Gastric blood flow, mast cell degranulation and micromorphology of gastric mucosa following experimental haemorrhagic shock in dogs

Kokoschka, R.; Göber, I; Gebhart, W.

doi:10.1002/bjs.1800690613

Cited by 4 publications

(2 citation statements)

References 18 publications

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“…In our study, the rapid release of histamine in tongue MC is consistent with the previous finding that stomach MC degranulate during HS (18, 19). Histamine can increase capillary permeability and low dose of histamine injection in humans induces a rapid decrease in mean arterial blood pressure (33, 34).…”

Section: Discussionsupporting

confidence: 93%

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Mast Cells Play a Critical Role in the Systemic Inflammatory Response and End-Organ Injury Resulting from Trauma

Cai

Cao

Loughran

et al. 2011

Journal of the American College of Surgeons

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Background Much of the morbidity following trauma results from excessive activation of the innate immune system. This is manifested as a systemic inflammatory response and associated end-organ damage. Although mast cells are known to be important in many immune responses, their role in the systemic response to severe trauma is unknown. Study Design C57BL/6J-KitW-sh/BsmJ (mast cell deficient) and wild type mice were subjected to 1.5h of hemorrhagic shock plus bilateral femur fracture and soft tissue injury (HS/T), followed by resuscitation at 4.5h. Blood withdrawal volumes, mean arterial pressures; circulating cytokine, chemokine, High Mobility Group Box-1 (HMGB-1), double strain DNA (dsDNA), transaminase levels, and histology in liver and lung were compared between groups. Results Mast cell deficient mice exhibited greater hemodynamic stability than wild type mice. At baseline, the mast cell deficient mice exhibited no difference in any of the organ injury or inflammatory markers measured. As expected, wild type mice subjected to HS/T exhibited end organ damage manifested by marked increases in circulating Alanine transaminase (ALT), aspartate aminotransferase (AST), and double-strain DNA (dsDNA) levels, as well as histological evidence of tissue necrosis. In clear contrast, mast cell deficient mice exhibited almost no tissue damage. Similarly, the magnitude of increased circulating cytokine and chemokine induced by HS/T was much less in the mast cell deficient mice than in the wild type group. Conclusions Mast cell deficiency resulted in a damped systemic inflammatory response, greatly attenuated multiple organ injury, and more stable hemodynamics in HS/T. Thus, mast cells appear to be a critical component of the initial host response to severe injury.

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Section: Discussionsupporting

confidence: 93%

“…MC stabilizer treatment reduced the induction of joint capsule fibrosis after traumatic injury (17). Previous work showed that HS could activate mast cells in the stomach (18, 19). However, the contribution of MC to trauma induced-inflammation is unknown.…”

Section: Introductionmentioning

confidence: 99%

Mast Cells Play a Critical Role in the Systemic Inflammatory Response and End-Organ Injury Resulting from Trauma

Cai

Cao

Loughran

et al. 2011

Journal of the American College of Surgeons

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Role of mast cells in trauma and neuroinflammation in allergy immunology

Frieri

Kumar

Boutin

2015

Annals of Allergy, Asthma & Immunology

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The Fundamental Hemodynamic Mechanism Underlying Gastric “Stress Ulceration” in Cardiogenic Shock

et al. 1987

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Acute hemorrhagic ulceration of the gastric mucosa is seen frequently in patients with hypovolemic or cardiogenic shock. Although such lesions clearly are related to regional gastric ischemia, little attention has been directed at the underlying mechanism(s) mediating the ischemia itself. To this end, anesthetized pigs were subjected to sustained cardiogenic shock (mild hemorrhage and pericardial tamponade) such that cardiac output was reduced to 38 +/- 1% of the baseline level for 4 hours, followed by release of the tamponade, reinfusion of the shed blood, and resuscitation for 2 hours. During the period of shock, there was profound regional gastric ischemia, resulting from severe and disproportionate gastric vasoconstriction. "Blinded" gross and microscopic evaluation of the stomachs removed after the experiment revealed severe mucosal ischemic necrosis, hemorrhage, and ulceration, whereas sham-operated pigs showed no lesions. The characteristics of this model therefore mimic the essential features of the gastric "stress ulceration" syndrome. Prior confirmed total alpha-adrenergic blockade with phenoxybenzamine failed to alter these features significantly. In contrast, prior ablation of the renin-angiotensin axis, whether by angiotensin-converting enzyme inhibition with teprotide or by bilateral nephrectomy, significantly and substantially ameliorated the ischemia, vasospasm, and mucosal injury. In this model of cardiogenic shock, acute gastric mucosal "stress ulceration" is caused by a disproportionately severe regional gastric ischemia resulting from selective splanchnic vasospasm that is unaffected by sympathetic blockade but abolished by prior ablation of the renin-angiotensin axis. Like nonocclusive small bowel ischemia, ischemic colitis, and the "shock liver" syndrome, gastric "stress ulceration" is yet another component of the multiple splanchnic organ failure syndrome that appears to be mediated primarily by the remarkable sensitivity of the splanchnic vascular bed to the renin-angiotensin axis.

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Gastric blood flow, mast cell degranulation and micromorphology of gastric mucosa following experimental haemorrhagic shock in dogs

Cited by 4 publications

References 18 publications

Mast Cells Play a Critical Role in the Systemic Inflammatory Response and End-Organ Injury Resulting from Trauma

Mast Cells Play a Critical Role in the Systemic Inflammatory Response and End-Organ Injury Resulting from Trauma

Role of mast cells in trauma and neuroinflammation in allergy immunology

The Fundamental Hemodynamic Mechanism Underlying Gastric “Stress Ulceration” in Cardiogenic Shock

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