Learning and memory is preserved after induced asanguineous hyperkalemic hypothermic arrest in a swine model of traumatic exsanguination

Alam, Hasan B.; Bowyer, Mark W.; Koustova, Elena; Gushchin, Vadim; Anderson, Daniel M.; Stanton, Kathleen; Kreishman, Peter; Cryer, Chad; Hancock, Timothy; Rhee, Peter

doi:10.1067/msy.2002.125787

Cited by 71 publications

(50 citation statements)

References 21 publications

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“…Several studies have demonstrated that the induction of suspended animation in mammals is possible for a few hours at a time through a procedure in which exsanguination is followed by an aortic flush with cold saline (16,17). Because these animals are blood-free while in suspension and thus would not be subject to the toxic effects of irreversible carbon monoxide binding to hemoglobin, it is intriguing to consider the possibility that the suspended animation procedure in these mammals might be enhanced by concurrent perfusion with carbon monoxide to ensure that low levels of residual oxygen do not induce damage.…”

Section: Discussionmentioning

confidence: 99%

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Carbon monoxide-induced suspended animation protects against hypoxic damage in Caenorhabditis elegans

Nystul

Roth²

2004

Proc. Natl. Acad. Sci. U.S.A.

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Oxygen deprivation is a major cause of cellular damage and death. Here we demonstrate that Caenorhabditis elegans embryos, which can survive both in anoxia (<0.001 kPa O 2) by entering into suspended animation and in mild hypoxia (0.25-1 kPa O 2) through a hypoxia-inducible factor 1-mediated response, cannot survive in intermediate concentrations of oxygen, between 0.01 and 0.1 kPa O 2 . Moreover, we show that carbon monoxide can protect C. elegans embryos against hypoxic damage in this sensitive range. Carbon monoxide can also rescue the hypoxia-sensitive mutant hif-1(ia04) from lethality in hypoxia. This work defines the oxygen tensions over which hypoxic damage occurs in C. elegans embryos and demonstrates that carbon monoxide can prevent this damage by inducing suspended animation.O xygen metabolism is a fundamental requirement for life in aerobic metazoans. Aerobic respiration accounts for the vast majority of energy production in most animals and also serves to maintain the redox potential necessary to carry out important cellular reactions. In hypoxia, decreased oxygen availability results in inefficient transfer of electrons to molecular oxygen in the final step of the electron transport chain. This inefficiency results in both a decrease in aerobic energy production and an increase in the production of damaging free radicals, mainly caused by the premature release of electrons at complex III and the formation of O 2 Ϫ by cytochrome oxidase (1). Limited energy supplies and free radical damage can interfere with essential cellular processes, such as protein synthesis and maintenance of membrane potentials (2), and will ultimately lead to cell death.Hypoxia is a common natural stress, and several well conserved responses exist that facilitate cellular adaptation to hypoxic environments. To compensate for the decrease in the capacity for aerobic energy production in hypoxia, the cell must either increase anaerobic energy production or decrease energy demand (2). Examples of both of these responses are common in metazoans, and the particular response used depends, in general, on the amount of oxygen available to the cell.In mild hypoxia, oxidative phosphorylation is still partially active, so some aerobic energy production is possible. The cellular response to this situation, which is mediated in part by hypoxia-inducible transcription factor 1 (HIF-1), is to supplement the reduced aerobic energy production by up-regulating genes involved in anaerobic energy production, such as glycolytic enzymes and glucose transporters (3,4). This response also promotes the up-regulation of antioxidants such as catalase and superoxide dismutase, which guard against free radical-induced damage. As a result, the cell is able to maintain near normoxic levels of activity in mild hypoxia.In an extreme form of hypoxia, which we call anoxia and define here as Ͻ0.001 kPa of O 2 , oxidative phosphorylation ceases and thus the capacity to generate energy is drastically reduced. To survive in this environment, the cell must decrease ...

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Section: Discussionmentioning

confidence: 99%

“…For example, mammals have both heme oxygenase 1 and HIF-1, and some evidence suggests that suspended animation is possible in mammals as well (16,17). Yet hypoxic damage caused by trauma such as heart attack, stroke, or blood loss is a major cause of death.…”

mentioning

confidence: 99%

Carbon monoxide-induced suspended animation protects against hypoxic damage in Caenorhabditis elegans

Nystul

Roth²

2004

Proc. Natl. Acad. Sci. U.S.A.

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“…Several studies have been carried out in experimental animals with uncontrolled hemorrhagic shock with a retroperitoneal bleeding [9,10], vascular injury with intraperitoneal bleeding [11,12], and bleeding of extremities [13].…”

Section: Introductionmentioning

confidence: 99%

Intraosseous Hypertonic Saline Solution for Resuscitation of Uncontrolled, Exsanguinating Liver Injury in Young Swine

Carrera

Pacheco²,

Caruso³

et al. 2004

Eur Surg Res

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Fluid resuscitation administered before hemorrhage control for trauma victims sustaining blunt abdominal injury is controversial. Prehospital fluid resuscitation is limited by difficulty in delivering large volumes of fluid in the field and time delays associated with gaining vascular access. Venous access is often a clinical dilemma in severely hypovolemic children. Intraosseous infusion is considered a useful technique for the administration of fluids in emergency situations when peripheral intravascular access is not possible. This study investigated the effectiveness of intraosseous versus intravenous infusion of hypertonic saline solution in an uncontrolled hemorrhagic shock swine model. We also tested the effect of the different sites of infusion on the intra-abdominal bleeding. Relevant hemodynamic parameters were monitored and blood samples were collected. After liver injury, 20 anesthetized immature pigs were randomized to three groups: intraosseous access, intravenous access and control. After 20 min of uncontrolled hemorrhage, the hypertonic saline solution begins in the intraosseous access and intravenous access groups of animals. Thirty minutes later, the animals were killed and intra-abdominal blood loss was measured. All the pigs presented lower pressures and lower cardiac output after 20 min of hemorrhagic shock. The intravenous and intraosseous access groups did not show a better hemodynamic performance after 10 min of fluid resuscitation. At the end of the experiment, all animals were hemodynamically similar without an improved answer to a fluid resuscitation. There were no significant differences between groups regarding intra-abdominal blood loss. It was concluded that the hypertonic saline solution in this experimental model did not promote hemodynamic improvement and there were no differences between the two sites of fluid resuscitation regarding intra-abdominal blood loss.

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“…Unisol has been evaluated for the preservation of a variety of cell, tissues, organs, and large mammals. 14,24,[30][31][32][33][34][35][36] In this study, Unisol maintained bt3 cells better than BMPS in the absence of any supplements. Similar numbers of cells survived 24 h of hypothermic exposure, but the bt3 cell proliferation was significantly better, suggesting that there may have been higher levels of delayed cell death in the BMPS stored group.…”

Section: Discussionmentioning

confidence: 99%

Development of Pancreas Storage Solutions: Initial Screening of Cytoprotective Supplements for β-Cell Survival and Metabolic Status after Hypothermic Storage

Campbell

Taylor

Brockbank

2013

Biopreservation and Biobanking

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Insulin-dependent diabetes mellitus is one of the leading causes of death world-wide. Donor-derived pancreas and Islet of Langerhans transplantation are potential cures; however, postmortem ischemia impacts islet quality. The murine bt3 cell line was employed as a model to study cell viability and proliferation after hypothermic storage by comparing Belzer's Machine Perfusion Solution with UnisolÔ Solution. The objective was to determine which of these solutions provided the best base line support for bt3 cells and to screen potential cytoprotective additives to the solutions. Initial bt3 cell viability was similar in the two storage solutions; however, better proliferation was observed after storage in Unisol Solution. The caspase inhibitor, Q-VD-OPH, and a-tocopherol improved viability in both storage solutions, suggesting that apoptotic pathways may be responsible for cell death during hypothermic storage of bt3 cells. Analysis of apoptosis markers, caspase activity, and DNA laddering showed a reduction in apoptosis when these additives were included. The effects of Q-VD-OPH and a-tocopherol were also synergistic when employed together during either hypothermic exposure, post-hypothermic physiologic incubation, or combinations of hypothermic exposure and physiologic incubation. These results suggest that both supplements should be included in pancreas hypothermic storage solutions and in islet culture media during post-isolation culture prior to transplantation.

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Learning and memory is preserved after induced asanguineous hyperkalemic hypothermic arrest in a swine model of traumatic exsanguination

Cited by 71 publications

References 21 publications

Carbon monoxide-induced suspended animation protects against hypoxic damage in Caenorhabditis elegans

Carbon monoxide-induced suspended animation protects against hypoxic damage in Caenorhabditis elegans

Intraosseous Hypertonic Saline Solution for Resuscitation of Uncontrolled, Exsanguinating Liver Injury in Young Swine

Development of Pancreas Storage Solutions: Initial Screening of Cytoprotective Supplements for β-Cell Survival and Metabolic Status after Hypothermic Storage

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