thromboxane-b2 and Burns--Electric

thromboxane-b2 has been researched along with Burns--Electric* in 2 studies

Other Studies

2 other study(ies) available for thromboxane-b2 and Burns--Electric

Article	Year
[The effect of the molecular triggers of hemostatic activity on thrombosis in early stage of electrical injuries]. Zhonghua zheng xing shao shang wai ke za zhi = Zhonghua zheng xing shao shang waikf [i.e. waike] zazhi = Chinese journal of plastic surgery and burns, 1999, Volume: 15, Issue:5 To evaluate the mechanisms of thrombosis in the early stage of electrical injury.. Endothelin-1(ET-1), prostacylin(PGI2), platelet alpha-granule membrane protein (Gmp-140), thromboxane (TXB2), and plasminogen(PLG-A) were measured in 26 patients with electrical injury.. It was found that GMP-140 and ET-1 increased significantly(P < 0.01), PLG-A showed a significant change 2 weeks after the injury, while there was an imbalance between TXB2 and PGI2.. It is believed that change in one or several mediators mentioned above may trigger thrombosis after electrical injury. Topics: Adolescent; Adult; Burns, Electric; Endothelin-1; Epoprostenol; Female; Humans; Male; Middle Aged; P-Selectin; Thrombosis; Thromboxane B2	1999
A new explanation for the progressive tissue loss in electrical injuries. Plastic and reconstructive surgery, 1984, Volume: 73, Issue:3 A reproducible electrical injury to the hind limb was produced in rats, an injury characterized by progressive tissue necrosis. Serial histochemical examinations of cross sections with a peroxidase-antiperoxidase method revealed increased production of arachidonic acid metabolites, especially thromboxane, at distal sites near the entrance wound and in periosseous tissues more proximally. Levels of these vasoactive substances remained elevated during the time of progressive necrosis and demarcation of seemingly normal, uninjured tissue. Treatment with agents capable of blocking thromboxane production allowed tissue salvage, as evidenced by a decreased autoamputation rate and an increased total surviving length. From this study it appears that an electrical injury is thermal trauma, producing elevated levels of arachidonic acid metabolites in areas of greatest heat production. Prolonged thromboxane excess, with resultant vasoconstriction and thrombosis in the microcirculation, is seen to play a key role in the progressive tissue loss characteristic of the injury. The use of antithromboxane agents may be of benefit in halting this progression and salvaging tissue in these devastating injuries. Topics: Animals; Arachidonic Acid; Arachidonic Acids; Burns, Electric; Dinoprost; Dinoprostone; Imidazoles; Male; Prostaglandins E; Prostaglandins F; Rats; Rats, Inbred Strains; Thromboxane B2	1984

Article

Year

[The effect of the molecular triggers of hemostatic activity on thrombosis in early stage of electrical injuries].

Zhonghua zheng xing shao shang wai ke za zhi = Zhonghua zheng xing shao shang waikf [i.e. waike] zazhi = Chinese journal of plastic surgery and burns, 1999, Volume: 15, Issue:5

To evaluate the mechanisms of thrombosis in the early stage of electrical injury.. Endothelin-1(ET-1), prostacylin(PGI2), platelet alpha-granule membrane protein (Gmp-140), thromboxane (TXB2), and plasminogen(PLG-A) were measured in 26 patients with electrical injury.. It was found that GMP-140 and ET-1 increased significantly(P < 0.01), PLG-A showed a significant change 2 weeks after the injury, while there was an imbalance between TXB2 and PGI2.. It is believed that change in one or several mediators mentioned above may trigger thrombosis after electrical injury.

Topics: Adolescent; Adult; Burns, Electric; Endothelin-1; Epoprostenol; Female; Humans; Male; Middle Aged; P-Selectin; Thrombosis; Thromboxane B2

1999

A new explanation for the progressive tissue loss in electrical injuries.

Plastic and reconstructive surgery, 1984, Volume: 73, Issue:3

A reproducible electrical injury to the hind limb was produced in rats, an injury characterized by progressive tissue necrosis. Serial histochemical examinations of cross sections with a peroxidase-antiperoxidase method revealed increased production of arachidonic acid metabolites, especially thromboxane, at distal sites near the entrance wound and in periosseous tissues more proximally. Levels of these vasoactive substances remained elevated during the time of progressive necrosis and demarcation of seemingly normal, uninjured tissue. Treatment with agents capable of blocking thromboxane production allowed tissue salvage, as evidenced by a decreased autoamputation rate and an increased total surviving length. From this study it appears that an electrical injury is thermal trauma, producing elevated levels of arachidonic acid metabolites in areas of greatest heat production. Prolonged thromboxane excess, with resultant vasoconstriction and thrombosis in the microcirculation, is seen to play a key role in the progressive tissue loss characteristic of the injury. The use of antithromboxane agents may be of benefit in halting this progression and salvaging tissue in these devastating injuries.

Topics: Animals; Arachidonic Acid; Arachidonic Acids; Burns, Electric; Dinoprost; Dinoprostone; Imidazoles; Male; Prostaglandins E; Prostaglandins F; Rats; Rats, Inbred Strains; Thromboxane B2

1984