scholarly journals Pre-Hospital Induced Hypothermia Improves Outcomes in a Pig Model of Traumatic Hemorrhagic Shock

2015 ◽  
Vol 24 (4) ◽  
pp. 571-578 ◽  
Author(s):  
Bo Zhou ◽  
Gang Wang ◽  
Nanhai Peng ◽  
Xiandi He ◽  
Xiaoxiang Guan ◽  
...  
Keyword(s):  
Hemorrhagic Shock ◽  
Pig Model ◽  
Induced Hypothermia ◽  
Traumatic Hemorrhagic Shock

Nitroglycerin Patch in Traumatic Hemorrhagic Shock to Improve Signs of Poor Peripheral Perfusion

2018 ◽  
Vol 86 (6) ◽  
pp. 1253-1261
Author(s):  
MEDHAT S. ALI, M.Sc.; HASSAN I.M. KOTB, M.D. ◽  
ALAA M. AHMED ATIA, M.D.; ABUALAUON M. ABD EL-MOHSEN, M.D.
Keyword(s):  
Hemorrhagic Shock ◽  
Peripheral Perfusion ◽  
Traumatic Hemorrhagic Shock ◽  
Poor Peripheral Perfusion

Protective Effect of Crocin on Liver Function and Survival in Rats With Traumatic Hemorrhagic Shock

2021 ◽  
Vol 261 ◽  
pp. 301-309
Author(s):  
Yang Liu ◽  
Caoyuan Yao ◽  
Yuan Wang ◽  
Xiaolin Liu ◽  
Shanggang Xu ◽  
...  
Keyword(s):  
Liver Function ◽  
Protective Effect ◽  
Hemorrhagic Shock ◽  
Traumatic Hemorrhagic Shock

scholarly journals Hemostatic Resuscitation in Traumatic Hemorrhagic Shock: Case Report

2013 ◽  
Vol 63 (1) ◽  
pp. 99-102
Author(s):  
José Osvaldo Barbosa Neto ◽  
Marcos Fernando Breda de Moraes ◽  
Ricardo Souza Nani ◽  
Joel Avancini Rocha Filho ◽  
Maria José Carvalho Carmona
Keyword(s):  
Case Report ◽  
Hemorrhagic Shock ◽  
Hemostatic Resuscitation ◽  
Traumatic Hemorrhagic Shock

Abstract 10679: Tissue-to-Arterial Carbon Dioxide Partial Pressure Gradient as a Useful Measure for Monitoring Tissue Perfusion in a Pig Model of Hemorrhagic Shock and Resuscitation

Circulation ◽  
2021 ◽  
Vol 144 (Suppl_2) ◽  
Author(s):  
Yusuke Endo ◽  
Lance B Becker ◽  
Ryosuke Takegawa ◽  
Santiago J Miyara ◽  
Ernesto P Molmenti ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Blood Transfusion ◽  
Pulmonary Artery ◽  
Hemorrhagic Shock ◽  
Laboratory Data ◽  
Tissue Perfusion ◽  
Pig Model ◽  
Carbon Dioxide Partial Pressure ◽  
End Diastolic Volume ◽  
O2 Supply

Introduction: Transcutaneous CO 2 (tcPCO 2 ) and arterial CO 2 (artPCO 2 ) become decoupled during shock. Aim: To test the hypotheses the gradient between tcPCO 2 and artPCO 2 (tc-artPCO 2 ) can be an early, sensitive measure to detect inadequate tissue perfusion in a pig model of hemorrhage shock. Methods: Six female pigs were used. A transcutaneous monitor was attached to the ear for measuring transcutaneous O 2 (tcPO 2 ) and tcPCO 2 . Pulmonary artery catheter and the pulse index continuous cardiac output (PiCCO) were instrumented for monitoring a variety of hemodynamic parameters. To induce massive hemorrhagic shock, blood was withdrawn stepwisely. Then, animals were resuscitated in stages with transfusions of the stored blood. The parameters were measured at the timings of 10, 20, and 30 ml/kg of blood withdrawals and the completions of 10, 20, and 30 ml/kg of blood transfusion . Levels of systemic oxygen delivery (DO 2 ) were also calculated at all measurement points. Results: Hemorrhage and blood transfusion impacted hemodynamic and laboratory data, such as cardiac output (CO), stroke volume, MAP, heart rate, pulmonary artery wedge pressure, global end-diastolic volume, hemoglobin, and arterial lactate. The tc-artPCO 2 markedly increased as CO decreased ( Figure A ). The critical level of DO 2 (DO 2crit ) was defined as 11.72 ml/kg/min according to tcPO 2 (a threshold as 30 mmHg). There was significant correlation between tc-artPCO 2 and DO 2 (r = -0.83, P<.0001). ROC analyses revealed that the AUCs to predict DO 2crit for tc-artPCO 2 , shock index (SI), and lactate were 0.94 (95% CI, 0.87-1.00), 0.78 (0.63-0.93), and 0.65 (0.47-0.82), respectively. The AUC for tc-artPCO 2 was greater with respect to the prediction of DO 2crit than for SI (P<.05) ( Figure B ). Conclusions: The tc-artPCO 2 strongly correlated with CO and DO 2 during hemorrhage shock and resuscitation. The less-invasive tc-artPCO 2 monitoring can sensitively detect systemic inadequate O2 supply in hemorrhagic shock.

scholarly journals The calcilytic drug Calhex-231 ameliorates vascular hyporesponsiveness in traumatic hemorrhagic shock by inhibiting oxidative stress and mitochondrial fission

2020 ◽  
Author(s):  
Yan Lei ◽  
Xiaoyong Peng ◽  
Tao Li ◽  
Liangming Liu ◽  
Guangming Yang
Keyword(s):  
Oxidative Stress ◽  
Hemorrhagic Shock ◽  
Vascular Reactivity ◽  
Mitochondrial Fission ◽  
Blood Perfusion ◽  
Mitochondrial Fusion ◽  
Vital Organ ◽  
Animal Survival ◽  
Traumatic Hemorrhagic Shock ◽  
Mlc Phosphorylation

Abstract Background The calcium-sensing receptor (CaSR) plays a fundamental role in extracellular calcium homeostasis in humans. Surprisingly, CaSR is also expressed in non-homeostatic tissues and is involved in regulating diverse cellular functions. The objective of this study was to determine if Calhex-231 (Cal), a negative modulator of CaSR, may be beneficial in the treatment of traumatic hemorrhagic shock (THS) by improving cardiovascular function, and investigated its relationship to oxidative stress and the mitochondrial fusion-fission pathway. Methods Rats that had been subjected to traumatic hemorrhagic shock were used as models in this study. Hypoxia-treated vascular smooth muscle cells (VSMCs) were also used. The effects of Cal on cardiovascular function, animal survival, hemodynamic parameters, and vital organ function in THS rats were observed, and the relationship to oxidative stress and mitochondrial fusion-fission was investigated. Results Cal significantly improved hemodynamics, elevated blood pressure, increased vital organ blood perfusion and local oxygen supply, and markedly improved the survival outcomes of THS rats. Furthermore, Cal significantly improved vascular reactivity after THS, including the pressor response of THS rats to norepinephrine (NE), and also the contractile response of superior mesenteric arteries, mesenteric arterioles, and isolated VSMCs to NE. Cal also restored the THS-induced decrease in myosin light chain (MLC) phosphorylation, which is the principal mechanism responsible for VSMC contraction and vascular reactivity. Inhibition of MLC phosphorylation antagonized the Cal-induced restoration of vascular reactivity following THS. Cal decreased oxidative stress indexes and increased antioxidant enzyme levels in THS rats, and also reduced reactive oxygen species levels in hypoxic VSMCs. In addition, THS induced expression of mitochondrial fission proteins Drp1 and Fis1, and decreased expression of mitochondrial fusion protein Mfn1 in vascular tissues. Cal reduced expression of Drp1 and Fis1, but did not affect Mfn1 expression. In hypoxic VSMCs, Cal inhibited hypoxia-induced mitochondrial fragmentation and preserved mitochondrial morphology. Conclusions Calhex-231 exhibits outstanding potential for effective therapy of traumatic hemorrhagic shock, due to its ability to improve hemodynamics, increase vital organ blood perfusion, and markedly prolong animal survival. These beneficial effects result from its protection of vascular function via inhibition of oxidative stress and mitochondrial fission.

Abstract 16745: It Would be Possible to Rescue Traumatic Hemorrhagic Shock Patients Who Failed to Fluid Resuscitation (Fluid Non-responder) but Succeed in REBOA Resuscitation (REBOA/IABO Responder)

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Tomohiko Orita ◽  
Tomohiro Funabiki ◽  
Motoyasu Yamazaki ◽  
Masayuki Shimizu ◽  
Tomohiro Sato ◽  
...  
Keyword(s):  
Survival Rate ◽  
Hemorrhagic Shock ◽  
Fluid Resuscitation ◽  
Recovery Rate ◽  
Balloon Occlusion ◽  
Shock State ◽  
Occlusion Time ◽  
Aortic Balloon Occlusion ◽  
Significant Difference ◽  
Traumatic Hemorrhagic Shock

Introduction: Fluid resuscitation (FR) and massive transfusion protocol (MTP) are important initial strategies for traumatic hemorrhagic shock cases. But poor responded patients to them are difficult to rescue. In such cases, open aortic cross clamping or intra-aortic balloon occlusion (IABO) would be performed as a temporary hemostasis treatment. Recently, IABO for severe trauma has been named resuscitative endovascular balloon occlusion of the aorta (REBOA). But it is still unclear which case can be rescued with REBOA. So we studied the relationship between the responsiveness to FR and REBOA. Methods: Consecutive 46 traumatic hemorrhagic shock patients underwent REBOA at our ER for last 86 months were included. All of their FAST were positive and done FR and MTP as a first-line resuscitation. 10Fr or 7Fr IABO devices were inserted at supraphrenic level (zone I) and underwent fundamental hemostasis by operative management (OM) and/or transcatheter arterial embolization (TAE). They were sorted into responded group or non-responded group for REBOA. The primary end point was a recovery rate from the shock state within 48 hours. Secondary end points were a survival rate in 30th days and a rate of complications. Results: 26 transient or non-responded patients (Fluid Non-responder) responded for REBOA (REBOA Responder group). 20 Fluid Non-responders did not respond for REBOA (REBOA Non-responder group). There were no significant differences in ISS (REBOA Responder vs. Non-responder: 45.8+/-15.2 vs. 54.8+/-22.3), amount of total fluid (7187+/-5782ml vs. 6772+/-4851) and total blood transfusion (4816+/-3006ml vs. 5080+/-3330), required time to occlude after arriving ER (25.3+/-12.6min vs. 19.4+/-9.8) and total occlusion time (76.4+/-66.5min vs. 92.7+/-34.4). There was significant difference in the changes of systolic blood pressure before and after of REBOA (59.3+/-25.7mmHg vs. 38.3+/-39.4, p=0.04). A recovery rate from shock state was 65%(12/26) vs. 0%(0/20) (p<0.01) and a survival rate was 14/26(54%) vs. 0/20(0%) (p<0.01). One complication occurred in REBOA Responder group but was not lethal. Conclusions: It would be necessary to recognize that Fluid Non-responder but REBOA Responder with traumatic hemorrhagic shock could be possible to rescue.

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