Abstract 218: Therapeutic Hypothermia Alone and Combination With Preconditioning Blunt Inflammation in Experimental Hemorrhagic Shock

Circulation ◽  
2019 ◽  
Vol 140 (Suppl_2) ◽  
Author(s):  
Jianru Shi ◽  
Wangde Dai ◽  
Juan Carreno ◽  
Sharon L Hale ◽  
Robert A Kloner
Keyword(s):  
Hemorrhagic Shock ◽  
Therapeutic Hypothermia ◽  
Absolute Lymphocyte Count ◽  
Control Group ◽  
Sprague Dawley ◽  
Term Survival ◽  
Shed Blood ◽  
Arterial Blood ◽  
The Absolute ◽  
Experimental Hemorrhagic Shock

Background: Recent studies by our group indicate that preconditioning, therapeutic hypothermia (TH) and TH combined with preconditioning improved long-term survival during resuscitation of hemorrhagic shock. The neutrophil-to-lymphocyte ratio (NLR) is a marker of inflammation associated with increased mortality in patients with severe hemorrhage shock. The aim of this study is to evaluate the effects of these three therapies on NLR level in rats with acute hemorrhagic shock. Methods and Results: In the preconditioning study, Sprague Dawley rats (both genders) were randomized to preconditioning (n=26) or control group (n=27); in the hypothermia study, rats were randomized to TH (n=16) or control group (n=15); in a combination study, rats were randomized to TH plus preconditioning (n=11) or control group (n=10). Rats were anesthetized with intraperitoneal Ketamine and xylazine. After heparinizing, hemorrhagic shock was induced by withdrawing blood to a fixed mean blood pressure (MBP) of 30 mmHg for 30 minutes and then shed blood was reinfused. Preconditioning was induced by 4 cycles of inflating small cuffs around the femoral arteries to 200 mmHg for 5 minutes, followed by 5-minute deflation of the cuffs prior to hemorrhagic shock. TH started at 5 minutes after MBP reached 30 mmHg. Core temperature was maintained at ~32 °C until blood volume was fully restored. In the control group, body temperature was maintained at ~ 37°C. Arterial blood samples were collected 1 hour after resuscitation. The NLR is an easily accessible biomarker, which is calculated by dividing the absolute neutrophil count by the absolute lymphocyte count. The NLR was significantly lower in TH group (0.20 ± 0.02) compared with the control group (0.32 ± 0.03; p=0.003). Similarly, the NLR level was significantly decreased in TH plus preconditioning group (0.19 ± 0.02) versus the control group (0.33 ± 0.02; p= 0.001). There was no difference in NLR level between the preconditioning group (0.41 ± 0.04) and the control group (0.41 ± 0.04; p=0.984). Conclusions: NLR is widely recognized inflammation marker associated with poor prognosis in severe hemorrhagic shock. TH alone and TH combined with preconditioning blunt the inflammation by decreasing the NLR level in experimental hemorrhagic shock.

Abstract 120: Effects of Therapeutic Hypothermia on Blood Parameters in Rats With Acute Hemorrhagic Shock

Circulation ◽  
2019 ◽  
Vol 140 (Suppl_2) ◽  
Author(s):  
Jianru Shi ◽  
Wangde Dai ◽  
Juan Carreno ◽  
Sharon L Hale ◽  
Robert A Kloner
Keyword(s):  
Hemorrhagic Shock ◽  
Potassium Chloride ◽  
Therapeutic Hypothermia ◽  
Early Phase ◽  
Group Versus ◽  
Blood Parameters ◽  
Term Survival ◽  
Shed Blood ◽  
Arterial Blood ◽  
Normothermic Group

Background: Our research group recently observed that therapeutic hypothermia (TH) compared with normothermia improved long-term survival in an experimental model of hemorrhagic shock. The effect of TH on blood counts, blood gases and chemistries during the early phase of recovery from hemorrhagic shock are unknown. Therefore, the purpose of the present study was to examine the effects of TH on blood parameters in the early phase of resuscitation from hemorrhagic shock. Methods and results: Sprague Dawley rats (both genders) were randomly assigned to TH (n= 16) or normothermia group (n= 15). Rats were anesthetized with intraperitoneal ketamine and xylazine. After heparinizing, hemorrhagic shock was induced by withdrawing blood to a fixed mean blood pressure (MBP) of 30 mmHg for 30 minutes and then shed blood was reinfused. TH was started 5 minutes after MBP reached 30 mmHg. Core temperature was maintained at ~ 32 °C until blood volume was fully restored, after which the rats were allowed to warm back to normal temperature. In the normothermia group, body temperature was maintained at ~ 37°C. Arterial blood samples were collected 1 hour after resuscitation with shed blood. We found that pO2 (partial pressure of oxygen) was significantly higher in TH group versus the normothermic group. The rats in normothermic group had significantly elevated potassium, chloride and lactate levels and more negative base excess compared to rats that in TH group (Table). The neutrophil was lower in the TH group; the lymphocyte (%) was higher in the TH group. There were no significantly differences in pH, pCO2, sodium, calcium or glucose between the normothermia and TH groups. Conclusions: pO2 remained normal and levels of potassium, chloride, lactate and neutrophil were lower in TH group. These results may contribute to the protective effect of TH during hemorrhagic shock.

Abstract 216: Therapeutic Hypothermia Alone and in Combination With Preconditioning Improves Long Term Survival During Resuscitation of Hemorrhagic Shock

Circulation ◽  
2019 ◽  
Vol 140 (Suppl_2) ◽  
Author(s):  
Wangde Dai ◽  
Jianru Shi ◽  
Juan Carreno ◽  
Robert A Kloner
Keyword(s):  
Blood Pressure ◽  
Hemorrhagic Shock ◽  
Therapeutic Hypothermia ◽  
Mean Blood Pressure ◽  
Control Group ◽  
Sprague Dawley ◽  
Term Survival ◽  
Long Term Survival ◽  
Combination Study

Background: We investigated the effects of hypothermia treatment alone and in combination with experimental bilateral lower limb remote ischemic preconditioning (RIPC) in rats undergoing experimental hemorrhagic shock. Previously we showed that RIPC alone improved survival. Methods: In the hypothermia alone study, adult Sprague Dawley rats (both genders) were randomized to hypothermia (n=16) or control group (n=15); in a combination study, rats were randomized to hypothermia plus RIPC (n=11) or control group (n=10). Rats were anesthetized with intraperitoneal ketamine/xylazine. Therapeutic hypothermia (Thermosuit) was started at 5 minutes after mean blood pressure (MBP) reached 30 mmHg. Core temperature was maintained at ~ 32 °C until blood volume was fully restored. RIPC was induced by 4 cycles of inflating small bilateral pressure cuffs to 200 mmHg around the femoral arteries for 5 minutes, followed by 5 minute deflation of the cuffs prior to hemorrhagic shock. In the control group, body temperature was maintained at 37 °C during the procedure. Hemorrhagic shock was induced by withdrawing blood from the carotid artery. Target mean blood pressure of 30 mmHg was maintained for 30 minutes followed by reinfusion of shed blood within the next 30 min. Rats were allowed recovery and the primary endpoint was survival rate at 6 weeks. Results: In the setting of hypothermia alone, 4 of 15 (26.7 %) rats in the control group and 11 of 16 (68.8 %; p = 0.032) rats in the hypothermia group survived at 6 weeks. In the combination study, 1 of 10 (10 %) rats in the control group and 7 of 11 (63.6 %; p = 0.024) rats in the hypothermia plus RIPC group survived at 6 weeks. Kaplan Meier Survival Curves are shown in Fig1. Conclusions: Hypothermia alone and combination with RIPC significantly improved long term survival in rats subjected to hemorrhagic shock. Hypothermia and RIPC did not show survival rates greater than hypothermia alone.

Decreases in organ blood flows associated with increases in sublingual P CO 2 during hemorrhagic shock

1998 ◽  
Vol 85 (6) ◽  
pp. 2360-2364 ◽  
Author(s):  
Xiaohua Jin ◽  
Max Harry Weil ◽  
Shijie Sun ◽  
Wanchun Tang ◽  
Joe Bisera ◽  
...  
Keyword(s):  
Blood Flow ◽  
Hemorrhagic Shock ◽  
Esophageal Wall ◽  
Sprague Dawley ◽  
Shed Blood ◽  
Blood Flows ◽  
Arterial Blood ◽  
Sprague Dawley Rats ◽  
Arterial Blood Lactate ◽  
Highly Correlated

Earlier studies demonstrated that not only the stomach but also the esophageal wall served as an appropriate site for estimating the severity of circulatory shock by using tonometric methods. We then conceived of the option of sublingual tonometry. In the present study, we tested the hypothesis that the changes in sublingual [Formula: see text] serve as indicators of decreases in blood flow to sublingual and visceral tissue. In Sprague-Dawley rats, sublingual[Formula: see text] increased from 50 to 127 Torr and arterial blood lactate increased from 0.9 to 11.2 mmol/l during bleeding. Sublingual blood flow simultaneously decreased to ∼32% of preshock values. After reinfusion of shed blood, organ blood flows and sublingual [Formula: see text] were promptly restored to near-baseline values. There were corresponding decreases in blood flows in the tongue, stomach, jejunum, colon, and kidneys during hemorrhagic shock. Increases in sublingual[Formula: see text] were highly correlated with decreases in sublingual blood flow ( r= 0.80), tongue blood flow ( r = 0.81), gastric blood flow ( r = 0.74), jejunal blood flow ( r = 0.65), colon blood flow ( r = 0.80), and renal blood flow ( r = 0.75). Unbled control animals demonstrated no significant changes. Therefore, we anticipate that sublingual tonometry will provide a useful, noninvasive alternative for monitoring visceral [Formula: see text].

Abstract 191: Effects of Anesthetic Agents on Blood Parameters in Rats With Acute Hemorrhagic Shock

Circulation ◽  
2018 ◽  
Vol 138 (Suppl_2) ◽  
Author(s):  
Jianru Shi ◽  
Wangde Dai ◽  
Juan Carreno ◽  
Sharon L Hale ◽  
Robert A Kloner
Keyword(s):  
Hemorrhagic Shock ◽  
Blood Parameters ◽  
Protective Role ◽  
Sprague Dawley ◽  
Shed Blood ◽  
Anesthetic Agents ◽  
Essentially Normal ◽  
Arterial Blood ◽  
Lactate Levels ◽  
Negative Base

Background: Recent studies in our laboratory indicate that isoflurane (ISO) has protective properties including improved survival in rats with hemorrhagic shock compared to ketamine and xylazine (K/X) anesthesia. The effects of these two anesthetic agents upon blood counts, gases and chemistries in the setting of hemorrhagic shock is unknown. The purpose of the present study was to examine the effects of these two commonly used anesthetic regimens on blood parameters in rats with acute hemorrhagic shock. Methods and Results: Sprague Dawley rats (both genders) were anesthetized with either intraperitoneal K/X (90mg/kg and 10mg/kg; n=12) or with isoflurane (5% isoflurane induction and 2% maintenance in room air; n=12). Rats were intubated and ventilated with room air. After heparinization, hemorrhagic shock was induced by withdrawing blood to a fixed mean blood pressure of 30 mmHg for one hour and then shed blood was reinfused. Arterial blood samples were collected at 1 hour after resuscitation with shed blood. We found that K/X was associated with lower PH and lower level of standard bicarbonate concentration (SBC) and oxygen saturation (SO 2 %) and more negative base excess; and had a significantly elevated anion gap, potassium, sodium and chloride levels compared to isoflurane (Table). Platelet counts were preserved and there was less elevation of white blood cell (WBC) in ISO (Table). There were no significant differences in PO 2 , PCO 2 , hematocrit, hemoglobin, glucose and lactate levels between the two types of anesthesia. Conclusions: The anesthesia influenced the levels of blood counts, gases and chemistries in rats with acute hemorrhagic shock, favoring ISO over K/X. Blood parameters remained essentially normal in ISO group, which may help explain the protective role of ISO in hemorrhagic shock.

Abstract 186: Remote Limb Ischemic Preconditioning Improves Short and Long Term Survival and Maintains Intravascular Blood Volume During Resuscitation of Hemorrhagic Shock

Circulation ◽  
2018 ◽  
Vol 138 (Suppl_2) ◽  
Author(s):  
Wangde Dai ◽  
Jianru Shi ◽  
Juan Carreno ◽  
Sharon Hale ◽  
Robert A Kloner
Keyword(s):  
Blood Pressure ◽  
Hemorrhagic Shock ◽  
Blood Volume ◽  
Ischemic Preconditioning ◽  
Control Group ◽  
Term Survival ◽  
Shed Blood ◽  
Short And Long Term ◽  
And Control

Background: We further examined the protective effects of experimental bilateral lower limb remote ischemic preconditioning (RIPC) in rats undergoing experimental hemorrhagic shock. Methods: Sprague Dawley rats (both genders) were randomized into RIPC (n= 26) or control group (n= 27), and anesthetized with intraperitoneal ketamine/xylazine. RIPC was induced by 4 cycles of inflating small bilateral pressure cuffs to 200 mmHg around the femoral arteries for 5 minutes, followed by 5 minute deflation of the cuffs. Hemorrhagic shock was induced by withdrawing blood from the carotid artery. Target mean blood pressure of 30 mmHg was maintained for 30 minutes followed by reinfusion of shed blood within the next 30 min. Rats remained anesthetized for another 30 min before recovery; endpoints were survival at 72 hours and 6 weeks. Results: The % of estimated total blood volume withdrawn to maintain a level of 30 mmHg was similar in the RIPC group (41.7 ± 1.0 %) and control group (41.9 ± 1.0 %). Recovery of blood pressure during the early resuscitation phase was significantly improved in the RIPC group. The diastolic internal dimension of the left ventricle (echocardiogram), which indicates circulating intravascular blood volume, was significantly larger in the RIPC group at 1 hour after initiation of shed blood reinfusion (5.8 ± 0.1 mm) compared to 5.4 ± 0.1mm in the control group (p=0.04). Left ventricular fractional shortening was comparable between RIPC (50.9 ± 1.9 %) and control group (49.6 ± 1.8 %; p=0.64) at 1 hour after initiation of resuscitation. At 48 hours after shock, BUN was within normal range in the RIPC group (17.3 ± 1.2 mg/dl); but elevated in the control group (22.0 ± 1.7 mg/dl). At 72 hours after hemorrhagic shock injury, 6 of 27 (22.2 %) rats in the control group and 13 of 26 (50 %, p = 0.047) rats in the RIPC group survived. At 6 weeks, 5 of 27 (18.5 %) rats in the control group and 13 of 26 (50 %; p = 0.021) rats in the RIPC group survived. RIPC significantly increased survival rate at both 72 hours and 6 weeks. Conclusions: RIPC improved recovery of blood pressure and maintained more circulating intravascular blood volume in the early phase of resuscitation, improved BUN, and markedly and significantly improved short and long term survival in rats subjected to hemorrhagic shock.

Abstract P126: Effects of Carvedilol on Mortality and Inflammatory Responses to Hemorrhagic Cardiac Arrest in Rats

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Takumi Taniguchi ◽  
Hideo Inaba
Keyword(s):  
Cardiac Arrest ◽  
Treatment Group ◽  
Oral Administration ◽  
Hemorrhagic Shock ◽  
Beta Blocker ◽  
Inflammatory Responses ◽  
Tnf Alpha ◽  
Control Group ◽  
Sprague Dawley ◽  
Arterial Blood

Recent studies showed that beta-blocker is often used in hypertensive and/or cardiac failure patients because of its drug efficacy. Moreover, several papers reported that beta-blocker has the beneficial effects in patients with cardiogenic shock. However, there are few studies about the effects of beta-blocker during hemorrhagic shock and hemorrhagic cardiac arrest. To evaluate the effects of beta-blocker in an animal model of hemorrhagic cardiac arrest. Carvedilol was used as the beta-blocker agents. Twenty-four male Sprague Dawley rats were used. Animals were randomly assigned to one of two groups (n = 12 per group): control group, no medication; treatment group, oral administration of carvedilol (10 mg/kg/day) for 5 days. After then, all animals were anesthetized with pentobarbital ip. Hemorrhagic cardiac arrest was induced with removing of blood. After 8 minutes of cardiac arrest, the all removing blood was administered. There were no other therapies before, during or after cardiac arrest. Hemodynamics and arterial blood gases were recorded, and mortality were calculated for the 5-hr observation period and plasma cytokine (TNF-alpha and Interleukin-6) concentrations were measured at 5-hr after cardiac arrest. The mortality rates at 5hrs after cardiac arrest were 8% and 50% for control and treatment groups, respectively. The increases of base deficit and lactate concentrations were less for the control group than the treatment group. Moreover, the increases of TNF-alpha and IL-6 concentrations were less for the control group than the treatment group. The present study showed that oral administration of carvedilol had the disadvantage effects on mortality and inflammatory effects to hemorrhagic cardiac arrest in rats. These finding suggest that beta-blocker may worsen the recovery of hemorrhagic shock.

Differing effects of anesthetics on splanchnic arterial blood flow during hemorrhagic shock

1994 ◽  
Vol 76 (6) ◽  
pp. 2304-2309 ◽  
Author(s):  
S. I. Myers ◽  
R. Hernandez ◽  
T. A. Miller
Keyword(s):  
Blood Flow ◽  
Hemorrhagic Shock ◽  
Arterial Blood Flow ◽  
Splanchnic Blood Flow ◽  
Aortic Blood Flow ◽  
Sprague Dawley ◽  
Acute Hemorrhage ◽  
Shed Blood ◽  
Arterial Blood ◽  
Aortic Blood

The effect of anesthesia on splanchnic blood flow was examined during hemorrhagic shock and resuscitation. Sprague-Dawley rats were anesthetized with the inhalation anesthetic, methoxyflurane, or pentobarbital (65 mg/kg). Transonic Doppler flow probes were placed around the superior mesenteric artery (SMA) and the abdominal aorta, and the animals were subjected to acute hemorrhage (or sham) to 30 mmHg for 90 min followed by 30 min of resuscitation with shed blood (n = 6/group). At 90, 105, and 120 min, sham animals in both anesthetic groups showed comparable blood pressures with a 50% decrease in SMA and aortic blood flow. Acute hemorrhage decreased SMA blood flow by 94.5 +/- 0.01 and 86.0 +/- 2.8%, respectively, in the pentobarbital and methoxyflurane groups, with similar changes occurring in aortic blood flow. During resuscitation, arterial pressure remained significantly depressed and SMA blood flow decreased by 65% in the pentobarbital group, whereas blood pressure returned to control levels and SMA blood flow increased to 56% of control values (P < 0.001) in the methoxyflurane group. The findings indicate that the choice of anesthetic agent may significantly impact splanchnic blood flow and needs to be taken into account when designing experiments examining effects of hemorrhagic shock.

Abstract 119: Influence of Anesthetics on the Hemodynamic Response in a Rat Model of Hemorrhagic Shock

Circulation ◽  
2019 ◽  
Vol 140 (Suppl_2) ◽  
Author(s):  
Claudius Balzer ◽  
Franz J Baudenbacher ◽  
Susan S Eagle ◽  
Michele M Salzman ◽  
William J Cleveland ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Hemorrhagic Shock ◽  
Rat Model ◽  
Cardiovascular Response ◽  
Femoral Vein ◽  
Blood Pressure Measurement ◽  
Experimental Models ◽  
Sprague Dawley ◽  
Compensatory Mechanisms ◽  
Arterial Blood

Introduction: Experimental models of hemorrhagic shock (HS) in rats are important to test new treatments that may improve outcomes in humans, and general anesthesia is required during these experiments. The volatile anesthetic Isoflurane is known for its beneficial effects in rat HS models. Focusing on cardiovascular compensatory mechanisms, we wanted to evaluate Isoflurane versus the injectable anesthetic Pentobarbital in our rat model of mild HS (class 2). We hypothesize that Isoflurane during development of HS improves hemodynamics compared to Pentobarbital. Methods: Twelve Sprague-Dawley rats were initially anesthetized with an intraperitoneal (IP) injection of Pentobarbital (45 mg/kg) and intubated (1 L/min, FiO 2 0.25); heart rate (HR) was monitored by subcutaneous ECG needles. Femoral artery and vein were cannulated for continuous blood pressure measurement and delivery of fluids, respectively. In one group (n=7), anesthesia was continued with repeated IP injections of Pentobarbital (dose mg/kg), the other group (n=5) received continuous Isoflurane (1%). After 30 min of stabilization and administration of Heparin (100 IU/kg), HS was induced by removal of 1 ml of blood over 1 min via the femoral vein, repeated every 3 min until a volume of 5 ml of blood was removed. Mean arterial blood pressure (MAP) and HR were recorded and analyzed in LabChart. Results: During baseline, rats showed no significant differences in HR and MAP between both groups. After 5 ml of hemorrhage, both groups showed significant changes compared to baseline, with significantly higher MAP and HR in rats given only Pentobarbital. Conclusions: In our rat model of HS, Isoflurane dampens the physiologic response to compensate for mild hemorrhage. The cardiovascular response of rats in the Isoflurane group was a decrease of HR and MAP to every ml of hemorrhage, while rats given only Pentobarbital were able to maintain their MAP by raising their HR until decompensation.

Abstract P14: Estradiol Does Not Improve Survival and Hemodynamic Parameters in Male Piglets after Hemorrhage and Ventricular Fibrillation

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Egidijus Semenas ◽  
Lars Wiklund
Keyword(s):  
Gender Differences ◽  
Cardiac Arrest ◽  
Ventricular Fibrillation ◽  
Hemorrhagic Shock ◽  
Repeated Measures ◽  
Troponin I ◽  
Control Group ◽  
Hemodynamic Parameters ◽  
Start Time ◽  
Arterial Blood

Introduction: Gender differences in organ functions and survival have been described in animal models of trauma and hemorrhagic shock. The female gender is associated with better cardiac, hepatic and immune functions compared to males after hemorrhagic shock. However, data about gender differences in hypovolemic normothermic cardiac arrest is lacking. Hypothesis: We hypothesized that the estradiol given during cardiopulmonary resuscitation (CPR) will improve survival and hemodynamic response in hypovolemic cardiac arrest and subsequent CPR. Methods: Twenty anesthetized male piglets (with a weight of 25.7 ± 1.7 kg [mean ± SD]) were bled 30% via the right femoral artery to a mean arterial blood pressure of 35 mm during 15 minutes. In the end of bleeding period estradiol group (n=10) received 17â-estradiol 50 ìg/kg intravenously, while the control group received no estradiol (n=10). Later all piglets were subjected to 4 min of untreated ventricular fibrillation followed by up to 15 min of open chest CPR. At 5 min of cardiac arrest piglets received vasopressin 0.4 U/kg, amiodarone 0.5 mg/kg, and hypertonic-hyperoncotic solution 3 ml/kg infusion for 20 minutes. Internal defibrillation was attempted from 8 min of cardiac arrest to achieve restoration of spontaneous circulation (ROSC). The experiment was terminated at 3 hours after initial resuscitation. Data were analyzed using Fisher’s exact test, Kaplan-Meier and repeated measures ANOVA methods. Results: All piglets were successfully resuscitated. No significant differences were observed in survival between the groups (p=0.24). All piglets needed dobutamine infusion and no differences were observed in either total dobutamin dose, or infusion start time (p=0.05). No significant changes were observed in any hemodynamic parameters (p>0.05). Troponin I levels did not differ between groups (p>0.75). Conclusions: Intravenous 17â-estradiol does not improve survival and hemodynamic parameters in male piglets after experimental hypovolemic cardiac arrest.

Humoral factor depletion and reticuloendothelial depression during hemorrhagic shock

1977 ◽  
Vol 232 (3) ◽  
pp. H283-H287
Author(s):  
D. J. Loegering
Keyword(s):  
Blood Pressure ◽  
Hemorrhagic Shock ◽  
Arterial Blood Pressure ◽  
Liver Slice ◽  
Phagocytic Index ◽  
Phagocytic Function ◽  
Opsonic Activity ◽  
Shed Blood ◽  
Arterial Blood

Circulating opsonic activity and reticuloendothelial system (RES) phagocytic function were determined in anesthetized rats subjected to hemorrhagic shock. Animals were hemorrhaged to and maintained at 40 mmHg arterial blood pressure until they spontaneously took back 5% or 40% of the maximum bled volume. The phagocytic index, as determined by colloid clearance kinetics, was decreased in both groups following reinfusion of the shed blood. The reduction in phagocytic index was associated with decreased liver, unchanged spleen, and increased lung test colloid localization. Plasma opsonic activity, as determined by liver slice bioassay, was decreased 50-60% at 5% and 40% uptake of the maximum shed volume, decreased further 15 min after reinfusion in both groups, and tended to recover 1 h after reinfusion in the 5% uptake group. In vitro hepatic phagocytic activity of liver slices from shocked animals in the presence of normal rat plasma was decreased only in the 40% uptake animals after reinfusion when the arterial blood pressure had decreased to 50 mmHg. These data indicate that the depression of RES phagocytic function during hemorrhagic shock is associated with and may be mediated, in part, by decreased circulating opsonic activity.

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