Arachidonic Acid Accumulation and Eicosanoid Synthesis During Ischemia and Reperfusion in Isolated Rat Hearts1

2015 ◽  
pp. 236-243 ◽  
Author(s):  
M. van Bilsen ◽  
W. Engels ◽  
P. H. M. Willemsen ◽  
W. A. Coumans ◽  
G. J. van der Vusse ◽  
...  
Keyword(s):  
Arachidonic Acid ◽  
Ischemia And Reperfusion ◽  
Eicosanoid Synthesis ◽  
Acid Accumulation ◽  
Isolated Rat

Ischemia and reperfusion induced formation of eicosanoids in isolated rat hearts

1990 ◽  
Vol 258 (6) ◽  
pp. H1865-H1871 ◽  
Author(s):  
W. Engels ◽  
M. Van Bilsen ◽  
M. J. De Groot ◽  
P. J. Lemmens ◽  
P. H. Willemsen ◽  
...  
Keyword(s):  
High Performance Liquid Chromatography ◽  
Arachidonic Acid ◽  
High Performance ◽  
Ischemia And Reperfusion ◽  
Rat Hearts ◽  
Conversion Rates ◽  
Time Courses ◽  
Prostacyclin Production ◽  
Krebs Henseleit Buffer ◽  
Isolated Rat

Isolated, ejecting rat hearts, perfused with Krebs-Henseleit buffer, were exposed to various periods of global ischemia. Arachidonic acid (AA) accumulated significantly in the ischemic heart when the duration of ischemia exceeded 45 min. During 30 min of reperfusion, tissue levels of AA raised steadily to values of 10.5, 17.7, and 63.1 nmol/g, after 30, 45, and 60 min of ischemia, respectively. During reperfusion, significant amounts of AA metabolite prostacyclin (determined as stable metabolite 6-ketoprostaglandin F1 alpha, by radioimmunoassay and high-performance liquid chromatography) were released after 30, 45, and 60 min of ischemia. Beside prostacyclin, only small amounts of thromboxane B2 could be found during reperfusion. In contrast to increasing amounts of AA in reperfused tissue, prostacyclin release was maximal during the first 5 min of reperfusion and declined rapidly thereafter. Relatively small proportions of the accumulated AA are converted into prostacyclin, i.e., less than 1%. When hearts were treated with mepacrine, AA accumulation was almost completely abolished during 60 min of ischemia. The cumulative release of prostacyclin was found to be reduced to 134 pmol/g during 30 min of subsequent reperfusion. A close, rectilinear correlation could be established between AA accumulation and cumulative prostacyclin release during reperfusion. It is likely, however, that the site of bulk AA accumulation and that of conversion of AA into eicosanoids does not coincide in the ischemic and reperfused heart because of the low conversion rates of AA into prostacyclin and the different time courses of AA accumulation and prostacyclin production after reinstallation of flow.

Independent dual perfusion of left and right coronary arteries in isolated rat hearts

1991 ◽  
Vol 261 (6) ◽  
pp. H2082-H2090 ◽  
Author(s):  
M. Avkiran ◽  
M. J. Curtis
Keyword(s):  
High Energy ◽  
Low Flow ◽  
Blue Dye ◽  
Ischemia And Reperfusion ◽  
Langendorff Preparation ◽  
Rat Hearts ◽  
Left And Right ◽  
Conventional Models ◽  
Aortic Cannula ◽  
Isolated Rat

A novel dual lumen aortic cannula was designed and constructed to permit independent perfusion of left and right coronary beds in isolated rat hearts without necessitating the cannulation of individual arteries. Stability of the dual-perfusion preparation was shown to be similar to that of the conventional Langendorff preparation, in terms of coronary flow, heart rate, and high-energy phosphate content. The independence of left and right perfusion beds was confirmed by unilateral infusion of disulfine blue dye and spectrophotometric detection of the dye in ventricular homogenates. Transient cessation of flow to the left coronary bed resulted in severe ventricular arrhythmias upon reperfusion, as in conventional models of regional ischemia and reperfusion. The dual-perfusion model is technically undemanding, reproducible, inexpensive, and can be used in several species. It enables studies with 1) regional low flow ischemia, 2) regional zero-flow ischemia without coronary ligation (with attendant damage to vasculature), 3) selective application of drugs or interventions to the ischemic-reperfused zone, and 4) selective application of components of ischemia and reperfusion to a site anatomically relevant to ischemic heart disease.

Abstract 1712: The P2Y 12 Antagonist Cangrelor and the GP IIb/IIIa Blocker Abciximab Reduce Platelet-Mediated Myocardial Injury After Ischemia and Reperfusion

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Jose A Barrabes ◽  
Javier Inserte ◽  
Maribel Mirabet ◽  
Adoracion Quiroga ◽  
Victor Hernando ◽  
...  
Keyword(s):  
Myocardial Injury ◽  
Myocardial Damage ◽  
Left Ventricular ◽  
Myocardial Salvage ◽  
Ischemia And Reperfusion ◽  
Activated Platelets ◽  
Rat Hearts ◽  
Developed Pressure ◽  
Enddiastolic Pressure ◽  
Isolated Rat

Objective: Platelets activated during experimental acute myocardial infarction (AMI) contribute to myocardial injury. We aimed to investigate whether platelets from patients with AMI increase myocardial damage after transient ischemia in isolated rat hearts and the modification of this effect by the P2Y 12 receptor antagonist cangrelor and the GPIIb/IIIa receptor blocker abciximab. Methods: Platelets were obtained from 9 AMI patients (7 thrombolyzed, all on aspirin) within 24 h after symptom onset. Incubation with 100 μM cangrelor or 50 μg/ml abciximab resulted, respectively, in 78 ± 4 and 90 ± 2% inhibition of aggregation (optical aggregometry). Isolated rat hearts (four simultaneous experiments per patient) were subjected to 40 min of global ischemia and 60 min of reperfusion. Hearts received no additional intervention (Control) or were infused during the 5 min prior to ischemia with platelets (22.5x10 6 /min), either untreated or treated with cangrelor or abciximab. Results: P-selectin expression (flow cytometry) in isolated platelets before infusion was 31 ± 3% (P = NS between groups). Platelets augmented myocardial injury, as demonstrated by worse left ventricular developed pressure (LVDevP), higher left ventricular enddiastolic pressure (LVEDP) and coronary resistance, and greater LDH release and infarct size (TTC staining), and both cangrelor and abciximab greatly attenuated these effects (Table ). Conclusions: Activated platelets from patients with AMI increase myocardial injury after ischemia and reperfusion, and cangrelor and abciximab attenuate this effect. The results support the notion that very early antiplatelet treatment may increase myocardial salvage by direct effects on the microcirculation in these patients.

Eicosanoids in Rat Brain during Ischemia and Reperfusion—Correlation to DC Depolarization

1990 ◽  
Vol 10 (3) ◽  
pp. 358-364 ◽  
Author(s):  
F. Tegtmeier ◽  
C. Weber ◽  
U. Heister ◽  
I. Haker ◽  
D. Scheller ◽  
...  
Keyword(s):  
Arachidonic Acid ◽  
Rat Brain ◽  
Direct Current ◽  
Eicosatetraenoic Acid ◽  
Ischemia And Reperfusion ◽  
Ischemic Time ◽  
Isolated Perfused Rat Brain ◽  
Current Potential

The effects of complete ischemia on cerebral arachidonic acid (AA) metabolism were investigated in the isolated perfused rat brain. During 12.5 min of ischemia, AA, 5-hydroxy-6,8,11,14-eicosatetraenoic acid, and 15-hydroxy-5,8,11,13-eicosatetraenoic acid increased 129-, 4-, and 10-fold, respectively, while subsequent reperfusion for 30 min resulted in normalized levels independently of the duration of preceding ischemia. Prostaglandin (PG) F2α, PGE2, PGD2, 6-keto-PGF1α, and thromboxane (Tx) B2 remained at preischemic levels during 12.5 min of complete ischemia. However, at the end of subsequent reperfusion for 30 min, the levels of the prostanoids PGF2α, PGE2, PGD2, 6-keto-PGF1α, and TxB2 increased according to the preceding ischemic time. The levels reached a maximum after 7.5 min of ischemia and were elevated by 7-, 14-, 48-, 3-, and 30-fold, respectively. A prolongation of ischemia of up to 12.5 min was not associated with further increases of prostanoids at the end of reperfusion. The mechanisms underlying the metabolism of eicosanoids are discussed in relation to the changes of cortical direct current potential.

scholarly journals Cardioprotective Effects of 9-Hydroxyellipticine on Ischemia and Reperfusion in Isolated Rat Heart

2002 ◽  
Vol 89 (1) ◽  
pp. 21-28 ◽  
Author(s):  
Kazuhiko Saeki ◽  
Ichiro Obi ◽  
Noriko Ogiku ◽  
Munekazu Shigekawa ◽  
Toshiaki Imagawa ◽  
...  
Keyword(s):  
Rat Heart ◽  
Isolated Rat Heart ◽  
Ischemia And Reperfusion ◽  
Cardioprotective Effects ◽  
Isolated Rat

Enhancement of Ca2+-regulated exocytosis by indomethacin in guinea-pig antral mucous cells: arachidonic acid accumulation

2005 ◽  
Vol 91 (1) ◽  
pp. 249-259 ◽  
Author(s):  
Shoko Fujiwara ◽  
Chikao Shimamoto ◽  
Yoshihiko Nakanishi ◽  
Ken-ichi Katsu ◽  
Masumi Kato ◽  
...  
Keyword(s):  
Arachidonic Acid ◽  
Guinea Pig ◽  
Mucous Cells ◽  
Regulated Exocytosis ◽  
Acid Accumulation
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