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Breaking barriers in trauma research: A narrative review of opportunities to leverage veterinary trauma for accelerated translation to clinical solutions for pets and people
- Kelly E. Hall, Claire Tucker, Julie A. Dunn, Tracy Webb, Sarah A. Watts, Emrys Kirkman, Julien Guillaumin, Guillaume L. Hoareau, Heather F. Pidcoke
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- Journal:
- Journal of Clinical and Translational Science / Volume 8 / Issue 1 / 2024
- Published online by Cambridge University Press:
- 05 April 2024, e74
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- Article
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- Open access
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Trauma is a common cause of morbidity and mortality in humans and companion animals. Recent efforts in procedural development, training, quality systems, data collection, and research have positively impacted patient outcomes; however, significant unmet need still exists. Coordinated efforts by collaborative, translational, multidisciplinary teams to advance trauma care and improve outcomes have the potential to benefit both human and veterinary patient populations. Strategic use of veterinary clinical trials informed by expertise along the research spectrum (i.e., benchtop discovery, applied science and engineering, large laboratory animal models, clinical veterinary studies, and human randomized trials) can lead to increased therapeutic options for animals while accelerating and enhancing translation by providing early data to reduce the cost and the risk of failed human clinical trials. Active topics of collaboration across the translational continuum include advancements in resuscitation (including austere environments), acute traumatic coagulopathy, trauma-induced coagulopathy, traumatic brain injury, systems biology, and trauma immunology. Mechanisms to improve funding and support innovative team science approaches to current problems in trauma care can accelerate needed, sustainable, and impactful progress in the field. This review article summarizes our current understanding of veterinary and human trauma, thereby identifying knowledge gaps and opportunities for collaborative, translational research to improve multispecies outcomes. This translational trauma group of MDs, PhDs, and DVMs posit that a common understanding of injury patterns and resulting cellular dysregulation in humans and companion animals has the potential to accelerate translation of research findings into clinical solutions.
9 - Central control of cardiovascular responses to injury
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- By Emrys Kirkman, North Western Injury Research Centre, Stopford Building, University of Manchester, Roderick A. Little, North Western Injury Research Centre, Stopford Building, University of Manchester
- Edited by Nancy J. Rothwell, University of Manchester, Frank Berkenbosch, Vrije Universiteit, Amsterdam
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- Book:
- Brain Control of Responses to Trauma
- Published online:
- 05 August 2016
- Print publication:
- 15 September 1994, pp 202-238
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Summary
Introduction
The aim of this chapter is to review aspects of the central nervous organisation of the cardiovascular response to peripheral (non-central nervous) trauma. Two aspects of trauma are considered, namely haemorrhage or loss of circulating fluid and tissue damage or injury. In the context of this chapter, the term ‘injury’ is used to denote tissue damage and the associated activation of afferent nociceptive fibres, and does not itself involve loss of circulating fluid. The responses to haemorrhage and to injury are initially considered separately, before the interaction between the two responses, and the clinical implications of this interaction, are discussed. Finally, ways in which these responses may be modified by three groups of pharmacological agents are described: opioid agonists and antagonists, 5-hydroxytryptamine (5-HT) and ethanol.
Relatively little is known of the central nervous pathways specifically involved in the response to trauma. However, there is a wealth of knowledge regarding the pathways of individual cardiovascular reflexes that together may generate the response to trauma. It is therefore pertinent to describe first the cardiovascular responses to haemorrhage and injury, and their component reflexes, before discussing the relevant central nervous pathways.
The cardiovascular response to a progressive haemorrhage
The pattern of response to a ‘simple’ haemorrhage
A progressive ‘simple’ haemorrhage (loss of blood in the absence of major tissue damage, e.g. rupture of varices) produces a biphasic pattern of response (Figures 9.1, 9.2a). In the initial stages there is a progressive increase in heart rate and vascular resistance, which can maintain arterial blood pressure close to prehaemorrhage levels following blood losses of up to 10-15% of the blood volume in a young, otherwise healthy, individual (Barcroft et a\., 1944; Secher & Bie, 1985). However, as the severity of haemorrhage increases, and exceeds 20% of the blood volume, a very different pattern of response becomes apparent, namely a marked bradycardia and peripheral vasodilatation accompanied by a precipitous fall in blood pressure, which may lead to syncope (Barcroft et al, 1944; Figures 9.1, 9.2a).
Since the elucidation of the mechanisms (and central nervous pathways) of these responses to blood loss have involved investigations on animals, it should be stressed that the finer details of the response appear to vary depending on the species studied, and the choice of anaesthetic agent, if any (for example, see Schadt & Ludbrook, 1991).