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.

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 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 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.

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.

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.

Platelet-activating factor mediates gastric damage induced by hemorrhagic shock

1990 ◽  
Vol 259 (1) ◽  
pp. G140-G146 ◽  
Author(s):  
J. L. Wallace ◽  
C. M. Hogaboam ◽  
G. W. McKnight
Keyword(s):  
Hemorrhagic Shock ◽  
Marked Decrease ◽  
Ex Vivo ◽  
Platelet Activating Factor ◽  
Gastric Damage ◽  
Doppler Flowmetry ◽  
Shed Blood ◽  
Arterial Blood ◽  
Gastric Lumen

The role of platelet-activating factor (PAF) as a mediator of the gastric damage associated with hemorrhagic shock was investigated using a rat model. With use of an ex vivo gastric chamber preparation, the gastric mucosa was bathed with 0.1 M HCl for 90 min. At minute 10 the systemic arterial blood pressure (BP) was reduced to 25 mmHg by bleeding from the femoral artery. BP was maintained at this level for 15 min, then the shed blood was reinfused. In control rats subjected to this protocol, extensive gastric damage developed during and after the shock period and involved an average of 50 +/- 8% of the total area of glandular mucosa. A marked decrease in transmucosal potential difference (PD) was observed during shock, with little recovery thereafter. Also, significant appearance of protein and hemoglobin (Hb) in the gastric lumen was detected after induction of shock. Oral pretreatment of the rats with the PAF antagonist WEB 2086 (0.5-20 mg/kg) dose dependently reduced the extent of macroscopically visible gastric damage, the decrease in transmucosal PD, and the appearance in the lumen of protein and Hb. A similar protective effect was observed with another PAF antagonist, BN 52021 (10 mg/kg). With use of laser-Doppler flowmetry, changes in gastric blood flow were determined before, during, and after induction of shock.(ABSTRACT TRUNCATED AT 250 WORDS)

Vasoactive agents in portal blood during hemorrhagic shock

1961 ◽  
Vol 200 (6) ◽  
pp. 1177-1184 ◽  
Author(s):  
Carl F. Rothe ◽  
Ewald E. Selkurt
Keyword(s):  
Hemorrhagic Shock ◽  
Vascular Tone ◽  
Portal Blood ◽  
Intestinal Loop ◽  
Vasoactive Agents ◽  
Systemic Blood ◽  
Shed Blood ◽  
Arterial Blood ◽  
Terminal Loop ◽  
Hypovolemic Hypotension

Vasoactive agents released from the intestine during hemorrhagic shock in dogs were studied by perfusing either an isolated terminal loop of ileum or an isolated gracilis muscle with oxygenated portal blood at 100 mm Hg pressure. At 10–20-min intervals femoral arterial blood at 100 mm Hg pressure was used as the perfusate to evaluate changes in the preparation and release of vasoactive agents into the systemic blood supply. By the end of the 40 mm Hg hypotensive period, vasodilators were consistently found in the portal blood. After transfusion of the shed blood, vasoconstrictors usually seen in the arterial blood during the hypovolemic phase were replaced or masked by vasodilators. However, during the remainder of the normotensive period, vascular tone slowly returned to near normal using either source. Terminally, vasodilators were often seen in both arterial and portal blood. Results with muscle were similar to those using an intestinal loop. Although the degree and pattern of vasodilatation do not appear to be adequate to explain the eventual circulatory collapse, it is suggested that the vasodilatation during the last phase of hypovolemic hypotension may be indicative of the release of agents which act on the cardiovascular system to contribute to irreversibility.

scholarly journals Brain Damage in a New Hemorrhagic Shock Model in the Rat Using Long-Term Recovery

1990 ◽  
Vol 10 (2) ◽  
pp. 207-212 ◽  
Author(s):  
Yoichi Yamauchi ◽  
Hiroyuki Kato ◽  
Kyuya Kogure
Keyword(s):  
Hemorrhagic Shock ◽  
Brain Damage ◽  
Neuronal Damage ◽  
Neuronal Loss ◽  
Shock Model ◽  
Shed Blood ◽  
Arterial Blood ◽  
Dentate Hilus ◽  
Hemorrhagic Shock Model

A new shock model in the rat using hemorrhagic hypotension for production of brain damage is described. Hemorrhagic shock was induced by lowering arterial blood pressure with bleeding. The MABP was maintained at ∼25 mm Hg, accompanied by isoelectric EEG, and then shed blood was retransfused. At 1 week of recovery, morphological and 45Ca autoradiographic changes were examined. No brain damage was observed in rats after 1 min of isoelectric EEG. Mild neuronal damage in the hippocampal CA1 subfield was seen in some animals after 2 min of isoelectric EEG. Severe and consistent neuronal loss in the hippocampal CA1 subfield was recognized after 3 min of isoelectric EEG. Additional damage was also seen in the dentate hilus and the thalamus in some animals. This model can be used to study the pathophysiology of postshock brain damage and to assess new therapies following shock.

scholarly journals Damage-associated molecular patterns in resuscitated hemorrhagic shock are mitigated by peritoneal fluid administration

2018 ◽  
Vol 315 (3) ◽  
pp. L339-L347
Author(s):  
Paul J. Matheson ◽  
Mark A. Eid ◽  
Matthew A. Wilson ◽  
Victoria S. Graham ◽  
Samuel A. Matheson ◽  
...  
Keyword(s):  
Blood Flow ◽  
Hemorrhagic Shock ◽  
Tissue Injury ◽  
High Mobility ◽  
Primary Response ◽  
Sprague Dawley ◽  
Shed Blood ◽  
Lung Blood Flow ◽  
Molecular Patterns ◽  
Damage Associated Molecular Patterns

Conventional resuscitation (CR) of hemorrhagic shock (HS), a significant cause of trauma mortality, is intravenous blood and fluids. CR restores central hemodynamics, but vital organ flow can drop, causing hypoperfusion, hypoxia, damage-associated molecular patterns (DAMPs), and remote organ dysfunction (i.e., lung). CR plus direct peritoneal resuscitation (DPR) prevents intestinal and hepatic hypoperfusion. We hypothesized that DPR prevents lung injury in HS/CR by altering DAMPs. Anesthetized male Sprague-Dawley rats were randomized to groups ( n = 8/group) in one of two sets: 1) sham (no HS, CR, or DPR), 2) HS/CR (HS = 40% mean arterial pressure (MAP) for 60 min, CR = shed blood + 2 volumes normal saline), or 3) HS/CR + DPR. The first set underwent whole lung blood flow by colorimetric microspheres. The second set underwent tissue collection for Luminex, ELISAs, and histopathology. Lipopolysaccharide (LPS) and DAMPs were measured in serum and/or lung, including cytokines, hyaluronic acid (HA), high-mobility group box 1 (HMGB1), Toll-like receptor 4 (TLR4), myeloid differentiation primary response 88 protein (MYD88), and TIR-domain-containing adapter-inducing interferon-β (TRIF). Statistics were by ANOVA and Tukey-Kramer test with a priori P < 0.05. HS/CR increased serum LPS, HA, HMGB1, and some cytokines [interleukin (IL)-1α, IL-1β, IL-6, and interferon-γ]. Lung TLR4 and MYD88 were increased but not TRIF compared with Shams. HS/CR + DPR decreased LPS, HA, cytokines, HMGB1, TLR4, and MYD88 levels but did not alter TRIF compared with HS/CR. The data suggest that gut-derived DAMPs can be modulated by adjunctive DPR to prevent activation of lung TLR-4-mediated processes. Also, DPR improved lung blood flow and reduced lung tissue injury. Adjunctive DPR in HS/CR potentially improves morbidity and mortality by downregulating the systemic DAMP response.

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