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.

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.

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)

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].

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.

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.

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.

Systemic and subcutaneous microvascular Po2 dissociation during 4-h hemorrhagic shock in conscious hamsters

1996 ◽  
Vol 270 (3) ◽  
pp. H827-H836 ◽  
Author(s):  
H. Kerger ◽  
D. J. Saltzman ◽  
M. D. Menger ◽  
K. Messmer ◽  
M. Intaglietta
Keyword(s):  
Hemorrhagic Shock ◽  
Blood Gases ◽  
Shed Blood ◽  
Arterial Blood ◽  
Cell Velocity ◽  
Tissue Po2 ◽  
Red Blood Cell Velocity ◽  
The Relationship ◽  
Arterial Po2 ◽  
Shock Outcome

The relationship between systemic and microvascular Po2 in subcutaneous connective tissue and hemodynamics was investigated during 4-h hemorrhagic shock (40 mmHg) in conscious Syrian hamsters (n = 66) fitted with a dorsal skinfold window. Systemic blood gases, metabolic parameters, arteriolar, venular, and tissue Po2, microvascular red blood cell velocity, and blood flow were evaluated in survivors (S) and nonsurvivors (NS). Surviving animals were resuscitated with shed blood. Microvascular and tissue Po2 were measured by phosphorescence decay of Pd-meso-tetra (4-carboxyphenyl) porphyrin (30 mg/kg body wt iv). Shock caused a significant dissociation between systemic arterial and microvascular arteriolar Po2 levels. Arterial Po2 increased from 59.7 +/- 12.0 to 110.8 +/- 19.7 mmHg (S) and from 64.0 +/- 13.7 to 128.5 +/- 10.1 mmHg (NS), whereas Po2 in large arterioles decreased from 56.9 +/- 5.5 (control) to 29.5 +/- 20.1 (S) and 6.0 +/- 5.7 mmHg (NS). Correspondingly, tissue Po2 fell from 24.1 +/- 6.8 (control) to 0.9 +/- 0.6 (S) and 0.4 +/- 0.3 mmHg (NS). Venous Po2 decreased from 28.8 +/- 3.7 to 20.4 +/- 4.1 (S) and from 28.0 +/- 2.9 to 16.3 +/- 0.5 mmHg (NS). Shock outcome and tissue oxygenation were predicted by arterial blood gases and metabolic and microcirculatory conditions but not by central venous Po2.

Hyperosmotic NaCl and severe hemorrhagic shock

1980 ◽  
Vol 239 (5) ◽  
pp. H664-H673 ◽  
Author(s):  
I. T. Velasco ◽  
V. Pontieri ◽  
M. Rocha e Silva ◽  
O. U. Lopes
Keyword(s):  
Hemorrhagic Shock ◽  
Circulatory System ◽  
Plasma Volume Expansion ◽  
Term Survival ◽  
Shed Blood ◽  
Acid Base Equilibrium ◽  
Restore Blood Pressure ◽  
Anesthetized Dogs ◽  
Metabolite Clearance ◽  
Critical Reduction

Intravenous infusions of highly concentrated NaCl (2,400 mosmol/l; infused volume 4 ml/kg; equivalent to 10% of shed blood), given to lightly anesthetized dogs in severe hemorrhagic shock, rapidly restore blood pressure and acid base equilibrium toward normality. No appreciable plasma volume expansion occurs for at least 12 h, indicating that fluid shift into the vascular bed plays no essential role in this response. Initial effects wee sustained indefinitely; long term survival was 100%, compared to 0% for a similar group of controls treated with saline. Hemodynamic analysis of the effects of hyperosmotic NaCl showed that these infusions substantially increase mean and pulse arterial pressure, cardiac output and mesenteric flow, whereas heart rate was slightly diminished. These effects immediately follow infusions with no tendency to dissipate with time (6-h observation). We conclude that hyperosmotic NaCl infusions increase the dynamic efficiency of the circulatory system, enabling it to adequately handle oxygen supply and metabolite clearance, despite a critical reduction of blood volume.

Sign in / Sign up

Export Citation Format

Share Document