Transfusion Of Shed Blood Research Articles

Adaptive Balloon Weaning Algorithm With Automated REBOA Facilitates Proximal Homeostasis During Reperfusion in a Swine Hemorrhagic Shock Model

Restoration of distal blood flow is critical to successfully salvage patients with resuscitative endovascular balloon occlusion of the aorta (REBOA). Yet, ideal methods for REBOA deflation to restore flow and simultaneously avoid proximal hypotension, remain undefined. Adaptive balloon titration algorithms to guide deflation may prevent large hemodynamic fluctuations during weaning. We hypothesize that automated REBOA weaning can both augment proximal hemodynamics and avoid hypotension during resuscitation in a swine model of hemorrhagic shock. Fifteen swine underwent 30% controlled hemorrhage followed by 30 minutes of zone 1 REBOA. Next, the REBOA was deflated with an automated syringe running an adaptive algorithm that prioritized proximal mean arterial blood pressure (pMAP) of >62.5 mm Hg during transfusion of shed blood. Upon post hoc analysis, animal pMAP responses (hypertensive [HTN] vs normotensive [NORM]) and the discovery of low volume distal flow during the intended complete REBOA allowed us to identify two distinct cohorts. The performance of the adaptive weaning algorithm was compared between the groups. The two cohorts (HTN, n = 5; NORM, n = 10) differed in pMAP (P = .001) and distal flow (P = .001) during REBOA. During the wean phase, cohorts were similar in pMAP, time with carotid flow within 90% of baseline, and time above the pMAP threshold of 62.5 mm Hg (P = .20, P = .59, and P = .95, respectively) despite the weaning algorithm permitting 14.5 mL/kg more distal aortic flow for the HTN cohort (P = .001). Automated REBOA weaning is feasible and maintains consistent hemodynamics across various physiological profiles. Automated endovascular devices that can interpret and adapt to a range of hemodynamic physiology will soon facilitate precision resuscitation for patients requiring endovascular aortic occlusion. These findings highlight the need for adaptive control to overcome variability in hemodynamics and differences in resuscitation intensity across clinical contexts.

A Novel Therapeutic Approach With Sodium Pyruvate on Vital Signs, Acid-Base, and Metabolic Disturbances in Rats With a Combined Blast and Hemorrhagic Shock.

BackgroundBlast injuries from improvised explosive devices (IEDs) are known to cause blast traumatic brain injuries (bTBIs), hemorrhagic shock (HS), organ damage, mitochondrial dysfunction, and subsequent free radical production. A pre-citric acid cycle reagent, pyruvate, is suggested to improve mitochondrial ATP production through the activation of the mitochondrial gatekeeper enzyme “pyruvate dehydrogenase complex (PDH).” Our study aimed to investigate the role of physiologic, metabolic, and mitochondrial effects of hypertonic sodium pyruvate resuscitation in rats with a combined blast and HS injury.MethodsA pre-clinical rat model of combined injury with repetitive 20 PSI blast exposure accompanied with HS and fluid resuscitation (sodium pyruvate as metabolic adjuvant or hypertonic saline as control), followed by transfusion of shed blood was used in this study. Control sham animals (instrumental and time-matched) received anesthesia and cannulation, but neither received any injury nor treatment. The mean arterial pressure and heart rate were recorded throughout the experiment by a computerized program. Blood collected at T0 (baseline), T60 (after HS), and T180 (end) was analyzed for blood chemistry and mitochondrial PDH enzyme activity.ResultsSodium pyruvate resuscitation significantly improved the mean arterial pressure (MAP), heart rate (HR), pulse pressure (PP), hemodynamic stability (Shock index), and autonomic response (Kerdo index) after the HS and/or blast injury. Compared with the baseline values, plasma lactate and lactate/pyruvate ratios were significantly increased. In contrast, base excess BE/() was low and the pH was also acidotic <7.3, indicating the sign of metabolic acidosis after blast and HS in all animal groups. Sodium pyruvate infusion significantly corrected these parameters at the end of the experiment. The PDH activity also improved after the sodium pyruvate infusion.ConclusionIn our rat model of a combined blast and HS injury, hypertonic sodium pyruvate resuscitation was significantly effective in hemodynamic stabilization by correcting the acid–base status and mitochondrial mechanisms via its pyruvate dehydrogenase enzyme.

Maintaining Zone 1 Occlusion is a Dynamic Process: The Effects of Proximal Pressure and Blood Transfusion During REBOA.

Resuscitative endovascular balloon occlusion of the aorta (REBOA) provides hemodynamic support to patients with non-compressible truncal hemorrhage. As cardiac output increases due to aortic occlusion (AO), aortic diameter will increase as a function of compliance, potentially causing unintended flow around the balloon. Swine (N = 10) were instrumented to collect proximal mean arterial blood pressure (pMAP), distal MAP (dMAP), balloon pressure (bP), balloon volume (bV), and distal aortic flow (Qaorta). A 7-Fr automated REBOA catheter was positioned in Zone 1. At T0, animals underwent 30% total blood volume hemorrhage over 30min followed by balloon inflation to complete AO. Automated balloon inflation occurred from T30-T60 when Qaorta was detected. Period of interest was T55-T60, while the balloon actively worked to maintain AO during transfusion of shed blood. Median weight of the cohort was 73.75 [IQR:71.58-74.45] kg. During T40-T55 and T55-T60, median pMAP was 88.95 [IQR:76.80-109.92] and 108.13 [IQR:99.13-119.51] mmHg, P = 0.07. Median Qaorta during T40-T55, and T55-T60 was 0.81 [IQR:0.41-0.96], and 1.53 [IQR:1.07-1.96] mL/kg/min, P = 0.06. Median number of balloon inflations during T40-T55 was 0.00 [IQR:0.00-0.75] and increased during active transfusion to 10.00 [IQR:5.25-14.00], P = 0.001. In clinical practice, following initial establishment of AO, progressive balloon inflations are required to maintain AO in response to intrinsic and transfusion-mediated increases in cardiac output, blood pressure, and aortic diameter.

Distal organ inflammation and injury after resuscitative endovascular balloon occlusion of the aorta in a porcine model of severe hemorrhagic shock.

Background and objectiveResuscitative Endovascular Balloon Occlusion of Aorta (REBOA) has emerged as a potential life-saving maneuver for the management of non-compressible torso hemorrhage in trauma patients. Complete REBOA (cREBOA) is inherently associated with the burden of ischemia reperfusion injury (IRI) and organ dysfunction. However, the distal organ inflammation and its association with organ injury have been little investigated. This study was conducted to assess these adverse effects of cREBOA following massive hemorrhage in swine.MethodsSpontaneously breathing and consciously sedated Sinclair pigs were subjected to exponential hemorrhage of 65% total blood volume over 60 minutes. Animals were randomized into 3 groups (n = 7): (1) Positive control (PC) received immediate transfusion of shed blood after hemorrhage, (2) 30min-cREBOA (A30) received Zone 1 cREBOA for 30 minutes, and (3) 60min-cREBOA (A60) given Zone 1 cREBOA for 60 minutes. The A30 and A60 groups were followed by resuscitation with shed blood post-cREBOA and observed for 4h. Metabolic and hemodynamic effects, coagulation parameters, inflammatory and end organ consequences were monitored and assessed.ResultsCompared with 30min-cREBOA, 60min-cREBOA resulted in (1) increased IL-6, TNF-α, and IL-1β in distal organs (kidney, jejunum, and liver) (p < 0.05) and decreased reduced glutathione in kidney and liver (p < 0.05), (2) leukopenia, neutropenia, and coagulopathy (p < 0.05), (3) blood pressure decline (p < 0.05), (4) metabolic acidosis and hyperkalemia (p < 0.05), and (5) histological injury of kidney and jejunum (p < 0.05) as well as higher levels of creatinine, AST, and ALT (p < 0.05).Conclusion30min-cREBOA seems to be a feasible and effective adjunct in supporting central perfusion during severe hemorrhage. However, prolonged cREBOA (60min) adverse effects such as distal organ inflammation and injury must be taken into serious consideration.

Blood pressure–targeted stepwise resuscitation of hemorrhagic shock in a swine model

BackgroundProlonged hemorrhagic shock and subsequent resuscitation frequently results in hemodynamic compromise. This study was designed to investigate the hemodynamic effect of the stepwise increase of blood pressure during initial resuscitation. Materials and methodsFifteen anesthetized male pigs (35 ± 5 kg) were used. Hemorrhagic shock was induced by losing 40% of estimated blood volume over 40 min and 10% of estimated blood volume over 20 min through the femoral artery and was maintained at a mean arterial pressure (MAP) of 30 ± 3 mm Hg for 2.5 h. The resuscitation of the rapid resuscitation (RR) group was targeted to reach MAP of 70 ± 5 mm Hg immediately by transfusion of shed blood via the femoral artery. The resuscitation of the pressure-targeted stepwise resuscitation (PSR) group was targeted to increase MAP by 10 mm Hg every 10 min up to 70 mm Hg, and then, the MAP was maintained at 70 ± 5 mm Hg until transfusion of the entire shed blood. ResultsDuring the initial resuscitation period of 30 min, the heart rate was significantly lower in the RR group than in the PSR group (P < 0.05), and mixed venous oxygen saturation was significantly higher in the RR group than in the PSR group during the 30 min of initial resuscitation (P < 0.05). After 2 h of resuscitation, cardiac output and stroke volume were significantly higher in the PSR group than in the RR group (P < 0.05), and the systemic vascular resistance was significantly lower in the PSR group than in the RR group (P < 0.05). ConclusionsA stepwise increase of blood pressure compared with rapid normalization improves hemodynamic parameters in the swine hemorrhagic shock model.

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Abstract : Learning Objectives: Resuscitative Endovascular Balloon Occlusion of the Aorta (REBOA) using generic balloon catheters placed into the descending aorta under fluoroscopy has been used to treat hemorrhagic shock in animal models. We tested a new non-image guided 7F ER-REBOA catheter (Pryor Medical Arvada, CO) for its potential to improve survival in a 100% lethal model of hemorrhagic shock. We hypothesized that ER-REBOA, placed without fluoroscopic guidance, improves survival. Methods: Spontaneously breathing, consciously sedated, sexually mature male Sinclair pigs undergone computerized exponential hemorrhage of 65% of their blood volume over 1 hour via an arterial line. Animals were then randomized into groups of 7 animals each including: negative control (NC), no resuscitation; positive control (PC), immediate transfusion of shed blood (TSB); ER30; 30 min of ERREBOA then TSB; ER60, 60 min of ER-REBOA then TSB; ER, 60 min of ERREBOA with TSB after 30 min of REBOA. After balloon deflation, epinephrine was given if mean arterial pressure was under 40 mm Hg. Up to 20 min of mechanical ventilation (FiO2 .21, RR 12, TV 10 ml/kg, ZEEP) was provided if animal suffered respiratory arrest. Animals were monitored for 240 min post-hemorrhage or until death. Survival was assessed via Kaplan-Meier analysis. Balloon placement was verified via post-mortem CT scan and at necropsy. Results: ER-REBOA was placed successfully in 100% of cases without fluoroscopy. Survival in the NC and PC groups was 0 and 71% respectively. Analysis showed significantly higher survival in the ER-REBOA groups: 100% in ER30 and ER60 groups and 86% in ER (p0.001). Epinephrine was given to 4/7 PC animals and to 6/7, 7/7, and 2/7 animals in ER30, ER60, and ER groups respectively. Ventilation support was given to 1/7, 2/7, and 3/7 in the ER30, ER60, and ER groups and to 2/7 in the PC group respectively.

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Belenkiy, Slava1; Park, Timothy2; Baker, William3; Jordan, Bryan3; Dubick, Michael4; Salinas, Jose4; Cancio, Leopoldo4; Batchinsky, Andriy5 Author Information

Tranexamic acid: more evidence for its use in joint replacement surgery

Tranexamic acid: more evidence for its use in joint replacement surgery

Role of p38MAPK signaling pathway in up-regulation of heme oxygenase-1 expression during hemorrhagic shock and resuscitation-induced acute lung injury in mice

Objective To evaluate the role of p38MAPK signaling pathway in the up-regulation of heme oxygenase-1 （HO-1） expression during hemorrhagic shock and resuscitation （HSR）-induced acute lung injury （ALI） in mice. Methods Thirty-two C3H/HeN （wild-type） mice, aged 10-12 weeks, weighing 20-25 g, were randomly divided into 4 groups （n = 8 each）： sham operation group （group S）; group HSR; FR167653 （a p38MAPK inhibitor） group （group FR） and FR167653 ＋ HSR group （group FR ＋ HSR）. HSR was induced according to the methods described by Ayala et al. MAP was reduced to 35-45 mm Hg and maintained for 60 min.Then the animals were resuscitated with transfusion of the shed blood and lactated Ringer＇s solution equivalent to the volume of shed blood. FR167653 5 mg/kg was injected intravenosly in group FR. FR167653 5 mg/kg was injected intravenously 30 min before blood-letting in group FR ＋ HSR. The animals were sacrificed by exsanguination at 6 h after resuscitation. The lungs were immediately removed for microscopic examination. The W/D lung weight ratio was calculated and the levels of myeloperoxidase （MPO）, IL-10, IL-6 and HO-1 and activated p38MAPK were determined （by ELISA）.Results Compared with group S, the pathological score, W/D ratio, the levels of MPO, IL-10, IL-6 and HO-1 and the level of activated p38MAPK were significantly increased in group HSR, the pathological score, W/D ratio and the level of HO-1 were significantly increased in group HSR ＋ FR （ P 〈 0.01） .Compared with group HSR, the pathological score, W/D ratio, the levels of MPO, IL-10, IL-6 and HO-1 and activated p38MAPK were significantly decreased in group HSR ＋ FR （ P 〈 0.01 ）. Conclusion p38MAPK signaling pathway mediates the up-regulation of HO-1 expression during HSR-induced ALI in mice. Key words: p38 Mitogen-activated protein kinases; Heme oxygenase-1; Shock, hemorrhagic; Respiratory distress syndrome, adult

Influence of ventilatory settings on static and functional haemodynamic parameters during experimental hypovolaemia

The influence of ventilatory settings on static and functional haemodynamic parameters during mechanical ventilation is not completely known. The purpose of this study was to evaluate the effect of positive end-expiratory pressure, tidal volume and inspiratory to expiratory time ratio variations on haemodynamic parameters during haemorrhage and after transfusion of shed blood. Ten anaesthetized pigs were instrumented and mechanically ventilated with a tidal volume of 8 mlkg(-1), a positive end-expiratory pressure of 5 cmH(2)O and an inspiratory to expiratory ratio of 1:2. Then, they were submitted in a random order to different ventilatory settings (tidal volume 16 mlkg(-1), positive end-expiratory pressure 15 cmH(2)O or inspiratory to expiratory time ratio 2:1). Functional and static haemodynamic parameters (central venous pressure, pulmonary artery occlusion pressure, right ventricular end-diastolic volume and pulse pressure variation) were evaluated at baseline, during hypovolaemia (withdrawal of 20% of estimated blood volume) and after an infusion of withdrawn blood (posttransfusion). During baseline, a positive end-expiratory pressure of 15 cmH(2)O significantly increased pulmonary artery occlusion pressure from 14.6 +/- 1.6 mmHg to 17.4 +/- 1.7 mmHg (P < 0.001) and pulse pressure variation from 15.8 +/- 8.5% to 25.3 +/- 9.5% (P < 0.001). High tidal volume increased pulse pressure variation from 15.8 +/- 8.5% to 31.6 +/- 10.4% (P < 0.001), and an inspiratory to expiratory time ratio of 2: 1 significantly increased only central venous pressure. During hypovolaemia, high positive end-expiratory pressure influenced all studied variables, and high tidal volume strongly increased pulse pressure variation (40.5 +/- 12.4% pre vs. 84.2 +/- 19.1% post, P < 0.001). The inversion of the inspiratory to expiratory time ratio only slightly increased filling pressures during hypovolaemia, without affecting pulse pressure variation or right ventricle end-diastolic volume. We concluded that pulse pressure variation measurement is influenced by cyclic variations in intrathoracic pressure, such as those caused by augmentations in tidal volume. The increase in mean airway pressure caused by positive end-expiratory pressure affects cardiac filling pressures and also pulse pressure variation, although to a lesser extent. Inversion of the inspiratory to expiratory time ratio does not induce significant changes in static and functional haemodynamic parameters.

Fat embolism and autologous blood transfusions in orthopaedic surgery

Fat embolism is a well-known complication associated with orthopaedic procedures like total hip or knee arthroplasty. The clinical relevance of fat embolism in association with orthopaedic procedures is, however, controversial. Although transesophageal echocardiography indicates echogenic material in the central circulation in more than 90% of patients undergoing cemented hip arthroplasty, the incidence of cardiac arrest due to pulmonary fat embolism is less than 1%. Cementation is known to increase the incidence of embolic complications. The duration of the pressure and the intensity of pressure inside the bone cavity are correlated with the incidence of fat emboli and the cardiopulmonary function. The use of modern cementing techniques and non-cemented arthroplasty reduces the incidence and the clinical risk of fat embolism. The disadvantages with allogeneic blood transfusions have encouraged the development of methods to reduce the need for such transfusions. Devices for salvage of blood during or after orthopaedic procedures have been shown to reduce the need for allogeneic transfusions. Shed blood may contain high concentrations of inflammatory mediators and may be contaminated with fat particles which may increase the risk of fat embolism. Transfusion of blood after washing and centrifugation and filtration of salvaged blood are available methods for transfusion of shed blood and that may reduce the amount of transfusion of fat.

Protective effect of urinary trypsin inhibitor on myocardial mitochondria during hemorrhagic shock and reperfusion.

To examine the mitochondrial function in the myocardium after hemorrhagic shock and reperfusion and to evaluate the protective effect of urinary trypsin inhibitor (UTI) on mitochondria. Animal experiment. University research laboratory. Wistar rats receiving 50,000 units/kg/hr of UTI (n = 27; UTI group) and control rats (n = 26; control group). Rats were subjected to low-perfusion ischemia with the left ventricular systolic pressure maintained at 50 mm Hg for 60 mins by bleeding, followed by a 60-min reperfusion by transfusion of shed blood. UTI was infused continuously from 10 mins before bleeding. Cardiac function was measured before bleeding, after bleeding, and after transfusion; at each determination point, the myocardial contents of adenosine triphosphate (ATP), creatine phosphate (P-Cr), pyruvate (Pyr), and lactate (Lac) were measured enzymatically. The cytosolic phosphorylation potential (PP) as well as the redox potential of the oxidized form of nicotinamide adenine dinucleotide/reduced form of nicotinamide adenine dinucleotide couple in mitochondria (Eh(NAD+/NADH)) and change of Gibbs free energy in ATP hydrolysis (deltaG(ATP hydrolysis) energy) were calculated. Cardiac function decreased during hemorrhagic shock but improved significantly in the UTI group after transfusion compared with the control group. Lac and the Lac/Pyr ratio were significantly lower in the UTI group than in the control group after transfusion. ATP and P-Cr were significantly higher in the UTI group than in the control group after transfusion. PP (x10(3) M-1), Eh(NAD+/NADH) (x - 1 mV), and deltaG(ATP hydrolysis) (x - 1 kcal/mol) were 1.9 +/- 0.4, 266 +/- 4, and 9.7 +/- 0.2, respectively, in the control group and 4.0 +/- 0.9, 274 +/- 5 and 13.0 +/- 0.2, respectively, in the UTI group after transfusion (p <.001, p <.001, and p <.001, respectively). In reperfusion after hemorrhagic shock, oxidative phosphorylation in myocardial mitochondria is impaired and energy production remains reduced, even after reperfusion. UTI contributed to the recovery of cardiac function after reperfusion, probably by reducing the severity of mitochondrial dysfunction during a state of shock and by maintaining energy production.

S100β after coronary artery surgery: release pattern, source of contamination, and relation to neuropsychological outcome

Background. S100β has been suggested as a marker of brain damage after cardiac operation. The aim of this study was to characterize the early S100β release in detail and relate it to neuropsychological outcome.Methods. Three groups of patients were investigated. All patients underwent coronary artery bypass surgery (CABG) with extracorporeal circulation. In group A, 110 patients had sampling of S100β for the first 10 postoperative hours and also underwent neuropsychological testing. In group B, 14 patients were examined for the effect of autotransfusion on S100β levels. Eight patients in group C had their intraoperative bleeding processed with a cell-saving device.Results. Group A had a heterogeneous release pattern with several rapid elevations in S100β concentration. In group B, high concentrations of S100β were found in the autotransfusion blood (range 0.2 to 210 μg/L) with a concurrent elevation of serum S100β levels after transfusion of shed blood. In group C, high levels of S100β were found in the blood from the surgical field (12.0 ± 6.0 μg/L) and decreased (1.1 ± 0.64 μg/L) after wash. Group C had significantly lower S100β values at the end of cardiopulmonary bypass compared to group A (0.53 ± 0.35 μg/L versus 2.40 ± 1.5 μg/L). S100β values were corrected for extracerebral contamination with a kinetic model. With this correction, an association was found between adverse neuropsychological outcome and S100β release in group A (r = 0.39, p < 0.02).Conclusions. A significant amount of S100β is found both in the blood from the surgical field and in the shed mediastinal blood postoperatively. Infusion of this blood will result in infusion of S100β into the blood and interfere in the interpretation of early systemic S100β values.

Formation of complement split products and proinflammatory cytokines by reinfusion of shed autologous blood

1. The purpose of this study was to determine whether shed autologous blood collected postoperatively contains complement split products (C3a and SC5b-9) and proinflammatory cytokines (TNF- α, IL-1 β, IL-6 and IL-8) and whether transfusion of shed blood increases the concentrations of inflammatory mediators in the circulation. 2. Twenty consecutive patients undergoing total hip replacement surgery under spinal anaesthesia were studied. The patients were transfused with whole blood collected postoperatively. 3. The median volume shed blood returned to the patients was 350 ml (25–75% range=300–450). Before transfusion of shed blood was filtered using a 40 μm filter (Solcotrans®). Samples for complement and cytokine determinations were drawn from the collected blood. 4. Venous blood samples were drawn 1 min before transfusion, 1 and 60 min after completed transfusion. High concentrations of C3a, SC5b-9, TNF- α, IL-1 β, IL-6 and IL-8 were found in shed blood. The concentrations were higher than the circulating levels ( P<0.05). The filtration procedure did not significantly reduce the concentrations. 5. Transfusion of the shed blood did not significantly alter the circulating concentrations of C3a, SC5b-9, TNF- α, IL-1 β, and IL-8. The plasma concentrations of IL-6 were increased both 1 and 60 min after completed transfusion compared to before ( P<0.05). 6. This study shows that whole blood collected from a surgical wound contains large concentrations of complement split products and proinflammatory cytokines. Transfusion of shed blood leads to elevated plasma levels of IL-6.

Levels of Troponin I and Cardiac Enzymes After Reinfusion of Shed Blood in Coronary Operations

Background. Reinfusion of shed blood after coronary artery bypass grafting might increase the levels of cardiac enzymes with consequent difficulties in the diagnosis of perioperative myocardial infarction. Methods. Thirty consecutive patients undergoing coronary artery bypass grafting who bled at least 400 mL within the first 4 hours after operation underwent reinfusion of shed blood. Thirty consecutive patients who were not autotransfused served as control. All patients underwent enzyme determination (total creatine kinase, MB fraction, lactate dehydrogenase, and troponin I) in the shed blood and in circulating blood preoperatively, at arrival in the intensive care unit, and 6, 24, and 48 hours after operation. Results. The shed blood contained significantly higher concentration of cardiac enzymes than the circulating blood at all time intervals ( p = 0.0001). The levels of creatine kinase, its MB fraction, and lactate dehydrogenase in circulating blood were significantly elevated in patients receiving autotransfusion up to 24 hours after autotransfusion. The blood levels of troponin I were not significantly different between the two group of patients at all time points. The percent fraction of MB did not increase after autotransfusion. Conclusions. The measurement of cardiac troponin I is a useful marker for the diagnosis of perioperative myocardial infarction in patients undergoing transfusion of shed blood after coronary operation.

Effects on complement activation of a new continuous autotransfusion system.

Allogeneic blood transfusions may subject patients to risks of infection and allergic reactions. Various techniques for transfusion of shed blood have been developed. The aim of this study was to evaluate a new continuous autotransfusion system (Fresenius CATS) as regards its impact on the complement system, and on erythrocytes and leucocytes. Eighteen consecutive patients undergoing hip replacement surgery were studied. Complement variables (C4d, factor Bb, C3a and terminal complement complex, SC5b-9) and free haemoglobin, haemoglobin, leucocytes, platelets, albumin and protein were determined in the patient's blood preoperatively, 1 min before the start of transfusion, 15 and 60 min after transfusion; and in the reservoir, in the waste bag and in the retransfusion blood. Increased concentrations of C3a and SC5b-9 were found in the collected reservoir blood (P < 0.05). The washing and centrifugation procedure reduced these concentrations (< 0.001). High levels of free haemoglobin were found in the collected blood as well as in the processed product. The median haemoglobin level in the processed blood was 260gL-1 (range 104-289gL-1). Inflammatory mediators from the complement cascade are removed by continuous autotransfusion technique. The processed blood contains high levels of free haemoglobin.

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.

Effects of ulinastation on rat renal energy metabolism and blood flow in hemorrhagic shock

The effect of ulinastation on rat renal energy metabolism and blood flow in hemorrhagic shock was studied by(31)P nuclear magnetic resonance spectroscopy. Hemorrhagic shock was induced by withdrawing blood from the left carotid artery into a reservoir until mean femoral arterial blood pressure stabilized as 20 mmHg. Ulinastatin (50000 units·kg(-1); UTI group, n=10) or saline (0.9% NaCl; NS group, n=10) was injected continuously during 30 min of hemorrhagic shock. Next, the total volume of blood shed in the reservoir was transfused into the right femoral vein over a period of 5 min. In the UTI group, 23.2±15.1% of adenosine triphosphate (ATP) remained and intracellular pH (pHi) was 6.77±0.07 at 30 min of hemorrhagic shock. However, ATP was not detected and pHi showed severe acidosis (pHi: 6.49±0.04) in the NS group. After the transfusion of shed blood, the UTI group exhibited higher ATP levels and pHi values than the NS group. Rats treated with UTI maintained mean arterial blood pressure and renal blood flow at significantly higher values than those administered NS.Ulinastatin improved the energy metabolism of the shocked kidney. We believe that ulinastatin maintains mitochondrial function against hemorrhagic shock by its membrane-stabilizing actions and might contribute beneficially in hemorrhagic shock.

Hemorrhagic shock and acid gastric injury in the rat: Comparison of gross and histologic findings

The purpose of this study was to compare the gross and histologic changes in the corpus and antrum in the rat hemorrhagic shock plus acid model of gastric injury, and to determine the effect of transfusion of shed blood or albumin on gastric lesion formation. The data indicate that (a) despite the gross appearance of more severe damage in the corpus, histologic damage was more severe in the antrum; (b) covering mucus and cell debris partly explain the difficulty in recognizing antral lesions grossly; (c) the severity of histologic injury was similar in transfused and nontransfused rats; and (d) transfusion of shed blood rendered corpus lesions more recognizable grossly but did not affect the severity of histologic injury. The latter findings raise questions about the pathogenetic importance of reperfusion in gastric ischemic injury and the validity of using gross lesions as an index of gastric injury.

Beneficial and detrimental actions of histamine H1- and H2-receptor antagonists in circulatory shock.

This study explores the use of both histamine H(1)- and H(2)-receptor antagonists in two different forms of circulatory shock and suggests that histamine may be involved in more than one way in the pathophysiology of circulatory shock. Various single doses of diphenhydramine, chlorpheniramine, promethazine, and burimamide were administered intravenously to Wistar rats subjected to hemorrhagic or bowel ischemia shock. Cumulative survival and mortality, as well as arterial blood pressures and microhematocrits, were monitored. Pretreatment of the animals with the three different H(1)-receptor antagonists exerted significant protection against both forms of shock. Rats pretreated with the H(2)-receptor antagonist, burimamide, demonstrated an exacerbated mortality after induction of shock. Animals pretreated with H(1)-receptor antagonists showed significantly higher mean arterial blood pressure, greater compensatory rebound of blood pressure after induction of shock, and greater responses to transfusion after hemorrhage than control, shocked animals. Similarly, rats pretreated with the H(1)-receptor blockers demonstrated significantly greater compensatory hemodilution which continued late in shock. In marked contrast, rats pretreated with burimamide exhibited opposite effects after hemorrhage and bowel ischemia, i.e., significant falls in blood pressure, lack of compensatory rebound and response to transfusion of shed blood, and a progressive hemoconcentration. This report clearly demonstrates beneficial actions of histamine H(1)-receptor antagonists and detrimental effects of H(2)-receptor antagonists on survival and other parameters in these forms of circulatory shock.