Interaction of Thromboxane A2 and Tissue Pathology during Graded Bacteremia

Slotman, Gus J.; Teplitz, Carl; Yellin, Scott A.; Farrugia, Ross

doi:10.1097/00005373-198702000-00013

Cited by 6 publications

(2 citation statements)

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“…15 Further, infusion of the Tx mimic in swine led to neutrophil sequestration in the lungs. 28 Activation of these sequestered neutrophils may lead to increased permeability. Although neutrophils may enhance Tx induced permeability they are not necessary for its expression.…”

Section: Discussionmentioning

confidence: 99%

Thromboxane Modulates Endothelial Permeability

Klausner

Abu-Abid

Alexander

et al. 1994

Mediators of Inflammation

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Section: Discussionmentioning

confidence: 99%

Thromboxane Modulates Endothelial Permeability

Klausner

Abu-Abid

Alexander

et al. 1994

Mediators of Inflammation

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“…Thromboxane A2 is produced by both platelets (for references, see Halushka et at., 1989) and vascular smooth muscle (Salzman et al, 1980;Greenberg et al, 1980Greenberg et al, , 1981 in response to platelet stimulation, trauma, inflammation, bacterial infection, physiological concentrations of epinephrine, and during nerve stimulation (Connor et al, 1989;Esplugues and Whittle, 1988;Greenberg and Palmer, 1978;Slotman et al, 1987;Vesterqvist et al, 1989). Continuous production of TXA2 by platelets and smooth muscle can reduce organ blood flow by constricting vascular smooth muscle (Eidt et al, 1989).…”

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confidence: 99%

The Effect of Thromboxane on Contraction of Canine Mesenteric and Lingual Arteries

Greenberg¹,

Wang²,

Xie³

et al. 1991

J Dent Res

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Thromboxane A2 (TXA2), a potent vasoconstrictor agent, is released from platelets and smooth muscle during inflammation and trauma. TXA2 may cause lingual artery (LA) contraction, leading to lingual paresthesia. The effects of U-46619, a TxA2 mimetic, on isolated rings of canine LA and mesenteric artery (MA) were examined. U-46619 (1 nmol/L to 1 mumol/L) caused a triphasic contraction of LA and MA; a rapid, phasic contraction; a slow, sustained contraction; and, upon washout of U-46619, a maintained contraction. The MA relaxed slowly, but the LA remained contracted for at least three h after washout. Decreasing extracellular calcium ion (Ca2+o) to less than 0.1 mumol/L with 2 mmol/L EGTA relaxed MA, but not LA. EGTA (4 mmol/L) partially relaxed the maintained contraction of LA. Inhibition of protein kinase C with amphotericin B or staurosporine inhibited the phasic and sustained contractions of LA, but did not affect the maintained contraction in the presence or absence of EGTA. Thus, CA2+o was required for the initial contraction of the LA by U-46619, but did not appear to be required for the maintained contraction following washout of U-46619. The data support the conclusion that following a brief exposure to U-46619, maintained contraction of LA persists by a unique mechanism that may be independent of Ca2+ and protein kinase C. Sustained LA contraction after exposure to endogenous TXA2 during inflammation and trauma may contribute to impaired lingual blood flow and orofacial tissue injury.

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Hypoxia reoxygenation-induced injury of cultured pulmonary microvessel endothelial cells

Wiles

Hechtman

Morel

et al. 1993

Journal of Leukocyte Biology

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Polymorphonuclear leukocyte (PMN) sequestration within the pulmonary microvasculature is known to occur in association with ischemia/reoxygenation (I/R). This sequestration is dependent on eicosanoids and reactive oxygen species. PMN sequestration within the lungs suggests that pulmonary microvascular endothelial cells (MECs) may in part regulate the I/R response. Simulating I/R, we examined the effect of hypoxia/reoxygenation (H/R) on pulmonary MECs in vitro, with and without PMNs. Significant cellular injury, assessed by 51Cr release, occurred upon reoxygenation of MECs (P < .01). Addition of PMNs to the H/R-injured monolayers did not increase MEC injury. Reoxygenation of MECs also resulted in increased thromboxane (Tx) B2 production compared to controls (P < .01). Inhibition of Tx secretion by aspirin reduced H/R-induced PMN adhesion to MECs (P < .01). Furthermore, H/R-induced increases in PMN-MEC adhesion were prevented by allopurinol and superoxide dismutase (P < .01). These data suggest that the pulmonary response to H/R is mediated by MEC generation of reactive oxygen radical species and Tx, which promotes increased PMN adhesion.

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Interaction of Thromboxane A2 and Tissue Pathology during Graded Bacteremia

Cited by 6 publications

References 0 publications

Thromboxane Modulates Endothelial Permeability

Thromboxane Modulates Endothelial Permeability

The Effect of Thromboxane on Contraction of Canine Mesenteric and Lingual Arteries

Hypoxia reoxygenation-induced injury of cultured pulmonary microvessel endothelial cells

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