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  • Resuscitative Endovascular Balloon Occlusion of the Aorta for Hemorrhagic Shock

    Abstract Full Text
    JAMA Surg. 2017; 152(11):1072-1073. doi: 10.1001/jamasurg.2017.3428

    This article reports the development, benefits, and applications of resuscitative endovascular balloon occlusion of the aorta in the setting of hemorrhagic shock.

  • Association Between MC-2 Peptide and Hepatic Perfusion and Liver Injury Following Resuscitated Hemorrhagic Shock

    Abstract Full Text
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    JAMA Surg. 2016; 151(3):265-272. doi: 10.1001/jamasurg.2015.4050

    This laboratory study examines the MC-2 peptide’s association with reduced liver injury following rescuscitated hemorrhagic shock in rats.

  • JAMA Surgery March 1, 2016

    Figure 3: Hematoxylin-eosin–Stained Liver Samples From the Groups

    There were no differences evident in injury score between the sham and sham+MC-2 groups, and all samples were graded as no or minimal injury. In the hemorrhagic shock (HS)/conventional resuscitation (CR) group, focal and centrilobular necrosis is evident, while in the HS/CR+MC-2 group, most samples were graded as focal necrosis. Original magnification is ×10.
  • JAMA Surgery March 1, 2016

    Figure 2: Heart Rate, Mean Arterial Pressure, and Effective Hepatic Blood Flow for Each Group

    Effective hepatic blood flow was stable across the entire protocol in the sham and sham+MC-2 groups. In the hemorrhagic shock (HS)/conventional resuscitation (CR) groups, EHBF was decreased during the period of shock and restored by resuscitation (RES) in both the HS/CR groups. However, EHBF decreased incrementally over the 4 hour post RES period. HS/CR+MC-2 increased EHBF compared to HS/CR alone at 3 hours and 4-hours postresuscitation. P values calculated by 2-way analysis of variance and Tukey-Kramer honestly significant difference test.aP < .05 vs baseline (BL).bP < .05 vs sham. cP < .05 vs sham+MC-2.dP < .05 vs HS/CR.
  • JAMA Surgery March 1, 2016

    Figure 1: Experimental Protocol

    The protocol was carried out to 4 hours postresuscitation (PR). Rats were hemorrhaged (H) to 40% of their baseline (BL) mean arterial pressure (MAP) and maintained at this pressure for 60 minutes by infusion or withdrawal of shed blood as needed. For resuscitation (R), shed blood was returned over 5 minutes, followed by infusion of 2 equal volumes of lactated Ringers (LR) solution over 25 minutes. This hemorrhagic shock model carries a mortality of 27% at 24 hours postresuscitation. MC-2 was given (50 mg/kg, intravenously [IV]) at the time of return of shed blood.
  • JAMA Surgery April 1, 2015

    Figure 5: A Summary of Hemorrhagic Shock Class by Model

    A, Taking into account the percentage of loss of total blood volume (TBV) and the hemodynamic profile, the tail-cut and liver punch biopsy models correlate best with class I hemorrhagic shock, whereas the liver laceration and spleen transection models correlate best with class II hemorrhagic shock. B, Loss of TBV by model. C, Heart rate by model. D, Mean arterial pressure (MAP) by model.aP < .001 vs tail-cut and liver punch biopsy models and P = .003 vs liver laceration model.
  • Development and Validation of 4 Different Rat Models of Uncontrolled Hemorrhage

    Abstract Full Text
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    JAMA Surg. 2015; 150(4):316-324. doi: 10.1001/jamasurg.2014.1685

    This experimental rat model study of hemorrhage provides a foundation to design novel nonsurgical therapies to control hemorrhage and allows flexibility in experimental design.

  • JAMA Surgery September 21, 2009

    Figure 1: Lyophilized Plasma for Resuscitation in a Swine Model of Severe Injury

    Swine model of severe injury and hemorrhagic shock. 3:1 ISCS indicates isotonic sodium chloride solution at a volume 3 times the controlled hemorrhage volume.
  • JAMA Surgery July 20, 2009

    Figure 3: Modulation of Mesenteric Lymph Flow and Composition by Direct Peritoneal Resuscitation From Hemorrhagic Shock

    Mesenteric lymph flow rate. Flow rate increased significantly during the resuscitation period in all hemorrhagic shock groups. The addition of adjunct peritoneal resuscitation fluid modulated mesenteric lymph flow toward sham levels, whereas the addition of an equal volume of intraperitoneal saline (IPS) increased mesenteric lymph flow. DPR indicates direct peritoneal resuscitation; error bars, SEM. * P < .05 vs sham group. † P < .05 vs hemorrhagic shock and resuscitation alone. ‡ P < .05 vs hemorrhagic shock and resuscitation plus IPS by 2-way analysis of variance and the Tukey-Kramer honestly significant difference test.
  • JAMA Surgery July 20, 2009

    Figure 1: Modulation of Mesenteric Lymph Flow and Composition by Direct Peritoneal Resuscitation From Hemorrhagic Shock

    Experimental time line of the study protocol. With the exception of the sham rats, all animals underwent the hemorrhage protocol, which consisted of mean arterial blood pressure held at 50% of individual baseline values for 30 minutes. All hemorrhagic shock groups received standard fluid resuscitation of the shed blood plus 2 equal volumes of intraperitoneal saline (IPS) delivered during a total of 30 minutes. The hemorrhagic shock and resuscitation plus IPS and hemorrhagic shock and resuscitation plus direct peritoneal resuscitation groups received IPS at the time of the return blood infusion. Mesenteric lymph fluid was collected throughout the protocol, and the lymph flow rate was calculated.
  • JAMA Surgery July 20, 2009

    Figure 2: Modulation of Mesenteric Lymph Flow and Composition by Direct Peritoneal Resuscitation From Hemorrhagic Shock

    Central hemodynamics. Mean arterial pressure (A) and heart rate (B) responses in the 4 groups. These values were restored to baseline or suprabaseline levels during the resuscitation period in the animals of each hemorrhagic group. Animals in the hemorrhagic shock and resuscitation alone group developed tachycardia at the 160-minute postresuscitation time point despite stable mean arterial pressure. DPR indicates direct peritoneal resuscitation. Error bars indicate SEM. * P < .05 vs sham group. † P < .05 vs hemorrhagic shock and resuscitation alone.
  • JAMA Surgery July 20, 2009

    Figure 4: Modulation of Mesenteric Lymph Flow and Composition by Direct Peritoneal Resuscitation From Hemorrhagic Shock

    Lymph and serum hyaluronic acid and CD44 levels after hemorrhagic shock and resuscitation. Lymph hyaluronic acid levels (A) peaked by 60 minutes after resuscitation in the hemorrhagic shock (HS) and resuscitation group, whereas CD44 levels (B) peaked at 120 minutes after resuscitation. The addition of direct peritoneal resuscitation (DPR) decreased the hyaluronic acid content of the mesenteric lymph, which was also reflected in lower levels of CD44 in lymph fluid with adjunct DPR at 120 minutes after resuscitation. C, Serum hyaluronic acid levels at 240 minutes after resuscitation. D, Serum CD44 levels at 240 minutes after resuscitation. Error bars indicate SEM. * P < .05 vs sham group. † P < .05 vs hemorrhagic shock and resuscitation alone. ‡ P < .05 vs hemorrhagic shock and resuscitation plus intraperitoneal saline (IPS) by 2-way analysis of variance and the Tukey-Kramer honestly significant difference test.
  • JAMA Surgery July 20, 2009

    Figure 6: Modulation of Mesenteric Lymph Flow and Composition by Direct Peritoneal Resuscitation From Hemorrhagic Shock

    Lymph fluid and serum interleukin (IL) 10 and transforming growth factor β (TGF-β) levels. Levels of both IL-10 and TGF-β were elevated in the mesenteric lymph by hemorrhagic shock and resuscitation at 60 minutes after resuscitation (A) and 120 minutes after resuscitation (B), and the addition of adjunct peritoneal resuscitation prevented these changes in cytokine expression. Similar patterns were observed in the serum levels of these cytokines at 240 minutes after resuscitation (C) and 240 minutes after resuscitation (D). * P < .05 vs sham group. † P < .05 vs hemorrhagic shock and resuscitation alone.
  • JAMA Surgery July 20, 2009

    Figure 5: Modulation of Mesenteric Lymph Flow and Composition by Direct Peritoneal Resuscitation From Hemorrhagic Shock

    Mesenteric lymph cytokine levels. Hemorrhagic shock and resuscitation increased levels of interleukin (IL) 1β (A), IL-6 (B), and interferon γ (IFN-γ) (D) in the mesenteric lymph, and these levels were modulated by adjunct peritoneal resuscitation with commercially available dialysate. Tumor necrosis factor α (TNF-α) (C) was not affected by hemorrhagic shock in these experimental groups. None of these cytokines differed among groups in the serum at 4 hours after resuscitation (data not shown). DPR indicates direct peritoneal resuscitation; error bars, SEM. * P < .05 vs sham group. † P < .05 vs hemorrhagic shock and resuscitation alone. ‡ P < .05 vs hemorrhagic shock and resuscitation plus intraperitoneal saline (IPS) by 2-way analysis of variance and the Tukey-Kramer honestly significant different test.
  • Modulation of Mesenteric Lymph Flow and Composition by Direct Peritoneal Resuscitation From Hemorrhagic Shock

    Abstract Full Text
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    Arch Surg. 2009; 144(7):625-634. doi: 10.1001/archsurg.2009.125
  • JAMA Surgery August 1, 2005

    Figure 3: Role of Thromboxane in Producing Hepatic Injury During Hepatic Stress

    Mechanisms of thromboxane A2 (TXA2)–mediated liver injury. Thromboxane A2 is produced commonly in response to different types of hepatic stress and elicits various effects. These lead to an activation of inflammatory process and microcirculatory disturbance. The major source of TXA2 in the liver may be Kupffer cells when the liver is exposed to stress. BDL indicates bile duct ligation; CCl4, carbon tetrachloride; HS-R, hemorrhagic shock and resuscitation; I-R, ischemia-reperfusion; LPS, lipopolysaccharide; LT, liver transplantation; and TNF-α, tumor necrosis factor α.
  • Hypothyroidism and Adrenal Insufficiency in Sepsis and Hemorrhagic Shock

    Abstract Full Text
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    Arch Surg. 2004; 139(11):1199-1203. doi: 10.1001/archsurg.139.11.1199
  • Sex Differences in Hepatic Heme Oxygenase Expression and Activity Following Trauma and Hemorrhagic Shock

    Abstract Full Text
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    Arch Surg. 2003; 138(12):1375-1382. doi: 10.1001/archsurg.138.12.1375
  • Administration of Progesterone After Trauma and Hemorrhagic Shock Prevents Hepatocellular Injury

    Abstract Full Text
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    Arch Surg. 2003; 138(7):727-734. doi: 10.1001/archsurg.138.7.727
  • Attenuation of Vascular Endothelial Dysfunction by Testosterone Receptor Blockade After Trauma and Hemorrhagic Shock

    Abstract Full Text
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    Arch Surg. 2001; 136(10):1158-1163. doi: 10.1001/archsurg.136.10.1158