Abstract:Although IV fluid administration is the mainstay of nonsurgical management of trauma patients with uncontrolled hemorrhagic shock, the efficacy of this strategy has been discussed controversially. In this animal model of severe liver trauma with uncontrolled hemorrhagic shock, vasopressin, but not saline placebo or fluid resuscitation, improved short-term survival.
“…Most animal models for uncontrolled hemorrhagic shock achieve blood withdrawal by tail amputation [14], or liver or spleen laceration [15,16]. These procedures greatly influence the rate and the amount of blood loss and require a long period of anesthetic or fasting state.…”
SummaryHemorrhagic shock is a common cause of death in emergency rooms. Current animal models of hemorrhage encounter a major problem that the volume and the rate of blood loss cannot be controlled. In addition, the use of anesthesia obscures physiological responses. Our experiments were designed to establish an animal model based on the clinical situation for studying hemorrhagic shock. Hemorrhagic shock was induced by withdrawing blood from a femoral arterial catheter. The blood volume withdrawn was 40% of the total blood volume for group 1 and 30% for group 2 and 3. Group 3 was anesthetized with sodium pentobarbital (25 mg/kg, i.v.) at the beginning of blood withdrawal. Our data showed that the survival rate was 87.5% at 48 h in the conscious group and 0% at 9 h in anesthetic group after hemorrhage. The levels of mean arterial pressure, heart rate, white blood count, TNF-a, IL1-b, CPK, and LDH after blood withdrawal in the anesthetic group were generally lower than those in conscious groups. These results indicated that anesthetics significantly affected the physiology of experimental animals. The conscious, unrestrained and cumulative volume-controlled hemorrhagic shock model was a good experimental model to investigate the physical phenomenon without anesthetic interfernce.
“…Most animal models for uncontrolled hemorrhagic shock achieve blood withdrawal by tail amputation [14], or liver or spleen laceration [15,16]. These procedures greatly influence the rate and the amount of blood loss and require a long period of anesthetic or fasting state.…”
SummaryHemorrhagic shock is a common cause of death in emergency rooms. Current animal models of hemorrhage encounter a major problem that the volume and the rate of blood loss cannot be controlled. In addition, the use of anesthesia obscures physiological responses. Our experiments were designed to establish an animal model based on the clinical situation for studying hemorrhagic shock. Hemorrhagic shock was induced by withdrawing blood from a femoral arterial catheter. The blood volume withdrawn was 40% of the total blood volume for group 1 and 30% for group 2 and 3. Group 3 was anesthetized with sodium pentobarbital (25 mg/kg, i.v.) at the beginning of blood withdrawal. Our data showed that the survival rate was 87.5% at 48 h in the conscious group and 0% at 9 h in anesthetic group after hemorrhage. The levels of mean arterial pressure, heart rate, white blood count, TNF-a, IL1-b, CPK, and LDH after blood withdrawal in the anesthetic group were generally lower than those in conscious groups. These results indicated that anesthetics significantly affected the physiology of experimental animals. The conscious, unrestrained and cumulative volume-controlled hemorrhagic shock model was a good experimental model to investigate the physical phenomenon without anesthetic interfernce.
“…Animal studies demonstrate that vasopressin increases blood pressure and prevents hypovolemic cardiac arrest from fatal hemorrhage. (11,12) In addition, to improve perfusion pressure of vital organs, exogenous administration of vasopressin provides the added benefit of enhancing clot formation. (13) Therefore, it seems reasonable to consider vasopressin for treating hemorrhagic shock patients at the scene.…”
Section: Discussionmentioning
confidence: 99%
“…(8)(9)(10) Vasopressin is a potent vasopressor with extended purposes in the treatment of severe trauma, septic shock, cardiac diseases and during cardiopulmonary resuscitation. (11)(12)(13)(14)(15)(16)(17)(18)(19)(20)(21)(22) In addition, a few researchers have found that vasopressin is absorbed well via the mucosa of the airway and alveoli. (23)(24)(25) The combination of a LMA and vasopressin could be a practical management tool in pre-hospital settings.…”
“…These volumes are equivalent to more than twice the normal blood volumes (i.e., >12 L in adult human subjects). Resuscitation with such a large volume of fluid is difficult to achieve, especially under combat conditions, and a rapid increase in blood pressure during resuscitation is detrimental for the trauma victim with uncontrolled hemorrhage (16). In view of this, to resuscitate the animals we used Ringer's lactate in volumes equal to the lost blood to make the study more relevant clinically.…”
Section: Effects Of Am/ambp-1 In a Rat Model Of Controlled Hemorrhagementioning
Traumatic injury is a major, largely unrecognized public health problem in the US that cuts across race, gender, age, and economic boundaries. The resulting loss of productive life years exceeds that of any other disease, with societal costs of $469 billion annually. Most trauma deaths result either from insufficient tissue perfusion due to excessive blood loss, or the development of inflammation, infection, and vital organ damage following resuscitation. Clinical management of hemorrhagic shock relies on massive and rapid infusion of fluids to maintain blood pressure. However, the majority of victims with severe blood loss do not respond well to fluid restoration. The development of effective strategies for resuscitation of traumatic blood loss is therefore critically needed. We have recently discovered that the vascular responsiveness to a recently-discovered potent vasodilatory peptide, adrenomedullin (AM) is depressed after severe blood loss, which may be due to downregulation of a novel specific binding protein, AM binding protein-1 (AMBP-1). Using three different animal models of hemorrhage (controlled hemorrhage with large volume resuscitation, controlled hemorrhage with low volume resuscitation, and uncontrolled hemorrhage with minimum resuscitation), we have shown that cell and organ injury occurs after hemorrhage despite fluid resuscitation. Administration of AM/AMBP-1 significantly improves cardiac output, heart performance and tissue perfusion, attenuates hepatic and renal injury, decreases pro-inflammatory cytokines, prevents metabolic acidosis, and reduces hemorrhage-induced mortality. Thus, administration of AM/AMBP-1 appears to be a novel and useful approach for restoring cardiovascular responses, preventing organ injury, and reducing mortality after hemorrhagic shock.
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