Thromboxane A<sub>2</sub>mediates increased pulmonary microvascular permeability after intestinal reperfusion

Turnage, Richard H.; LaNoue, John L.; Kadesky, Kevin M.; Meng, Yan; Myers, Stuart I.

doi:10.1152/jappl.1997.82.2.592

Cited by 31 publications

(25 citation statements)

References 27 publications

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“…The concentration of U-46619 was chosen based on a dose-response curve relating increasing concentrations of U-46619 to increases in K f in this experimental system (data not shown). This concentration of U-46619 is associated with increases in K f similar to those seen with in vivo models of acute lung injury (29). Lastly, the increases in K f associated with U-46619 have been found to be completely inhibited by the thromboxane receptor antagonist SQ-29548 (2 µM; data not shown).…”

Section: Experimental Protocolsupporting

confidence: 54%

“…Pulmonary microvascular permeability was quantitated by determining K f as has been previously described by our laboratory (29) and that of other investigators (11,39). Briefly, 15 min after the addition of U-46619, the capillary pressure prior to elevating Ppv (Pc pre ) was measured using the double occlusion technique (1,28).…”

Section: Measurement Of Pulmonary Microvascular Dysfunctionmentioning

confidence: 99%

“…capillary filtration coefficient; pulmonary vascular resistance; isolated perfused lung model THROMBOXANE A 2 (TxA 2 ) has been incriminated as an important mediator of the pulmonary microvascular dysfunction that characterizes tissue ischemia and reperfusion injury (29), endotoxin exposure (9), and cutaneous thermal injury (14). In these conditions, as well as others, TxA 2 has been shown to cause vasoconstriction and enhanced microvascular permeability.…”

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confidence: 99%

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Prostaglandins potentiate U-46619-induced pulmonary microvascular dysfunction

Wright¹,

Kim²,

Rogers

et al. 2000

Journal of Applied Physiology

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.-The induction of cyclooxygenase is an important event in the pathophysiology of acute lung injury. The purpose of this study was to examine the synergistic effects of various cyclooxygenase products (PGE 2 , PGI 2 , PGF 2␣ ) on thromboxane A 2 (TxA 2 )-mediated pulmonary microvascular dysfunction. The lungs of SpragueDawley rats were perfused ex vivo with Krebs-Henseleit buffer containing indomethacin and PGE 2 (5 ϫ 10 Ϫ8 to 1 ϫ 10 Ϫ7 M), PGF 2␣ (7 ϫ 10 Ϫ9 to 5 ϫ 10 Ϫ6 M), or PGI 2 (5 ϫ 10 Ϫ8 to 2 ϫ 10 Ϫ5 M). The TxA 2 -receptor agonist U-46619 (7 ϫ 10 Ϫ8 M) was then added to the perfusate, and then the capillary filtration coefficient (K f ), pulmonary arterial pressure (Ppa), and total pulmonary vascular resistance (RT) were determined. The K f of lungs perfused with U-46619 was twice that of lungs perfused with buffer alone (P ϭ 0.05). The presence of PGE 2 , PGF 2␣ , and PGI 2 within the perfusate of lungs exposed to U-46619 caused 118, 65, and 68% increases in K f , respectively, over that of lungs perfused with U-46619 alone (P Ͻ 0.03). The RT of lungs perfused with PGE 2 ϩ U-46619 was ϳ30% greater than that of lungs exposed to either U-46619 (P Ͻ 0.02) or PGE 2 (P Ͻ 0.01) alone. When paired measurements of RT taken before and then 15 min after the addition of U-46619 were compared, PGI 2 was found to attenuate U-46619-induced increases in RT (P Ͻ 0.01). These data suggest that PGE 2 , PGI 2 , and PGF 2␣ potentiate the effects of TxA 2 -receptor activation on pulmonary microvascular permeability.capillary filtration coefficient; pulmonary vascular resistance; isolated perfused lung model THROMBOXANE A 2 (TxA 2 ) has been incriminated as an important mediator of the pulmonary microvascular dysfunction that characterizes tissue ischemia and reperfusion injury (29), endotoxin exposure (9), and cutaneous thermal injury (14). In these conditions, as well as others, TxA 2 has been shown to cause vasoconstriction and enhanced microvascular permeability. Upregulation of cyclooxygenase is an important event in the generation of TxA 2 during acute inflammatory states. Cyclooxygenase catalyzes the incorporation of molecular oxygen into arachidonic acid, yielding a cyclic endoperoxide (PGG 2 ); subsequent peroxidation yields PGH 2 , the precursor for the synthesis of TxA 2 and PGE 2 , PGI 2 , and PGF 2␣ . In general, each of these cyclooxygenase products is released by the lung in response to a particular inflammatory stimulus, albeit in varying amounts (9,14).Despite their common origin, the physiological effects of these substances on the pulmonary microvasculature are diverse. For example, TxA 2 and PGF 2␣ are constrictors of the pulmonary vasculature in rats, whereas PGI 2 is a potent vasodilator (4, 5). Furthermore, TxA 2 profoundly increases microvascular permeability, whereas the other agents have little, if any, effect by themselves (20, 27). Several investigators have reported that PGE 2 and PGI 2 potentiate the effects of histamine, bradykinin, and interleukin-1 on microvascular permeability (2,34,35). Thi...

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Section: Experimental Protocolsupporting

confidence: 54%

Section: Measurement Of Pulmonary Microvascular Dysfunctionmentioning

confidence: 99%

mentioning

confidence: 99%

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Prostaglandins potentiate U-46619-induced pulmonary microvascular dysfunction

Wright¹,

Kim²,

Rogers

et al. 2000

Journal of Applied Physiology

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“…For example, both PGE 2 and PGI 2 enhance endothelial barrier and protect against ventilator-induced lung edema. 15 TXA 2 is reported to increase endothelial permeability and mediate intestinal reperfusion-induced pneumonia 16 and allergic nasal inflammation. 17 However, the mechanism by which PGD 2 modulates vascular permeability and inflammation remained unclear.…”

Section: Discussionmentioning

confidence: 99%

Prostaglandin D ₂ -DP Signaling Promotes Endothelial Barrier Function via the cAMP/PKA/Tiam1/Rac1 Pathway

Kobayashi

Tsubosaka

Hori

et al. 2013

ATVB

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Objective-Prostaglandin D 2 (PGD 2 ) is one of the prostanoids produced during inflammation. Although PGD 2 is known to decrease endothelial permeability through D prostanoid (DP) receptor stimulation, the detailed mechanism is unknown. Methods and Results-Treatment with PGD 2 (0.1-3 μmol/L) or the DP receptor agonist, BW245C (0.1-3 μmol/L), dosedependently increased transendothelial electrical resistance and decreased the FITC-dextran permeability of human umbilical vein endothelial cells. Both indicated decreased endothelial permeability. These phenomena were accompanied by Tiam1/Rac1-dependent cytoskeletal rearrangement. BW245C (0.3 μmol/L) increased the intracellular cAMP level and subsequent protein kinase A (PKA) activity. Pretreatment with PKA inhibitory peptide, but not gene depletion of exchange protein directly activated by cAMP 1 (Epac1), attenuated BW245C-induced Rac1 activation and transendothelial electric resistance increase. In vivo, application of 2.5% croton oil or histamine (100 μg) caused vascular leakage indexed by dye extravasation. Pretreatment with BW245C (1 mg/kg) attenuated the dye extravasation. Gene deficiency of DP abolished, or inhibition of PKA significantly reduced, the DP-mediated barrier enhancement. Conclusion-PGD

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“…Previous studies have suggested that the vasoactive effects of prostaglandins are likely involved in the pathogenesis of acute lung injury (Halushka et al, 1981;Wisner et al, 1988;Schuster and Haller, 1990;Stephenson et al, 1992;Schuster et al, 1993Schuster et al, , 1996Turnage et al, 1997;Gust et al, 1999b). In fact, acute lung injury is associated with increased tissue concentrations of the thromboxane metabolite TXB 2 (Gust et al, 1999a).…”

Section: Introductionmentioning

confidence: 99%

Components of diesel exhaust particles differentially affect lung expression of cyclooxygenase‐2 related to bacterial endotoxin

Inoue

Takano

Yanagisawa

et al. 2004

J of Applied Toxicology

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We have reported previously that components of diesel exhaust particles (DEP) differently affect acute lung injury related to lipopolysaccharide (LPS) in mice. This study examined the effects of components of DEP on the lung expression of cyclooxygenase (COX)-1 and -2 in the presence or absence of LPS. ICR mice were divided into six experimental groups that received vehicle, LPS (2.5 mg kg(-1)), organic chemicals in DEP (DEP-OC) extracted with dichloromethane (4 mg kg(-1)), residual carbonaceous nuclei after the extraction (washed DEP: 4 mg kg(-1)), DEP-OC (4 mg kg(-1)) + LPS (2.5 mg kg(-1)) or washed DEP (4 mg kg(-1)) + LPS (2.5 mg kg(-1)) intratracheally. The expression of mRNA for both COXs in the lung was evaluated 4 h after the intratracheal administration. The magnitude of COX-1 mRNA expression was not altered in each group. The LPS treatment enhanced the COX-2 gene expression compared with vehicle treatment. Washed DEP combined with LPS further increased its expression compared with LPS alone. In contrast, combined treatment of DEP-OC with LPS decreased COX-2 gene expression compared with LPS alone. These results suggest that the residual carbonaceous nuclei of DEP predominantly enhance lung expression of COX-2 rather than the extracted organic chemicals from DEP in the presence of LPS, which is concomitant with the magnitude of acute lung injury in our previous study.

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Thromboxane A₂mediates increased pulmonary microvascular permeability after intestinal reperfusion

Cited by 31 publications

References 27 publications

Prostaglandins potentiate U-46619-induced pulmonary microvascular dysfunction

Prostaglandins potentiate U-46619-induced pulmonary microvascular dysfunction

Prostaglandin D ₂ -DP Signaling Promotes Endothelial Barrier Function via the cAMP/PKA/Tiam1/Rac1 Pathway

Components of diesel exhaust particles differentially affect lung expression of cyclooxygenase‐2 related to bacterial endotoxin

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Thromboxane A2mediates increased pulmonary microvascular permeability after intestinal reperfusion

Cited by 31 publications

References 27 publications

Prostaglandins potentiate U-46619-induced pulmonary microvascular dysfunction

Prostaglandins potentiate U-46619-induced pulmonary microvascular dysfunction

Prostaglandin D 2 -DP Signaling Promotes Endothelial Barrier Function via the cAMP/PKA/Tiam1/Rac1 Pathway

Components of diesel exhaust particles differentially affect lung expression of cyclooxygenase‐2 related to bacterial endotoxin

Contact Info

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Thromboxane A₂mediates increased pulmonary microvascular permeability after intestinal reperfusion

Prostaglandin D ₂ -DP Signaling Promotes Endothelial Barrier Function via the cAMP/PKA/Tiam1/Rac1 Pathway