Postischemic extremities exhibit immediate release of tumor necrosis factor

Sternbergh, W. Charles; Tuttle, Todd M.; Makhoul, Raymond G.; Bear, Harry D.; Sobel, Michael; Fowler, Alpha A.

doi:10.1016/0741-5214(94)90148-1

Cited by 46 publications

(20 citation statements)

References 29 publications

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“…In this model, the aorta is cross-clamped and the lower torso is not perfused while a segment of aorta is infused with elastase. Ischemia-reperfusion of the lower torso produces various chemical mediators [13,14] such as arachidonic acid metabolites and proinflammatory cytokines, the presence of which results in systemic inflammation [13,15]. Cohen et al [13] reported that all rats subjected to 2 h of lower torso ischemia by cross-clamping of the infrarenal aorta followed by reperfusion died within 12 h of pulmonary, hepatic, and renal injuries.…”

Section: Discussionmentioning

confidence: 98%

Shortened Elastase Infusion Time in the Elastase-Induced Rat Aneurysm Model

Yamaguchi¹,

Yokokawa

Suzuki

et al. 1999

Journal of Surgical Research

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Section: Discussionmentioning

confidence: 98%

Shortened Elastase Infusion Time in the Elastase-Induced Rat Aneurysm Model

Yamaguchi¹,

Yokokawa

Suzuki

et al. 1999

Journal of Surgical Research

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“…Much experimental evidence from models in animals including rats, rabbits and dogs has strongly implicated endothelin as a causative player in the injuries that follow ischaemia/reperfusion [13], and here there is good evidence that in all species there are increases in cytokine production [14]. Following an ischaemic period, for instance, the hindquarters of rats release an early, transient burst of TNF-c~ on reperfusion, and treatment with antibodies against TNF-~ maintains post-ischaemic flow [15]. Similarly, focal cerebral ischaemia in rats increases TNF-ct production by ischaemic neurones [16] supporting a role for ET-1 in stroke.…”

Section: Td Warner and P Klemmmentioning

confidence: 93%

What turns on the endothelins?

Warner

Klemm

1996

Inflamm Res

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Production of the potent vasoconstrictor peptide endothelin-1 (ET-1) within the circulation is increased markedly in a number of pathologies, such as the damage following from ischaemia and reperfusion, vasculitis, congestive heart failure, and systemic inflammatory response (septic shock syndrome) and related pathological states. All these conditions are associated with marked increases in the production of cytokines such as tumour necrosis factor-alpha and interleukin-2. Our experiments indicate that in rats administration of either of these cytokines results in a rapid increase in the circulating levels of ET-1 and a very pronounced ET-1-dependent coronary vasoconstriction. Furthermore, in rats suffering from adjuvant polyarthritis, in which there is marked joint inflammation and associated cytokine production, there are dramatic increases in coronary perfusion pressure which are absent when rats are treated with an endothelin receptor antagonist. This does not imply that inflammation must be associated with coronary vasoconstriction and myocardial dysfunction, but rather that in the rat, where ET-1 is a strong and almost irreversible constrictor of coronary vessels, coronary perfusion pressure serves as a very good bioassay for ET-1 activity. What our results do imply is that the ET-1 system is latent, but that in numerous disease states it can become rapidly upregulated following endothelial activation by cytokines.

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“…Die Unterschenkel wurden auf Höhe des rechten Vorhofs in einer Vakuummatratze gelagert. Mögliche Ursachen dafür sind Beinvenenthrombosen [15], Beeinträchtigung des Lymphabflusses der betroffenen Extremitäten durch Zerstörung der ableitenden Lymphgefäße [11,30] und Veränderungen in der Mikrozirkulation der ischämischen Extremitäten [6,20] sowie ein Reperfusionsschaden durch Freisetzung von Mediatoren und Sauerstoffradikalen [16,22,35,40,42]. Das so entstandene Signal wurde mit einer im Computer gespeicherten Kalibrationskurve verrechnet [13].…”

Section: Allgemeines Untersuchungsprotokollunclassified

Perioperative Veränderungen der Flüssigkeitsfiltrationskapazität bei gefäßchirurgischen Patienten

et al. 1999

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The data presented suggests an increase in extravascular fluid loss in patients undergoing vascular surgery, which becomes evident after the induction of general anaesthesia or completion of epidural anaesthesia. The positive correlation with the intraoperative fluid requirements may partially explain the often reported large intraoperative fluid requirements of patients undergoing AAA repair. The fact that the maximum change in fluid filtration capacity is found postoperatively may be explained by the additional effect of an ischemia/reperfusion injury in response to both the clamping an declamping of the artery and the increase in arterial blood flow to the limb due to the successful reconstruction of the blood vessel.

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Postischemic extremities exhibit immediate release of tumor necrosis factor

Cited by 46 publications

References 29 publications

Shortened Elastase Infusion Time in the Elastase-Induced Rat Aneurysm Model

Shortened Elastase Infusion Time in the Elastase-Induced Rat Aneurysm Model

What turns on the endothelins?

Perioperative Veränderungen der Flüssigkeitsfiltrationskapazität bei gefäßchirurgischen Patienten

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