A Mathematical Model for the Study of Hemorrhagic Shock and Fluid Resuscitation: The Systemic and Pulmonary Vasculature

1993 ◽  
Author(s):  
Tammy J. Doherty
Keyword(s):  
Mathematical Model ◽  
Hemorrhagic Shock ◽  
Fluid Resuscitation ◽  
Pulmonary Vasculature

Abstract 188: Investigation of the Mechanism of Action of Hydrogen Gas in Hemorrhagic Shock

Circulation ◽  
2018 ◽  
Vol 138 (Suppl_2) ◽  
Author(s):  
Tomoyoshi Tamura ◽  
Motoaki Sano ◽  
Tadashi Matsuoka ◽  
Kei Hayashida ◽  
Koichiro Homma ◽  
...  
Keyword(s):  
Hemorrhagic Shock ◽  
Reperfusion Injury ◽  
Mechanism Of Action ◽  
Fluid Resuscitation ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Hydrogen Gas ◽  
Endothelial Glycocalyx ◽  
Pulmonary Vasculature ◽  
Control Group

Background: Molecular hydrogen gas (H 2 ) is known to alleviate ischemia-reperfusion injury; however, the mechanism of action involved remains unknown. Metabolome analysis of tissue subjected to ischemia-reperfusion injury has revealed xanthine oxidoreductase (XOR) as a candidate target molecule for H 2. Purpose: The effects of H 2 and the XOR inhibitor (XORi) on resuscitation after hemorrhagic shock (HS) were examined. Methods: Male Sprague-Dawley rats were subjected to HS by the withdrawal of blood to maintain a mean arterial pressure (MBP) of 35 mmHg for 60 minutes (T0 to T60). They were then resuscitated with lactated Ringer’s solution with 3 times the shed blood volume over 30 minutes (T60 to T90). The animals were randomly assigned into 3 groups: H 2 inhalation (1.3% H 2 ) from T30 (n=6), XORi administration (Topiroxostat 10 mg/kg, orally administered at 60 minutes before induction of HS) (n=5), and control (CTL) (n=5). The rats were observed until 2 hours after fluid resuscitation (T210). Results: Compared to that in the control group, the lactate level at 60 minutes after introduction of HS was lower in the XORi group, while the MBP after 2 hours of fluid resuscitation was higher in the H 2 group. XOR activity in the plasma, liver, kidney, and lung tissue was suppressed in the XORi group, but not in the H 2 group. Increased permeability of the pulmonary vasculature associated with increased levels of plasma inflammatory cytokines and plasma Syndecan-1 (a marker of endothelial glycocalyx degradation) after 2 hours of fluid resuscitation was ameliorated only in the H 2 group. Conclusion: The mechanisms of action possibly differ between H 2 and XORi. XORi confers resistance to ischemia by suppressing anaerobic glycolysis during ischemia. On the other hand, H 2 stabilizes hemodynamics via suppression of inflammation and vascular hyperpermeability after resuscitation.

P68 Self-resuscitation and limited fluid resuscitation (FR) for severe “prehospital” hemorrhagic shock (HS) in rats

Resuscitation ◽  
1994 ◽  
Vol 28 (2) ◽  
pp. S13
Author(s):  
A. Capone ◽  
P. Safar ◽  
D. Crippen ◽  
Y. Leonov ◽  
S. Tisherman ◽  
...  
Keyword(s):  
Hemorrhagic Shock ◽  
Fluid Resuscitation

scholarly journals Is restrictive fluid resuscitation beneficial not only for hemorrhagic shock but also for septic shock?

Medicine ◽  
2021 ◽  
Vol 100 (12) ◽  
pp. e25143
Author(s):  
Shuaiyu Jiang ◽  
Mengmeng Wu ◽  
Xiaoguang Lu ◽  
Yilong Zhong ◽  
Xin Kang ◽  
...  
Keyword(s):  
Septic Shock ◽  
Hemorrhagic Shock ◽  
Fluid Resuscitation

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.

Influence of Hemorrhagic Shock and Subsequent Fluid Resuscitation on the Electroencephalographic Effect of Isoflurane in a Swine Model

2005 ◽  
Vol 103 (6) ◽  
pp. 1189-1194
Author(s):  
Tadayoshi Kurita ◽  
Koji Morita ◽  
Kazushige Fukuda ◽  
Masahiro Uraoka ◽  
Kotaro Takata ◽  
...  
Keyword(s):  
Hemorrhagic Shock ◽  
Fluid Resuscitation ◽  
Swine Model

scholarly journals Heart Protective Effects of Electroacupuncture in an Animal Experimental Study with Delayed Fluid Resuscitation after Hemorrhagic Shock

2018 ◽  
Vol 2018 ◽  
pp. 1-7 ◽  
Author(s):  
Huan Wang ◽  
Zhen Liu ◽  
Yuanshi Liu ◽  
Zhanqi Tong ◽  
Yan Qian ◽  
...  
Keyword(s):  
Nervous System ◽  
Autonomic Nervous System ◽  
Blood Loss ◽  
Protective Effect ◽  
Hemorrhagic Shock ◽  
Fluid Resuscitation ◽  
Cardiac Tissue ◽  
Protective Effects ◽  
Sprague Dawley ◽  
Autonomic Nervous

Fluid resuscitation could hardly be performed immediately after fatal hemorrhagic shock in outpatients. We investigated whether electroacupuncture (EA) at Zusanli (ST36) could prevent fatal hemorrhagic shock induced heart failure with delayed fluid resuscitation and whether the protective role of EA is related to the autonomic nervous system. Sixty Sprague Dawley rats were randomly divided into five groups (n=12 each): group of sham hemorrhagic shock (SHAM), group of EA, group of sham EA (SEA), group of delayed fluid resuscitation with EA (EA + DR), and group of delayed fluid resuscitation with SEA (SEA + DR). After blood loss for 6 hours, caspase-3 activity and positive rate of TUNEL in EA + DR group were significantly lower than in other hemorrhagic shock groups (e.g., versus SEA + DR: 0.156±0.039 versus 0.301±0.042; P<0.05). Immediately EA treatment after the blood loss enhanced the protective effect of delayed resuscitation on the cardiac tissue of hemorrhagic shock rats. Considering the significant changes of epinephrine (137.8±6.9 ng/L versus 98.6±7.4 ng/L; P<0.05) and acetylcholine (405±8.6 pmol/L versus 341±10.1 pmol/L; P<0.05) after EA treatment (SEA + DR versus EA + DR), this cardiac protective effect may be related to regulation of the autonomic nervous system.

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