the clots were more adherent (p < 0.05) in the FSF group than in the IgGF group. CONCLUSION: In rats with a severe liver injury, spraying fibrin foam directly on the cut liver surface decreased blood loss when compared with placebo foam and no treatment. This pilot study suggests a future possible treatment for noncompressible truncal hemorrhage.

Administration, Topical↗
PubMed2000

Starch-deferoxamine conjugate inhibits hepatocyte Ca2+ uptake during hemorrhagic shock and resuscitation.

BACKGROUND: This study investigated whether hepatocyte Ca2+ dysregulation after hemorrhagic shock and resuscitation could be modulated by the iron chelator hydroxyethyl starch-conjugated deferoxamine (HES-DFO). METHODS: In a randomized experimental study, anesthetized rats (n = 7) were bled for 60 minutes to maintain mean arterial blood pressure at 40 mm Hg. They were then resuscitated with 60% of shed blood and threefold the shed-blood volume as lactated Ringer's solution, 1 mL of pentastarch solution (hydroxyethyl starch 10%) per mL of shed blood, or 1 mL of HES-DFO solution (10%) per mL of shed blood. In isolated hepatocytes, the rate of Ca2+ influx (Ca2+ in), total Ca2+ uptake (Ca2+ up), and membrane Ca2+ flux (Ca2+ flux) were determined by 45Ca incubation. Reduced or oxidized glutathione and malondialdehyde concentrations were assessed fluorometrically. RESULTS: Significant increases of hepatocellular Ca2+ in, Ca2+ up, and Ca2+ flux were observed in rats resuscitated with lactated Ringer's solution compared with control groups (p < 0.05). Although hydroxyethyl starch decreased Ca2+ in but not Ca2+ up, HES-DFO not only prevented the increase of Ca2+ in and Ca2+ up but also inhibited hepatocyte oxidative injury. CONCLUSION: Iron-catalyzed oxyradical production and membrane peroxidation seem to alter hepatocyte Ca2+ homeostasis after hemorrhagic shock and resuscitation.

Animals↗
PubMed2001

Resuscitation with a blood substitute abrogates pathologic postinjury neutrophil cytotoxic function.

BACKGROUND: Resuscitation with oxygen-carrying fluids is critically important in the patient with hemorrhagic shock caused by trauma. However, it is clear that a number of biologic mediators present in stored blood (packed red blood cells [PRBCs]) have the potential to exacerbate early postinjury hyperinflammation and multiple organ failure through priming of circulating neutrophils (PMNs). PolyHeme (Northfield Laboratories, Evanston, IL), a hemoglobin-based substitute that is free of priming agents, provides an alternative. We hypothesized that PMN priming would be attenuated in patients resuscitated with PolyHeme in lieu of stored blood. METHODS: Injured patients requiring urgent transfusion were given either PolyHeme (up to 20 units) or PRBCs. Early postinjury PMN priming was measured via beta-2 integrin expression, superoxide production, and elastase release. RESULTS: Treatment groups were comparable with respect to extent of injury and early physiologic compromise. PMNs from patients resuscitated with PRBCs showed priming in the early postinjury period by all three measures. No such priming was evident in patients resuscitated with PolyHeme. CONCLUSION: The use of a blood substitute in the early postinjury period avoids PMN priming and may thereby provide an avenue to decrease the incidence or severity of postinjury multiple organ failure.

Blood Pressure↗
PubMed2001

Monitoring tissue oxygenation during resuscitation of major burns.

BACKGROUND: Because subcutaneous and splanchnic oxygenation indices are sensitive indicators of evolving hemorrhagic shock and adequacy of resuscitation, we postulated that these indices might have an equivalent role in the monitoring of severely burned patients. This observational study was undertaken to examine changes in tissue oxygenation indices during burn resuscitation. METHODS: Seven patients with major burns (54 +/- 21% total body surface area) were studied during the first 36 hours of fluid resuscitation. Silastic tubing was placed in the subcutaneous tissue just beneath both normal skin and deep partial thickness burn. Fiberoptic sensors inserted into the tubing measured subcutaneous oxygen and carbon dioxide tensions in the burnt skin (PO2scb and PCO2scb) and normal skin (PO2scn and PCO2scn) continuously. Gastric intramucosal pH (pHi) and the mucosal CO2 (PCO2m) gap were calculated using gastric tonometers. Mean arterial pressure, arterial pH, lactate, and pHi measurements were obtained for 36 hours. RESULTS: There were no significant differences in mean arterial pressure, arterial pH, or lactate concentrations throughout the study period, whereas indices of tissue oxygenation showed deterioration: pHi decreased from 7.2 +/- 0.1 to 6.7 +/- 0.3 (p = 0.06), the PCO2m gap increased from 12 +/- 17 to 108 +/- 123 mm Hg (p < 0.01), PO2scn decreased from 112 +/- 18 to 50 +/- 11 mm Hg (p < 0.01), PO2scb decreased from 62 +/- 23 to 29 +/- 16 mm Hg (p < 0.01), PCO2scn increased from 42 +/- 4 to 46 +/- 10 mm Hg (p = 0.2), and PCO2scb increased from 42 +/- 10 to 52 +/- 5 mm Hg (p = 0.05). CONCLUSION: Despite adequate global indices of tissue perfusion after 36 hours of resuscitation, tissue monitoring indicated significant deterioration in the splanchnic circulation and in the normal and burnt skin.

Adult↗
PubMed2002

Evaluation of staff workload during resuscitation of trauma patients.

OBJECTIVE: Evaluating the medical staff workload during resuscitation of trauma patients is one of the important quality assurance activities to provide adequate medical manpower, especially for patients with life-threatening or severe injuries. Nevertheless, there is no method available to measure and calculate the amount of workload during resuscitation. We sought to develop a new framework of Workload Scoring System (WSS) to evaluate and quantify the medical staff workload during resuscitation. METHODS: From July 1996 to July 1998, the records of 11,800 trauma patients were prospectively collected from our computer-stored medical record system. The Workload Scoring System points with reference to age, different triage category on the basis of triage version of the Revised Trauma Score (RTS), level category on the basis of Injury Severity Score (ISS), and Abbreviated Injury Scale (AIS) in six body regions were calculated to survey the medical staff workload. RESULTS: The WSS points were 18.51 +/- 0.80 for triage I, 11.88 +/- 0.17 for triage II, and 6.90 +/- 0.04 for triage III trauma patients. The WSS points were 23.10 +/- 0.67 for Level I, 20.34 +/- 0.25 for Level II, 12.87 +/- 0.08 for Level III, and 6.03 +/- 0.02 for Level IV trauma patients. There were statistically significant differences among triage I, II, and III trauma patients, and among Level I, II, III, and IV trauma patients (p < 0.01). The worse the physiologic status and the greater the anatomic damage, the more medical staff workload was needed. Multiple regression with linear model may predict WSS points as an equation of -8.920 + 1.375 ISS + 1.785 RTS + 0.424 Age (r2 = 0.621), which accounts for 62.1% of the variance in WSS points. CONCLUSION: WSS provides a valuable tool to measure and quantify the medical staff workload during resuscitation as a function of -8.920 + 1.375 ISS + 1.785 RTS + 0.424 Age. The greatest benefit of this methodology is to forecast the expected medical staff workload to allocate sufficient medical manpower to provide the desired trauma care.

Analysis of Variance↗
PubMed2002

Evaluation of trauma team performance using an advanced human patient simulator for resuscitation training.

BACKGROUND: Human patient simulation (HPS) has been used since 1969 for teaching purposes. Only recently has technology advanced to allow application to the complex field of trauma resuscitation. The purpose of our study was to validate an advanced HPS as an evaluation tool of trauma team resuscitation skills. METHODS: The pilot study evaluated 10 three-person military resuscitation teams from community hospitals that participated in a 28-day rotation at a civilian trauma center. Each team consisted of physicians, nurses, and medics. Using the HPS, teams were evaluated on arrival and again on completion of the rotation. In addition, the 10 trauma teams were compared with 5 expert teams composed of experienced trauma surgeons and nurses. Two standardized trauma scenarios were used, representing a severely injured patient with multiple injuries and with an Injury Severity Score of 41 (probability of survival, 50%). Performance was measured using a unique human performance assessment tool that included five scored and eight timed tasks generally accepted as critical to the initial assessment and treatment of a trauma patient. Scored tasks included airway, breathing, circulation, and disability assessments as well as overall organizational skills and a total score. The nonparametric Wilcoxon test was used to compare the military teams' scores for scenarios 1 and 2, and the comparison of the military teams' final scores with the expert teams. A value of p < 0.05 was considered significant. RESULTS: The 10 military teams demonstrated significant improvement in four of the five scored (p < or = 0.05) and six of the eight timed (p < or = 0.05) tasks during the final scenario. This improvement reflects the teams' cumulative didactic and clinical experience during the 28-day trauma refresher course as well as some degree of simulator familiarization. Improved final scores reflected efficient and coordinated team efforts. The military teams' initial scores were worse than the expert group in all categories, but their final scores were only lower than the expert groups in 2 of 13 measurements (p < or = 0.05). CONCLUSION: No studies have validated the use of the HPS as an effective teaching or evaluation tool in the complex field of trauma resuscitation. These pilot data demonstrate the ability to evaluate trauma team performance in a reproducible fashion. In addition, we were able to document a significant improvement in team performance after a 28-day trauma refresher course, with scores approaching those of the expert teams.

Computer Simulation↗
PubMed2003

Hypertonic saline resuscitation attenuates neutrophil lung sequestration and transmigration by diminishing leukocyte-endothelial interactions in a two-hit model of hemorrhagic shock and infection.

BACKGROUND: Hypertonic saline (HTS) attenuates polymorphonuclear neutrophil (PMN)-mediated tissue injury after hemorrhagic shock. We hypothesized that HTS resuscitation reduces early in vivo endothelial cell (EC)-PMN interactions and late lung PMN sequestration in a two-hit model of hemorrhagic shock followed by mimicked infection. METHODS: Thirty-two mice were hemorrhaged (40 mm Hg) for 60 minutes and then given intratracheal lipopolysaccharide (10 microg) 1 hour after resuscitation with shed blood and either HTS (4 mL/kg 7.5% NaCl) or Ringer's lactate (RL) (twice shed blood volume). Eleven controls were not manipulated. Cremaster intravital microscopy quantified 5-hour EC-PMN adherence, myeloperoxidase assay assessed lung PMN content (2 1/2 and 24 hours), and lung histology determined 24-hour PMN transmigration. RESULTS: Compared with RL, HTS animals displayed 55% less 5-hour EC-PMN adherence (p = 0.01), 61% lower 24-hour lung myeloperoxidase ( p= 0.007), and 57% lower mean 24-hour lung histologic score ( p= 0.027). CONCLUSION: Compared with RL, HTS resuscitation attenuates early EC-PMN adhesion and late lung PMN accumulation in hemorrhagic shock followed by inflammation. HTS resuscitation may attenuate PMN-mediated organ damage.

Animals↗
PubMed1994

A proposed model for the cost of cardiopulmonary resuscitation.

In-hospital cardiopulmonary resuscitation (CPR) is associated with substantial costs beyond those of the resuscitation itself. These costs are important to understand because health care resources are limited. To that end, a model of CPR is proposed, including an examination of the effect of several variables on the cost per patient surviving to discharge. The cost of CPR was estimated using a model that describes the CPR process as a series of decision points, each with an associated survival rate and cost. Sensitivity analyses were performed for critical variables to examine their effect on cost. The cost per patient surviving to discharge increases exponentially as the rate of survival to discharge decreases. This cost was $117,000 for a rate of survival to discharge of 10%, $248,271 for a rate of 1%, and $544,521 for a rate of 0.2%. Analysis of the model shows that health care costs related to CPR could be reduced most by decreasing the hospital length of stay and charges for patients who survive the initial resuscitation event, by increases in the overall survival rate, and by the prospective stratification of hospitalized patients according to their anticipated response to resuscitation efforts. The model allows the marginal cost-effectiveness of CPR to be quantitatively evaluated relative to survival rate.

Cardiopulmonary Resuscitation↗
PubMed1990

Evaluation of resuscitation proficiency in simulations: the impact of a simultaneous cognitive task.

In order to evaluate the impact of simulation complexity on resuscitation skill performance, 15 pediatric residents were observed in bag-valve-mask ventilation on an infant manikin. Performance was evaluated in a simple exercise in which ventilation was performed as a single isolated task. For each subject, this was compared to performance when a cognitive task involving clinical problem solving was simultaneously presented. Performance was expressed as frequency, tidal volume, and estimated hypothetical alveolar Pco2 in each resuscitation. A correlation was observed (P less than 0.05) between simple and complex resuscitation simulations for each measure of performance. The only subject with inadequate performance in the complex exercise was also identified as deficient in the simple exercise. These observations suggest that an adequate evaluation of performance of some resuscitation skills may be obtained in simple, efficient simulation exercises.

Carbon Dioxide↗
PubMed1994

Role of Kupffer cells in interleukin-6 release following trauma-hemorrhage and resuscitation.

Although interleukin-6 (IL-6) plays an important role in the pathophysiology of trauma-hemorrhage and resuscitation, the cellular origin of this inflammatory cytokine remains unknown. This study was undertaken to determine whether Kupffer cells (KC) are a major source of IL-6 release following trauma-hemorrhage and resuscitation. KC numbers were significantly (p < .05) reduced in vivo with gadolinium chloride (GdCl3; 10 mg/kg IV). KC-reduced (KC(-)) and KC-normal (saline-treated; KC(+)) rats underwent laparotomy (i.e., trauma-induced), followed by either sham operation or hemorrhage. Hemorrhaged rats were bled to and maintained at a mean arterial pressure of 40 mmHg until 40% of the shed blood volume was returned as Ringer's lactate, and then resuscitated with Ringer's lactate (four times shed blood volume over 1 h). Results indicate that KC reduction per se had no effect on any measured parameter at any time. At 0.5 and 2.0 h postresuscitation, mean arterial pressure, heart rate, cardiac output, stroke volume, and hematocrit were reduced to a similar extent in both the KC(+) and KC(-) hemorrhage groups. KC reduction did, however, significantly reduce plasma IL-6 concentration (means +/- S.E.; U/ml) at both 0.5 h (KC(+) = 709 +/- 391 vs. KC(-) = 159 +/- 5) and at 2.0 h (KC(+) = 527 +/- 394 vs. KC(-) = 83 +/- 20) postresuscitation. In conclusion, this study demonstrates that KC are a major source of in vivo IL-6 release following trauma-hemorrhage and resuscitation.

Animals↗
PubMed1996

Progressive gastric intramucosal acidosis follows resuscitation from hemorrhagic shock.

The time course of gastric intramucosal pH (pHi) during the early phase of resuscitation of hemorrhagic shock has not been adequately characterized. We examined pHi using gastric tonometry catheters in an anesthetized dog model of hemorrhagic shock. Shock was induced in 10 animals to maintain mean arterial blood pressure (MAP) at 40-45 mmHg for 30 min, followed by transfusion of shed blood plus additional saline as needed to maintain MAP at pre-shock values. Five animals served as controls. Baseline pHi values were nearly identical in both groups. Resuscitation promptly restored MAP. Following a precipitous drop of pHi during shock, there was only partial recovery 60 min post-shock, followed by progressive worsening of intramucosal acidosis (7.02 +/- .10 vs. 6.82 +/- .24 at 60 and 210 min post-shock, respectively; p < .002). MAP, heart rate, and pHi did not change significantly during the experiment in the control group. These results indicate that prompt and adequate MAP response to resuscitation failed to prevent significant decreases of pHi in the first few hours post-resuscitation. This finding may be related to persistent splanchnic hypoperfusion or reperfusion injury.

Acidosis↗
PubMed1997

Impaired enterocyte triglyceride synthesis after trauma-hemorrhage and resuscitation.

Although gut lipid absorptive capacity is depressed after trauma and hemorrhagic shock, it remains unknown whether this is associated with an impairment in the enterocyte triglyceride (TG) synthesis, and if so, whether villus or crypt cells participate in the lipid absorption under such conditions. To study this, midline laparotomy (i.e., trauma induction) was performed in the rats, and then the animals were bled to and maintained at a mean arterial pressure of 40 mmHg until 40% of shed blood volume was returned in the form of Ringer's lactate. The rats were then resuscitated with four times the volume of maximal bleedout with Ringer's lactate over 60 min. For lipid loading test, 1 mL of olive oil was given intraduodenally as a bolus injection upon the completion of resuscitation. The enterocytes along the crypt-villus axis from the proximal small intestine were isolated at either 0, 1.5, or 5 h after fat feeding. The intracellular and pre-chylomicron TG contents as well as the microsomal enzyme activities associated with TG synthesis were determined thereafter. The results indicated that intracellular and pre-chylomicron TG contents and lipid esterifying enzyme (i.e., acyl-coenzyme A:monoglyceride acyltransferase) activity decreased significantly in villus tip cells after trauma-hemorrhage and resuscitation. The intracellular TG content and lipid esterifying enzyme activity in crypt cells after trauma and hemorrhagic shock were also reduced. However, there was no significant decrease in pre-chylomicron TG content in the crypt cells isolated from trauma-hemorrhaged rats. It is unlikely that crypt cells participate in lipid transport after trauma and hemorrhagic shock. In contrast, the TG synthesis in villus tip cells decreased significantly following trauma-hemorrhage and resuscitation, which may contribute, at least in part, to the impaired gut lipid absorptive capacity observed under such conditions.

Animals↗
PubMed2003

Picroliv modulates antioxidant status and down-regulates AP1 transcription factor after hemorrhage and resuscitation.

Resuscitation from hemorrhagic shock initiates profound changes in the liver that are likely to contribute to end organ damage and resultant dysfunction after shock. Extensive research in this area has indicated the potential of free radical scavenging strategy for better management of the pathophysiology following hemorrhage-resuscitation (H/R) injury. We studied the effect of a novel pharmacological agent, picroliv, on hepatocellular injury and redox status, as well as its possible mechanism of action in a H/R model in adult rats. Anesthetized rats were subjected to hemorrhagic shock by bleeding 30 mL/kg body weight. After 60 min of shock, rats were resuscitated with twice the shed blood volume of lactated Ringer's solution and were sacrificed 2 h after resuscitation. We observed that picroliv (12 mg/kg) pretreatment, given orally for 7 days, resulted in a significant decrease in serum aspartate transaminase and gamma-glutamyl transpeptidase levels. Picroliv also inhibited the lipid peroxidation and nitric oxide release that occurred after H/R and altered the activity of glutathione reductase in a favorable manner, thereby suggesting better antioxidant status. Picroliv significantly down-regulated the stress-sensitive transcription factor AP1 and decreased the level of c-fos mRNA as well as c-jun and c-fos proteins in liver tissue, indicating that its actions could be mediated through AP1 and associated signal transduction pathways. These findings suggest that picroliv has the potential to be developed as a protective agent against H/R injury.

Animals↗