Intestinal Ischemia-Reperfusion Leads to Platelet Dysfunction

Aydemir-Koksoy, Aslihan; Köksoy, Cüneyt; Kuzu, Mehmet Ayhan; Demirpençe, Ediz; Cinel, İsmail; Kesenci, M; Yavuzer, Sema

doi:10.1016/s0049-3848(99)00012-2

Cited by 11 publications

(6 citation statements)

References 23 publications

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“…A deficiency in T or B cells, depletion of complement with cobra venom factor, or inhibiting complement activity with sCD55 or CrIg significantly reduces, but does not completely ameliorate, intestinal villi damage after mesenteric I/R (4,8,9,33,77,78,80). A role for platelets in I/R-mediated tissue damage has not been fully investigated, although a recent report demonstrates that I/R injury led to dysfunctional activity of platelets (81).…”

Section: Discussionmentioning

confidence: 99%

“…Recent reports have demonstrated that platelets activate the complement pathway, complement components can activate platelets, and platelets can become coated with C fragments (19, 34, 59 -63, 66, 69). A number of clinical reports demonstrate that trauma, including burn injury and I/R injury, leads to platelet dysregulation (26,27,32,42,44,53,66,69,81). While there is ample evidence demonstrating a functional role for platelets in ischemic stroke (30,49,54,64,65), there is little published evidence supporting a pathological role for platelets in local and remote tissue damage after I/R injury.…”

mentioning

confidence: 99%

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Platelets orchestrate remote tissue damage after mesenteric ischemia-reperfusion

Lapchak

Kannan

Ioannou

et al. 2012

American Journal of Physiology-Gastrointestinal and Liver Physi

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Ischemia-reperfusion (I/R) injury is a leading cause of morbidity and mortality. A functional role for platelets in tissue damage after mesenteric I/R is largely unknown. The hypothesis that mesenteric I/R local and remote injury are platelet dependent was tested. Using a murine mesenteric I/R model, we demonstrate that platelets orchestrate remote lung tissue damage that follows mesenteric I/R injury and also contribute, albeit to a lesser degree, to local villi damage. While lung damage is delayed compared with villi damage, it increased over time and was characterized by accumulation of platelets in the pulmonary vasculature early, followed by alveolar capillaries and extravasation into the pulmonary space. Both villi and lung tissues displayed complement deposition. We demonstrate that villi and lung damage are reduced in mice made platelet deficient before I/R injury and that platelet transfusion into previously platelet-depleted mice before I/R increased both villi and lung tissue damage. Increased C3 deposition accompanied platelet sequestration in the lung, which was mostly absent in platelet-depleted mice. In contrast, C3 deposition was only minimally reduced on villi of platelet-depleted mice. Our findings position platelets alongside complement as a significant early upstream component that orchestrates remote lung tissue damage after mesenteric I/R and strongly suggest that reperfusion injury mitigating modalities should consider the contribution of platelets.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Platelets orchestrate remote tissue damage after mesenteric ischemia-reperfusion

Lapchak

Kannan

Ioannou

et al. 2012

American Journal of Physiology-Gastrointestinal and Liver Physi

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“…These substances can cause vasoconstriction (TXA 2 , LTC 4 , LTD 4 , LTE 4 ), vasodilatation (PGI 2 , PGE 1 , PGE 2 , PGD 2 ), increased vascular permeability (LTC 4 , LTD 4 , LTE 4 ), can stimulate platelet aggregation and chemotaxia in the PMNs (LTB 4 , HETE) 11 . Aydemir-Koksoy et al 19 observed a reduction in the velocity and intensity in platelet aggregation after reperfusion in intestinal ischemia of rabbits.…”

Section: Reperfusionmentioning

confidence: 97%

Pathophysiology of mesenteric ischemia/reperfusion: a review

2005

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During ischemia, the cell structures are progressively damaged, but restoration of the blood flow, paradoxically, intensifies the lesions caused by the ischemia. The mechanisms of ischemia injury and reperfusion (I/R) have not been completely defined and many studies have been realized in an attempt to find an ideal therapy for mesenteric I/R. The occlusion and reperfusion of the splanchnic arteries provokes local and systemic alterations principally derived from the release of cytotoxic substances and the interaction between neutrophils and endothelial cells. Substances involved in the process are discussed in the present review, like oxygen-derived free radicals, nitric oxide, transcription factors, complement system, serotonin and pancreatic proteases. The mechanisms of apoptosis, alterations in other organs, therapeutic and evaluation methods are also discussed.

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“…Platelet aggregation decreases after reperfusion in small intestinal ischemia [5] and liver transplantation [6]. Platelet aggregation is generally measured as the light transmission rate using platelet-rich plasma (PRP), the so-called Born method [7].…”

Section: Introductionmentioning

confidence: 99%