Comparing the effects of various fluid resuscitative strategies on Glycocalyx damage in a canine hemorrhage model.

Hemorrhagic shock and subsequent resuscitation can cause significant dysregulation of critical systems, including the vascular endothelium. Following hemorrhage, the endothelial lining (glycocalyx) can shed, causing release of glycocalyx components, endothelial activation, and systemic inflammation. A canine model of hemorrhagic shock was used to evaluate five resuscitation fluids, including Lactated Ringers+Hetastarch, Whole Blood (WB), Fresh Frozen Plasma+packed Red Blood Cells (FFP+pRBC), and two hemoglobin-based oxygen carrier (HBOC) fluids, for their impact on glycocalyx shedding.

Cellular and Biochemical Effects of Combined X-Ray Radiation and Storage on Whole Blood.

Background: Evaluating the impact of ionizing radiation on stored blood is relevant since blood banks are major assets in emergency conditions such as radiation incident/attack. This study aimed to fill our knowledge gap of combined radiation and storage effects on blood.

Methods: Blood collected from 16 anesthetized rats was anticoagulated, aliquoted into storage bags, and assigned to 8 groups using protocols combining storage (1-day vs 3-day 4C) plus irradiation (75 Gy vs 0 Gy - control).

Cremaster muscle perfusion, oxygenation, and heterogeneity revealed by a new automated acquisition system in a rodent model of prolonged hemorrhagic shock.

Local blood flow/oxygen partial pressure (Po) distributions and flow-Po relationships are physiologically relevant. They affect the pathophysiology and treatment of conditions like hemorrhagic shock (HS), but direct noninvasive measures of flow, Po, and their heterogeneity during prolonged HS are infrequently presented. To fill this void, we report the first quantitative evaluation of flow-Po relationships and heterogeneities in normovolemia and during several hours of HS using noninvasive, unbiased, automated acquisition.

Automated noninvasive evaluation of blood flow and oxygenation in rats integrated with systemic physiological monitoring.

Background: Many studies evaluating blood flow and oxygen partial pressure (PO2) do not directly measure both parameters, are confined to few locations/microvessels, and depend on investigator's selection of measuring sites. Moreover, clinically/physiologically relevant systemic parameters are not simultaneously recorded. We implemented an automated system for prolonged blood flow/PO2 acquisition in large areas while collecting relevant systemic information.

Fatty Acid-Saturated Albumin Reduces High Mortality and Fluid Requirements in a Rat Model of Hemorrhagic Shock Plus Tourniquet and Hypotensive Resuscitation.

Military prehospital care for hemorrhage is often characterized by use of tourniquets (TQ) and permissive hypotensive resuscitation (PHR) with crystalloids or colloids, but these treatments have not been previously combined in an animal model. Although albumin resuscitation solutions have been tested, the potential effects of nonesterified fatty acids (NEFAs) bound to albumin have not been evaluated in vivo, and few studies have investigated concentrated albumin solutions to reduce fluid requirements. We created a militarily relevant rat model of trauma and hemorrhagic shock (T/HS) (27 mL/kg hemorrhage) with TQ and PHR.

p53 and rapamycin are additive.

Mechanistic target of rapamycin (mTOR) is a kinase found in a complex (mTORC1) that enables macromolecular synthesis and cell growth and is implicated in cancer etiology. The rapamycin-FK506 binding protein 12 (FKBP12) complex allosterically inhibits mTORC1. In response to stress, p53 inhibits mTORC1 through a separate pathway involving cell signaling and amino acid sensing.

Rapamycin extends life span of Rb1+/- mice by inhibiting neuroendocrine tumors.

Chronic treatment of mice with an enterically released formulation of rapamycin (eRapa) extends median and maximum life span, partly by attenuating cancer. The mechanistic basis of this response is not known. To gain a better understanding of thesein vivo effects, we used a defined preclinical model of neuroendocrine cancer, Rb1+/- mice.