Effect of aspirin on the fibrinolytic response in perfused rat hindquarters

The role of aspirin in tissue plasminogen activator (t-PA) release was studied in rats after experimental venous occlusion. For this purpose, we developed a new experimental model which combines a vascular perfusion system (isolated rat hindquarters) with vascular stimulation, namely the application...

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Veröffentlicht in:European journal of pharmacology 1992-12, Vol.229 (1), p.39-44
Hauptverfasser: Iacoviello, Licia, De Curtis, Amalia, Amore, Concetta, D'Adamo, Maria Cristina, Buczko, Wlodzimierz, de Gaetano, Giovanni, Donati, Maria Benedetta
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container_end_page 44
container_issue 1
container_start_page 39
container_title European journal of pharmacology
container_volume 229
creator Iacoviello, Licia
De Curtis, Amalia
Amore, Concetta
D'Adamo, Maria Cristina
Buczko, Wlodzimierz
de Gaetano, Giovanni
Donati, Maria Benedetta
description The role of aspirin in tissue plasminogen activator (t-PA) release was studied in rats after experimental venous occlusion. For this purpose, we developed a new experimental model which combines a vascular perfusion system (isolated rat hindquarters) with vascular stimulation, namely the application of venous stasis. Application of venous stasis for 30 min induced the release of t-PA from the vascular endothelium into the perfusate (from 0.19 ± 0.05 to 0.39 ± 0.05 UI/ml), reaching a peak 90 s after reperfusion. Aspirin administered to rats 60 min before the experiments (100 mg/kg i.v.), or dissolved in Tyrode solution (100 μM), suppressed 6-keto-prostaglandin F 1α (6-keto-PGF 1α) synthesis (0.38 ± 0.09 in control and
doi_str_mv 10.1016/0014-2999(92)90283-A
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For this purpose, we developed a new experimental model which combines a vascular perfusion system (isolated rat hindquarters) with vascular stimulation, namely the application of venous stasis. Application of venous stasis for 30 min induced the release of t-PA from the vascular endothelium into the perfusate (from 0.19 ± 0.05 to 0.39 ± 0.05 UI/ml), reaching a peak 90 s after reperfusion. Aspirin administered to rats 60 min before the experiments (100 mg/kg i.v.), or dissolved in Tyrode solution (100 μM), suppressed 6-keto-prostaglandin F 1α (6-keto-PGF 1α) synthesis (0.38 ± 0.09 in control and &lt;0.01 and 0.15 ± 0.09 ng/ml, respectively, in aspirin-treated groups) but did not prevent the increase in fibrinolytic activity after venous occlusion (from 0.20 ± 0.04 to 0.38 ± 0.06 and from 0.07 ± 0.03 to 0.27 ± 0.03 IU/ml, respectively, in the aspirin-treated group). Our results suggest that the increase in fibrinolytic activity after experimental venous occlusion in isolated rat hindlegs is modulated by mechanism(s) other than the cyclooxygenase pathway in the vascular wall.</description><identifier>ISSN: 0014-2999</identifier><identifier>EISSN: 1879-0712</identifier><identifier>DOI: 10.1016/0014-2999(92)90283-A</identifier><identifier>PMID: 1473562</identifier><identifier>CODEN: EJPHAZ</identifier><language>eng</language><publisher>Amsterdam: Elsevier B.V</publisher><subject>6-Ketoprostaglandin F1 alpha - metabolism ; Animals ; Aspirin ; Aspirin - pharmacology ; Biological and medical sciences ; Blood. Blood coagulation. Reticuloendothelial system ; Disease Models, Animal ; Endothelium, Vascular - drug effects ; Endothelium, Vascular - metabolism ; Fibrinolysis - drug effects ; Fibrinolytic activity ; Hindlimb - blood supply ; Ligation ; Male ; Medical sciences ; Perfusion ; Pharmacology. 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For this purpose, we developed a new experimental model which combines a vascular perfusion system (isolated rat hindquarters) with vascular stimulation, namely the application of venous stasis. Application of venous stasis for 30 min induced the release of t-PA from the vascular endothelium into the perfusate (from 0.19 ± 0.05 to 0.39 ± 0.05 UI/ml), reaching a peak 90 s after reperfusion. Aspirin administered to rats 60 min before the experiments (100 mg/kg i.v.), or dissolved in Tyrode solution (100 μM), suppressed 6-keto-prostaglandin F 1α (6-keto-PGF 1α) synthesis (0.38 ± 0.09 in control and &lt;0.01 and 0.15 ± 0.09 ng/ml, respectively, in aspirin-treated groups) but did not prevent the increase in fibrinolytic activity after venous occlusion (from 0.20 ± 0.04 to 0.38 ± 0.06 and from 0.07 ± 0.03 to 0.27 ± 0.03 IU/ml, respectively, in the aspirin-treated group). Our results suggest that the increase in fibrinolytic activity after experimental venous occlusion in isolated rat hindlegs is modulated by mechanism(s) other than the cyclooxygenase pathway in the vascular wall.</description><subject>6-Ketoprostaglandin F1 alpha - metabolism</subject><subject>Animals</subject><subject>Aspirin</subject><subject>Aspirin - pharmacology</subject><subject>Biological and medical sciences</subject><subject>Blood. Blood coagulation. Reticuloendothelial system</subject><subject>Disease Models, Animal</subject><subject>Endothelium, Vascular - drug effects</subject><subject>Endothelium, Vascular - metabolism</subject><subject>Fibrinolysis - drug effects</subject><subject>Fibrinolytic activity</subject><subject>Hindlimb - blood supply</subject><subject>Ligation</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Perfusion</subject><subject>Pharmacology. 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Blood coagulation. Reticuloendothelial system</topic><topic>Disease Models, Animal</topic><topic>Endothelium, Vascular - drug effects</topic><topic>Endothelium, Vascular - metabolism</topic><topic>Fibrinolysis - drug effects</topic><topic>Fibrinolytic activity</topic><topic>Hindlimb - blood supply</topic><topic>Ligation</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Perfusion</topic><topic>Pharmacology. Drug treatments</topic><topic>Rats</topic><topic>Tissue Plasminogen Activator - metabolism</topic><topic>Veins</topic><topic>Venous Insufficiency - blood</topic><topic>Venous stasis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Iacoviello, Licia</creatorcontrib><creatorcontrib>De Curtis, Amalia</creatorcontrib><creatorcontrib>Amore, Concetta</creatorcontrib><creatorcontrib>D'Adamo, Maria Cristina</creatorcontrib><creatorcontrib>Buczko, Wlodzimierz</creatorcontrib><creatorcontrib>de Gaetano, Giovanni</creatorcontrib><creatorcontrib>Donati, Maria Benedetta</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>European journal of pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Iacoviello, Licia</au><au>De Curtis, Amalia</au><au>Amore, Concetta</au><au>D'Adamo, Maria Cristina</au><au>Buczko, Wlodzimierz</au><au>de Gaetano, Giovanni</au><au>Donati, Maria Benedetta</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Effect of aspirin on the fibrinolytic response in perfused rat hindquarters</atitle><jtitle>European journal of pharmacology</jtitle><addtitle>Eur J Pharmacol</addtitle><date>1992-12-08</date><risdate>1992</risdate><volume>229</volume><issue>1</issue><spage>39</spage><epage>44</epage><pages>39-44</pages><issn>0014-2999</issn><eissn>1879-0712</eissn><coden>EJPHAZ</coden><abstract>The role of aspirin in tissue plasminogen activator (t-PA) release was studied in rats after experimental venous occlusion. For this purpose, we developed a new experimental model which combines a vascular perfusion system (isolated rat hindquarters) with vascular stimulation, namely the application of venous stasis. Application of venous stasis for 30 min induced the release of t-PA from the vascular endothelium into the perfusate (from 0.19 ± 0.05 to 0.39 ± 0.05 UI/ml), reaching a peak 90 s after reperfusion. Aspirin administered to rats 60 min before the experiments (100 mg/kg i.v.), or dissolved in Tyrode solution (100 μM), suppressed 6-keto-prostaglandin F 1α (6-keto-PGF 1α) synthesis (0.38 ± 0.09 in control and &lt;0.01 and 0.15 ± 0.09 ng/ml, respectively, in aspirin-treated groups) but did not prevent the increase in fibrinolytic activity after venous occlusion (from 0.20 ± 0.04 to 0.38 ± 0.06 and from 0.07 ± 0.03 to 0.27 ± 0.03 IU/ml, respectively, in the aspirin-treated group). Our results suggest that the increase in fibrinolytic activity after experimental venous occlusion in isolated rat hindlegs is modulated by mechanism(s) other than the cyclooxygenase pathway in the vascular wall.</abstract><cop>Amsterdam</cop><pub>Elsevier B.V</pub><pmid>1473562</pmid><doi>10.1016/0014-2999(92)90283-A</doi><tpages>6</tpages></addata></record>
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ispartof European journal of pharmacology, 1992-12, Vol.229 (1), p.39-44
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subjects 6-Ketoprostaglandin F1 alpha - metabolism
Animals
Aspirin
Aspirin - pharmacology
Biological and medical sciences
Blood. Blood coagulation. Reticuloendothelial system
Disease Models, Animal
Endothelium, Vascular - drug effects
Endothelium, Vascular - metabolism
Fibrinolysis - drug effects
Fibrinolytic activity
Hindlimb - blood supply
Ligation
Male
Medical sciences
Perfusion
Pharmacology. Drug treatments
Rats
Tissue Plasminogen Activator - metabolism
Veins
Venous Insufficiency - blood
Venous stasis
title Effect of aspirin on the fibrinolytic response in perfused rat hindquarters
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