Contribution of prostaglandins to reperfusion-induced ventricular failure in isolated rat hearts

1986 ◽  
Vol 251 (1) ◽  
pp. H133-H140 ◽  
Author(s):  
M. Karmazyn
Keyword(s):  
Coronary Flow ◽  
Initial Period ◽  
Hydrolysis Product ◽  
Contractile Force ◽  
Ventricular Contractility ◽  
Endogenous Prostaglandin ◽  
Resting Tension ◽  
Rat Hearts ◽  
Contractile Recovery ◽  
Isolated Rat

This study was carried out to investigate the possible contribution of endogenous prostaglandin (PG) production to failure of contractile recovery following reperfusion of hypoperfused isolated rat hearts. A 90% reduction in coronary flow rate for 60 min resulted in a time-dependent depression of contractile force and an elevation in resting tension. Reperfusion produced a slight (approximately 11%) recovery of contractile force, whereas resting tension remained elevated. Reperfusion was a potent stimulus for PG (as assessed by 6 keto-PGF1 alpha) release and resulted in levels that were significantly higher than those observed prior to ischemia. When PG synthesis was inhibited by the nonsteroidal anti-inflammatory drugs ibuprofen, indomethacin, or acetylsalicylic acid (ASA), recovery of ventricular contractility on reperfusion was significantly higher than that seen in the absence of drugs. Ibuprofen was the most effective, producing an average recovery of 70% (P less than 0.05 from control). Indomethacin and ASA produced approximately a 40% (P less than 0.05) and 35% (P less than 0.05) recovery of contractile force, respectively. The improved recovery in contractility was significantly depressed by the addition of low concentrations of prostacyclin (PGI2) and PGF2 alpha, whereas PGE2 and 6 keto-PGF1 alpha, the hydrolysis product of PGI2, were ineffective. The effects on resting tension were inconsistent. PG release during reperfusion was unrelated either to the length of the initial period of reduced coronary flow or the degree of contractile recovery; it was attenuated either by a reduction in or by an elevation of Ca concentration. These results indicate that endogenous PGs mediate, at least in part, reperfusion-associated failure of ventricular function.

Dissociation of hypoxia-induced calcium gain and rise in resting tension in isolated rat hearts

1988 ◽  
Vol 254 (4) ◽  
pp. H678-H685
Author(s):  
W. G. Nayler ◽  
J. S. Elz ◽  
D. J. Buckley
Keyword(s):  
Perfusion Defect ◽  
Creatine Phosphate ◽  
Ventricular Muscle ◽  
Isolated Hearts ◽  
Resting Tension ◽  
Rat Hearts ◽  
Early Increase ◽  
Butanedione Monoxime ◽  
Tension Generation ◽  
Isolated Rat

When isolated hearts are perfused with substrate-free hypoxic buffer for prolonged periods of time, resting tension and tissue Ca increase. These two events may be interrelated. Isolated rat hearts were used to establish whether the hypoxia-induced increase in tissue Ca can be dissociated from the rise in resting tension. Tension generation was inhibited at the start of hypoxic perfusion by adding 2,3-butanedione monoxime (BDM, 30 mM). In other experiments the Ca2+ in the hypoxic buffer was reduced from 1.3 to 0.1 mM. After 30-120 min of hypoxia, ventricular muscle was assayed for ATP, creatine phosphate, Ca, and Na, and the perfusion defect was established. Resting tension was recorded before and throughout the hypoxic perfusion. Sixty minutes of perfusion with 1.3 mM Ca2+ glucose-free hypoxic buffer caused the tissue Ca to increase (P less than 0.01). Resting tension increased by 7.9 +/- 0.6 g (P less than 0.01). Sixty minutes of perfusion with 0.1 mM Ca2+ glucose-free hypoxic buffer failed to cause an increase in tissue Ca, but resting tension increased (P less than 0.01). During perfusion with glucose-free hypoxic buffer containing 2.6 mM Ca2+ and 30 mM BDM, resting tension remained low for up to 120 min, but after 60 min Ca accumulation occurred. After 120 min of BDM-hypoxic perfusion, tissue Ca reached 11.8 +/- 0.9 mumol/g dry wt. With or without BDM, hypoxia caused an early increase in tissue Na ahead of any increase in tissue Ca.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of Salidroside on Cardiac Functional Recovery

2013 ◽  
Vol 798-799 ◽  
pp. 1030-1032
Author(s):  
Yan Zhang ◽  
Zhong Hua Zheng ◽  
Yue Peng Wang ◽  
Guo Liang Peng ◽  
Liu Hang Wang
Keyword(s):  
Flow Rate ◽  
Functional Recovery ◽  
Rat Heart ◽  
Coronary Flow ◽  
Left Ventricular ◽  
Cardioprotective Effect ◽  
Decrease Rate ◽  
Rat Hearts ◽  
Developed Pressure ◽  
Isolated Rat

To investigate the cardioprotective effect of salidroside to rat heart subjected to 8-hour hypothermic storage and 2-hour normothermic reperfusion. Isolated rat hearts were perfused with Langendorff model; after 30 minutes of baseline, the hearts were arrested and stored by St. Thomas solution (STS) without (STS group) or with different concentration salidroside at 4 °C for 8 hours, then reperfused for 2 hours. Compared with STS group, both middle and high dosage in STS greatly improved the recovery of left ventricular developed pressure (LVDP), maximum LVDP increase and decrease rate (±dp/dt), coronary flow rate (CF). Our study demonstrated that the salidroside was beneficial to improving cardiac functional recovery.

scholarly journals Postischemic Na+-K+-ATPase reactivation is delayed in the absence of glycolytic ATP in isolated rat hearts

2001 ◽  
Vol 280 (5) ◽  
pp. H2189-H2195 ◽  
Author(s):  
Jan G. Van Emous ◽  
Carmen L. A. M. Vleggeert-Lankamp ◽  
Marcel G. J. Nederhoff ◽  
Tom J. C. Ruigrok ◽  
Cees J. A. Van Echteld
Keyword(s):  
Pyruvate Dehydrogenase ◽  
Functional Coupling ◽  
Glycogen Depletion ◽  
Postischemic Reperfusion ◽  
Rat Hearts ◽  
Perfused Rat Hearts ◽  
Glycolytic Atp ◽  
Contractile Recovery ◽  
Isolated Rat ◽  
Isolated Perfused Rat Hearts

Normalization of intracellular sodium (Na[Formula: see text]) after postischemic reperfusion depends on reactivation of the sarcolemmal Na+-K+-ATPase. To evaluate the requirement of glycolytic ATP for Na+-K+-ATPase function during postischemic reperfusion, 5-s time-resolution23Na NMR was performed in isolated perfused rat hearts. During 20 min of ischemia, Na[Formula: see text] increased approximately twofold. In glucose-reperfused hearts with or without prior preischemic glycogen depletion, Na[Formula: see text]decreased immediately upon postischemic reperfusion. In glycogen-depleted pyruvate-reperfused hearts, however, the decrease of Na[Formula: see text] was delayed by ∼25 s, and application of the pyruvate dehydrogenase (PDH) activator dichloroacetate (DA) did not shorten this delay. After 30 min of reperfusion, Na[Formula: see text]had almost normalized in all groups and contractile recovery was highest in the DA-treated hearts. In conclusion, some degree of functional coupling of glycolytic ATP and Na+-K+-ATPase activity exists, but glycolysis is not essential for recovery of Na[Formula: see text] homeostasis and contractility after prolonged reperfusion. Furthermore, the delayed Na+-K+-ATPase reactivation observed in pyruvate-reperfused hearts is not due to inhibition of PDH.

Atenolol and fentanyl effects upon the heart rate, myocardial contractility, and coronary flow in isolated rat hearts

2001 ◽  
Vol 33 (6) ◽  
pp. A75
Author(s):  
H.K. Maués ◽  
W.C. Pádua Filho ◽  
M. Faraj ◽  
H. Junqueira Neves ◽  
E.S. Gomes ◽  
...  
Keyword(s):  
Heart Rate ◽  
Myocardial Contractility ◽  
Coronary Flow ◽  
Rat Hearts ◽  
Isolated Rat

Tadalafil in Increasing Doses: The Influence on Coronary Blood Flow and Oxidative Stress in Isolated Rat Hearts

Pharmacology ◽  
2021 ◽  
pp. 1-10
Author(s):  
Nada M. Banjac ◽  
Velibor M. Vasović ◽  
Nebojša P. Stilinović ◽  
Dušan V. Prodanović ◽  
Ana D. Tomas Petrović ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Superoxide Anion ◽  
Coronary Flow ◽  
Albino Rats ◽  
Dependent Manner ◽  
Superoxide Anion Production ◽  
Nitrite Oxide ◽  
Rat Hearts ◽  
And Oxidative Stress ◽  
Isolated Rat

<b><i>Introduction:</i></b> This study aimed to assess the influence of different doses of tadalafil on coronary flow and oxidative stress in isolated rat hearts. <b><i>Methods:</i></b> The hearts of male Wistar albino rats (<i>n</i> = 48) were retrogradely perfused according to the Langendorff technique at gradually increased constant perfusion pressure (CPP) (40–120 mm Hg). Coronary flow and oxidative stress markers: nitrite oxide (NO) outflow and superoxide anion production in coronary effluent were measured. The experiments were performed during control conditions and in the presence of tadalafil (10, 20, 50, and 200 nM) alone or with Nω-nitro-L-arginine monomethyl ester (L-NAME) (30 μM). <b><i>Results:</i></b> Tadalafil administration significantly increased coronary flow at all CPP values at all administered doses. Tadalafil led to an increase in the NO levels, but a statistically significant NO release increase was found only at the highest dose and highest CPP. Tadalafil did not significantly affect the release of O<sup>2−</sup>. After inhibiting the nitrite oxide synthase system by L-NAME, tadalafil-induced changes in cardiac flow and NO levels were reversed. L-NAME administration had no pronounced effect on the O<sup>2−</sup> release. <b><i>Conclusion:</i></b> Tadalafil causes changes in the heart vasculature in a dose-dependent manner. It does not lead to a significant increase in the production of superoxide anion radicals.

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