Ideal target arterial pressure after control of bleeding in a rabbit model of severe traumatic hemorrhagic shock: results from volume loading-based fluid resuscitation

Zhao, Xiaogang; Jiang, Shouyin; Zhang, Mao; Zhou, Guozhong; Zhao, Yingying; Yi, Huixing; Jiang, Libing; Wang, Jianan

doi:10.1016/j.jss.2015.02.052

Cited by 6 publications

(5 citation statements)

References 30 publications

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“…Several reports indicated that mean arterial pressure values of 40 to 50 mm Hg constituted a critical level in rabbit hemorrhagic shock . In line with this, rabbit mean arterial pressure decreased to 40 to 50 mm Hg in the current study, suggesting the rabbits were subjected to severe shock conditions.…”

Section: Discussionsupporting

confidence: 87%

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Combination therapy using fibrinogen γ‐chain peptide‐coated, ADP‐encapsulated liposomes and hemoglobin vesicles for trauma‐induced massive hemorrhage in thrombocytopenic rabbits

et al. 2019

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BACKGROUND: We previously developed substitutes for red blood cells (RBCs) and platelets (PLTs) for transfusion. These substitutes included hemoglobin vesicles (HbVs) and fibrinogen γ-chain (dodecapeptide HHLGGAKQAGDV, H12)-coated, adenosine diphosphate (ADP)-encapsulated liposomes [H12-(ADP)liposomes]. Here, we examined the efficacy of combination therapy using these substitutes instead of RBC and PLT transfusion in a rabbit model with traumainduced massive hemorrhage with coagulopathy. ABBREVIATIONS: ADP = adenosine diphosphate; APTT = activated partial thromboplastin time; AT = antithrombin; CR = clot rate; CT = clotting time; HbVs = hemoglobin vesicles; HSA = human serum albumin; MAP = mannitol adenine phosphate; NO = nitric oxide; NOx = NO 2 − /NO 3 ; PPP = plateletpoor plasma; PRP = platelet-rich plasma; PT = prothrombin time.From the

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Section: Discussionsupporting

confidence: 87%

“…Several animal studies showed that both normal and lethal physiological values for arterial pressure, Hb, and Hct in rabbits were similar to those in humans . Most studies of dilutional coagulopathy used mild to moderate dilution in which PLT counts decreased to one‐half of baseline .…”

Section: Discussionmentioning

confidence: 99%

Combination therapy using fibrinogen γ‐chain peptide‐coated, ADP‐encapsulated liposomes and hemoglobin vesicles for trauma‐induced massive hemorrhage in thrombocytopenic rabbits

et al. 2019

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“…Ischemia/reperfusion injury induces renal production of pro-inflammatory cytokines such as IL-18 49 , and inflammatory mediators lead to activation of the TLR4/NF-κB signaling pathway, which plays a key role in inflammation and immunity. In the present study, terlipressin treatment restored renal expression of NF-κB, IL-18, IL-6 as well as reducing CD68 infiltration 16 . However, there was no difference among the groups in terms of CD43 infiltration.…”

Section: Discussionsupporting

confidence: 68%

“…The current standard resuscitation protocol for HS mandates the use of liberal fluid management, which involves the infusion of large volumes of crystalloid solutions such as lactated Ringer’s (LR). However, that practice can have adverse effects, such as interstitial edema in the gut, lungs, and kidneys 13 – 16 ; increased production of pro-inflammatory cytokines 17 ; and increased intracranial pressure 18 . Other studies have demonstrated additional adverse effects, including coagulopathies due to the large dilution, hypothermia related to LR administration at an inappropriate temperature, and changes in the serum pH 19 , 20 .…”

Section: Introductionmentioning

confidence: 99%

Terlipressin combined with conservative fluid management attenuates hemorrhagic shock-induced acute kidney injury in rats

Castro

Otsuki

Sanches

et al. 2022

Sci Rep

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Hemorrhagic shock (HS), a major cause of trauma-related mortality, is mainly treated by crystalloid fluid administration, typically with lactated Ringer’s (LR). Despite beneficial hemodynamic effects, such as the restoration of mean arterial pressure (MAP), LR administration has major side effects, including organ damage due to edema. One strategy to avoid such effects is pre-hospitalization intravenous administration of the potent vasoconstrictor terlipressin, which can restore hemodynamic stability/homeostasis and has anti-inflammatory effects. Wistar rats were subjected to HS for 60 min, at a target MAP of 30–40 mmHg, thereafter being allocated to receive LR infusion at 3 times the volume of the blood withdrawn (liberal fluid management); at 2 times the volume (conservative fluid management), plus terlipressin (10 µg/100 g body weight); and at an equal volume (conservative fluid management), plus terlipressin (10 µg/100 g body weight). A control group comprised rats not subjected to HS and receiving no fluid resuscitation or treatment. At 15 min after fluid resuscitation/treatment, the blood previously withdrawn was reinfused. At 24 h after HS, MAP was higher among the terlipressin-treated animals. Terlipressin also improved post-HS survival and provided significant improvements in glomerular/tubular function (creatinine clearance), neutrophil gelatinase-associated lipocalin expression, fractional excretion of sodium, aquaporin 2 expression, tubular injury, macrophage infiltration, interleukin 6 levels, interleukin 18 levels, and nuclear factor kappa B expression. In terlipressin-treated animals, there was also significantly higher angiotensin II type 1 receptor expression and normalization of arginine vasopressin 1a receptor expression. Terlipressin associated with conservative fluid management could be a viable therapy for HS-induced acute kidney injury, likely attenuating such injury by modulating the inflammatory response via the arginine vasopressin 1a receptor.

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“…In our previous study, serum atrial natriuretic peptide (ANP) level was positively correlated with expression of intestinal Protein kinase B (Akt) protein in THS but negatively correlated with interleukin 10 (IL-10) expression in bronchoalveolar lavage fluids. 8 Although the study did not find a correlation between ANP and early survival, it does imply that ANP may have a potential role in the initial treatment of THS, which needs to be studied further. ANP has a blood pressure lowering effect, but it is not clear whether ANP can aggravate hemodynamic disorders during hemorrhagic shock.…”

Section: Introductionmentioning

confidence: 71%

Therapeutic role of atrial natriuretic peptide in early treatment of traumatic hemorrhagic shock

et al. 2021

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The biological effect of atrial natriuretic peptide (ANP) in traumatic hemorrhagic shock (THS) is unknown. This study was to evaluate whether ANP therapy can show organ protection in THS. Thirty male Sprague-Dawley rats were divided into three groups: ANP group, sham group, and control group. Pressure-controlled THS was induced in rats in ANP group and control group. ANP at a rate of 0.025 μg/kg/min was infused in ANP group during near-80 min of shock. After that, animals were resuscitated for 60 min and observed until 24 h. Hemodynamic parameters during shock and resuscitation were measured. Serum levels of ANP and lactate dehydrogenase, tissue oxidative stress and inflammatory factors, as well as liver and kidney function were determined. Tissue apoptosis was also assessed. There was no statistically significant difference between ANP group and control group in arterial pressure throughout the 150 min monitoring period. Blood urea nitrogen at 90 min and 24 h in ANP group was significantly lower than control group. Alanine transaminase and aspartate aminotransferase activity at 90 min in control group were significantly higher than that in sham group. However, hepatic enzyme activity at 90 min in ANP group was not significantly different compared with sham or control group. After 24 h, myocardial expression of caspase 3 protein in ANP group was significantly reduced compared with control group. Jejunal and hepatic Malondialdehyde was increased following ANP treatment. ANP therapy during early THS has no significant adverse effect on hemodynamics but can exert oxidative stress and certain protective effect on multiple organs. Our study may shed light on the novel therapy of THS with regard to organ protection. The mechanisms underlying the organ protection require further study.

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Ideal target arterial pressure after control of bleeding in a rabbit model of severe traumatic hemorrhagic shock: results from volume loading-based fluid resuscitation

Cited by 6 publications

References 30 publications

Combination therapy using fibrinogen γ‐chain peptide‐coated, ADP‐encapsulated liposomes and hemoglobin vesicles for trauma‐induced massive hemorrhage in thrombocytopenic rabbits

Combination therapy using fibrinogen γ‐chain peptide‐coated, ADP‐encapsulated liposomes and hemoglobin vesicles for trauma‐induced massive hemorrhage in thrombocytopenic rabbits

Terlipressin combined with conservative fluid management attenuates hemorrhagic shock-induced acute kidney injury in rats

Therapeutic role of atrial natriuretic peptide in early treatment of traumatic hemorrhagic shock

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