Gas tonometry for evaluation of gastrointestinal mucosal perfusion: experimental models of trauma, shock and complex surgical maneuvers - Part 1

Substantial clinical and animal evidences indicate that the mesenteric circulatory bed, particularly the gut mucosa, is highly vulnerable to reductions in oxygen supply and prone to early injury in the course of hemodynamic changes induced by trauma, shock, sepsis and several complex surgical maneuvers. Gut hypoxia or ischemia is one possible contributing factor to gastrointestinal tract barrier dysfunction that may be associated with the development of systemic inflammatory response and multiple organ dysfunction syndrome, a common cause of death after trauma, sepsis or major surgeries. Monitoring gut perfusion during experiments may provide valuable insights over new interventions and therapies highly needed to reduce trauma and sepsis-related morbidity and mortality. We present our experience with gas tonometry as a monitor of the adequacy of gastrointestinal mucosal perfusion in clinical and experimental models of trauma, shock and surgical maneuvers associated with abrupt hemodynamic changes, such as aortic occlusion and hepatic vascular exclusion. Next issue we will be presenting our experience with gas tonometry in experimental and clinical sepsis.

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Gas tonometry for evaluation of gastrointestinal mucosal perfusion: experimental and clinical sepsis¹. part 2

Acta Cirurgica Brasileira ◽

10.1590/s0102-86502002000500003 ◽

2002 ◽

Vol 17 (5) ◽

pp. 281-288 ◽

Cited By ~ 3

Author(s):

Eliezer Silva ◽

Luiz Francisco Poli de Figueiredo ◽

Ruy Jorge Cruz Jr ◽

Maurício Rocha e Silva

Keyword(s):

Septic Shock ◽

Organ Dysfunction ◽

Experimental Models ◽

Multiple Organ ◽

Multiple Organ Dysfunction ◽

Barrier Dysfunction ◽

Clinical Sepsis ◽

Mucosal Perfusion ◽

Early Injury ◽

Sepsis And Septic Shock

Substantial clinical and animal evidences indicate that the mesenteric circulatory bed, particularly the gut mucosa, is highly vulnerable to reductions in oxygen supply and prone to early injury in the course of hemodynamic changes induced by sepsis and septic shock. Gut hypoxia or ischemia is one possible contributing factor to gastrointestinal tract barrier dysfunction that may be associated with the development of systemic inflammatory response and multiple organ dysfunction syndrome, the principal cause of death after sepsis. Monitoring gut perfusion during experimental and clinical sepsis may provide valuable insights over new interventions and therapies highly needed to reduce multiple organ dysfunction and sepsis-related morbidity and mortality. We present our experience with gas tonometry as a monitor of the adequacy of gastrointestinal mucosal perfusion in experimental models sepsis and with the use of vasoactive agents for hemodynamic management in patients with septic shock.

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Early Detection of Junctional Adhesion Molecule-1 (JAM-1) in the Circulation after Experimental and Clinical Polytrauma

Mediators of Inflammation ◽

10.1155/2015/463950 ◽

2015 ◽

Vol 2015 ◽

pp. 1-7 ◽

Cited By ~ 12

Author(s):

Stephanie Denk ◽

Rebecca Wiegner ◽

Felix M. Hönes ◽

David A. C. Messerer ◽

Peter Radermacher ◽

...

Keyword(s):

Organ Dysfunction ◽

Adhesion Molecule ◽

Plasma Concentrations ◽

Occult Blood ◽

Multiple Organ ◽

Pulmonary Contusion ◽

Barrier Dysfunction ◽

Protein Levels ◽

Early Injury ◽

Polytrauma Patients

Severe tissue trauma-induced systemic inflammation is often accompanied by evident or occult blood-organ barrier dysfunctions, frequently leading to multiple organ dysfunction. However, it is unknown whether specific barrier molecules are shed into the circulation early after trauma as potential indicators of an initial barrier dysfunction. The release of the barrier molecule junctional adhesion molecule-1 (JAM-1) was investigated in plasma of C57BL/6 mice 2 h after experimental mono- and polytrauma as well as in polytrauma patients (ISS ≥ 18) during a 10-day period. Correlation analyses were performed to indicate a linkage between JAM-1 plasma concentrations and organ failure. JAM-1 was systemically detected after experimental trauma in mice with blunt chest trauma as a driving force. Accordingly, JAM-1 was reduced in lung tissue after pulmonary contusion and JAM-1 plasma levels significantly correlated with increased protein levels in the bronchoalveolar lavage as a sign for alveolocapillary barrier dysfunction. Furthermore, JAM-1 was markedly released into the plasma of polytrauma patients as early as 4 h after the trauma insult and significantly correlated with severity of disease and organ dysfunction (APACHE II and SOFA score). The data support an early injury- and time-dependent appearance of the barrier molecule JAM-1 in the circulation indicative of a commencing trauma-induced barrier dysfunction.

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Effects of mannitol in the prevention of lipid peroxidation during liver resection with hepatic vascular exclusion

Journal of Clinical Anesthesia ◽

10.1016/j.jclinane.2006.03.014 ◽

2006 ◽

Vol 18 (8) ◽

pp. 570-574 ◽

Cited By ~ 18

Author(s):

Georgia Kostopanagiotou ◽

Ageliki K. Pandazi ◽

Ioanna Andreadou ◽

Sofia L. Markantonis ◽

Dimitra Niokou ◽

...

Keyword(s):

Lipid Peroxidation ◽

Liver Resection ◽

Vascular Exclusion ◽

Hepatic Vascular Exclusion

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Severe Acute Respiratory Syndrome Coronavirus 2, COVID-19, and the Renin-Angiotensin System

Hypertension ◽

10.1161/hypertensionaha.120.15948 ◽

2020 ◽

Vol 76 (5) ◽

pp. 1350-1367 ◽

Cited By ~ 2

Author(s):

Matthew A. Sparks ◽

Andrew M. South ◽

Andrew D. Badley ◽

Carissa M. Baker-Smith ◽

Daniel Batlle ◽

...

Keyword(s):

Severe Acute Respiratory Syndrome ◽

Renin Angiotensin System ◽

Organ Damage ◽

Experimental Models ◽

Multiple Organ ◽

Host Cells ◽

Ang Ii ◽

Angiotensin System ◽

Renin Angiotensin ◽

Organ Systems

The coronavirus disease 2019 (COVID-19) pandemic is associated with significant morbidity and mortality throughout the world, predominantly due to lung and cardiovascular injury. The virus responsible for COVID-19—severe acute respiratory syndrome coronavirus 2—gains entry into host cells via ACE2 (angiotensin-converting enzyme 2). ACE2 is a primary enzyme within the key counter-regulatory pathway of the renin-angiotensin system (RAS), which acts to oppose the actions of Ang (angiotensin) II by generating Ang-(1–7) to reduce inflammation and fibrosis and mitigate end organ damage. As COVID-19 spans multiple organ systems linked to the cardiovascular system, it is imperative to understand clearly how severe acute respiratory syndrome coronavirus 2 may affect the multifaceted RAS. In addition, recognition of the role of ACE2 and the RAS in COVID-19 has renewed interest in its role in the pathophysiology of cardiovascular disease in general. We provide researchers with a framework of best practices in basic and clinical research to interrogate the RAS using appropriate methodology, especially those who are relatively new to the field. This is crucial, as there are many limitations inherent in investigating the RAS in experimental models and in humans. We discuss sound methodological approaches to quantifying enzyme content and activity (ACE, ACE2), peptides (Ang II, Ang-[1–7]), and receptors (types 1 and 2 Ang II receptors, Mas receptor). Our goal is to ensure appropriate research methodology for investigations of the RAS in patients with severe acute respiratory syndrome coronavirus 2 and COVID-19 to ensure optimal rigor and reproducibility and appropriate interpretation of results from these investigations.

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