scholarly journals The release of 3′:5′-cyclic monophosphate from the isolated perfused rat heart

1975 ◽  
Vol 152 (2) ◽  
pp. 429-432 ◽  
Author(s):  
John A. O'Brien ◽  
Richard C. Strange
Keyword(s):  
Cyclic Amp ◽  
Rat Heart ◽  
Perfused Rat Heart ◽  
Cyclic Monophosphate ◽  
Isolated Perfused Rat Heart ◽  
Rat Hearts ◽  
Basal Release ◽  
Perfused Rat Hearts ◽  
Isolated Perfused Rat Hearts

Although basal release of cyclic AMP from isolated perfused rat hearts was not measurable, isoprenaline induced substantial release of the nucleotide, suggesting that in vivo the myocardium can contribute to plasma cyclic AMP. Anoxia also increased the amount of cyclic AMP released, but insulin and nicotinate alone or in combination had no effect.

scholarly journals The inhibition in vivo of lipoprotein lipase (clearing-factor lipase) activity by triton WR-1339

1976 ◽  
Vol 156 (3) ◽  
pp. 539-543 ◽  
Author(s):  
J Borensztajn ◽  
M S Rone ◽  
T J Kotlar
Keyword(s):  
Lipoprotein Lipase ◽  
Lipase Activity ◽  
Lipoprotein Lipase Activity ◽  
Rat Hearts ◽  
Maximum Inhibition ◽  
Triton Wr 1339 ◽  
Perfused Rat Hearts ◽  
Hydrolysis Of ◽  
Isolated Perfused Rat Hearts

1. Lipoprotein lipase activity was measured in heart homogenates and in heparin-releasable and non-releasable fractions of isolated perfused rat hearts, after the intravenous injection of Triton WR-1339. 2. In homogenates of hearts from starved, rats, lipoprotein lipase activity was significantly inhibited (P less than 0.001) 2h after the injection of Triton. This inhibition was restricted exclusively to the heparin-releasable fraction. Maximum inhibition occurred 30 min after the injection and corresponded to about 60% of the lipoprotein lipase activity that could be released from the heart during 30 s perfusion with heparin. 3. Hearts of Triton-treated starved rats were unable to take up and utilize 14C-labelled chylomicron triacylglycerol fatty acids, even though about 40% of heparin-releasable activity remained in the hearts. 4. It is concluded that Triton selectively inhibits the functional lipoprotein lipase, i.e. the enzyme directly involved in the hydrolysis of circulating plasma triacylglycerols. 5. Lipoprotein lipase activities measured in homogenates of soleus muscle of starved rats and adipose tissue of fed rats were decreased by 25 and 39% respectively after Triton injection. It is concluded that, by analogy with the heart, these Triton-inhibitable activities correspond to the functional lipoprotein lipase.

scholarly journals The discovery of a rapidly metabolized polymeric tetraphosphate derivative of adenosine in perfused rat heart

1984 ◽  
Vol 223 (3) ◽  
pp. 627-632 ◽  
Author(s):  
J Mowbray ◽  
W L Hutchinson ◽  
G R Tibbs ◽  
P G Morris
Keyword(s):  
Organic Acid ◽  
Rat Heart ◽  
Purine Nucleoside ◽  
Acid Phosphate ◽  
Perfused Rat Heart ◽  
Rat Hearts ◽  
Adenosine Phosphate ◽  
Perfused Rat Hearts ◽  
Radioactive Labelling

The predicted presence in perfused rat hearts of a rapidly metabolized but hitherto unrecognized form of adenosine phosphate has been confirmed by specific radioactive labelling. The properties of the purified compound suggest that it is a heteropolymer of a small organic acid, phosphate and purine nucleoside in the proportions 1:4:1.

scholarly journals The effects of glucose, acetate, lactate and insulin on protein degradation in the perfused rat heart

1982 ◽  
Vol 206 (3) ◽  
pp. 467-472 ◽  
Author(s):  
P H Sugden ◽  
D M Smith
Keyword(s):  
Protein Degradation ◽  
Rat Heart ◽  
Plasma Concentrations ◽  
Normal Range ◽  
Perfused Rat Heart ◽  
Rat Hearts ◽  
Insulin Inhibition

Rat hearts were perfused as working preparations by the method of Taegtmeyer, Hems & Krebs [(1980 Biochem. J. 186, 701-711]. In the presence of glucose, insulin significantly inhibited protein degradation at concentrations as low as 50 mu units/ml. Acetate or lactate, when present either as sole fuel for contraction or in combination with glucose, did not inhibit protein degradation. Insulin inhibition or protein degradation was decreased with either lactate as sole fuel. We suggest that the inhibition of protein degradation occurs over the normal range of plasma concentrations of insulin present in vivo and that the presence of glucose may be at least in part necessary for this effect of insulin.

Preconditioning accelerates contracture and ATP depletion in blood-perfused rat hearts

1995 ◽  
Vol 269 (4) ◽  
pp. H1415-H1420 ◽  
Author(s):  
K. G. Kolocassides ◽  
M. Galinanes ◽  
D. J. Hearse
Keyword(s):  
Rat Heart ◽  
Contractile Function ◽  
Study Groups ◽  
Atp Depletion ◽  
Perfused Rat Heart ◽  
Ischemic Contracture ◽  
Isolated Hearts ◽  
Time To Peak ◽  
Rat Hearts ◽  
Perfused Rat Hearts

We investigated the effect of preconditioning on the ischemia-induced depletion of ATP in the blood-perfused rat heart. Isolated hearts (n = 5/group) were aerobically perfused with whole blood from a support rat and subjected to zero-flow global ischemia (37 degrees C) for periods up to 35 min. Frozen hearts were taken for metabolic analysis. Ischemic contracture was assessed with an isovolumic intraventricular balloon. The study groups were 1) control (C) with unprotected ischemia, 2) preconditioning (PC; 2 cycles of 3-min ischemia/3-min reperfusion), and 3) cardioplegia (CP; St. Thomas') before ischemia. Preconditioning accelerated, whereas cardioplegia delayed, ischemic contracture (time to peak contracture: PC = 8.1 +/- 0.3 and CP = 25.1 +/- 0.2 min vs. C = 15.6 +/- 0.3 min, P < 0.05). The ischemia-induced decline in ATP was delayed by cardioplegia but accelerated by preconditioning (P < 0.05). In a parallel study, preconditioning and cardioplegia protected postischemic contractile function to a similar extent. Thus, in the blood-perfused rat heart, preconditioning accelerated ischemic contracture and depletion of ATP. In contrast, cardioplegia slowed ischemic contracture and ATP depletion.

scholarly journals Anthrax edema toxin has cAMP-mediated stimulatory effects and high-dose lethal toxin has depressant effects in an isolated perfused rat heart model

2011 ◽  
Vol 300 (3) ◽  
pp. H1108-H1118 ◽  
Author(s):  
Caitlin W. Hicks ◽  
Yan Li ◽  
Shu Okugawa ◽  
Steven B. Solomon ◽  
Mahtab Moayeri ◽  
...  
Keyword(s):  
Rat Heart ◽  
Left Ventricular ◽  
Lethal Toxin ◽  
Heart Model ◽  
In Vivo Models ◽  
Inotropic Effects ◽  
Perfused Rat Heart ◽  
Isolated Perfused Rat Heart ◽  
Edema Toxin

While anthrax edema toxin produces pronounced tachycardia and lethal toxin depresses left ventricular (LV) ejection fraction in in vivo models, whether these changes reflect direct cardiac effects as opposed to indirect ones related to preload or afterload alterations is unclear. In the present study, the effects of edema toxin and lethal toxin were investigated in a constant pressure isolated perfused rat heart model. Compared with control hearts, edema toxin at doses comparable to or less than a dose that produced an 80% lethality rate (LD80) in vivo in rats (200, 100, and 50 ng/ml) produced rapid increases in heart rate (HR), coronary flow (CF), LV developed pressure (LVDP), dP/d tmax, and rate-pressure product (RPP) that were most pronounced and persisted with the lowest dose ( P ≤ 0.003). Edema toxin (50 ng/ml) increased effluent and myocardial cAMP levels ( P ≤ 0.002). Compared with dobutamine, edema toxin produced similar myocardial changes, but these occurred more slowly and persisted longer. Increases in HR, CF, and cAMP with edema toxin were inhibited by a monoclonal antibody blocking toxin uptake and by adefovir, which inhibits the toxin's intracellular adenyl cyclase activity ( P ≤ 0.05). Lethal toxin at an LD80 dose (50 ng/ml) had no significant effect on heart function but a much higher dose (500 ng/ml) reduced all parameters ( P ≤ 0.05). In conclusion, edema toxin produced cAMP-mediated myocardial chronotropic, inotropic, and vasodilatory effects. Vasodilation systemically with edema toxin could contribute to shock during anthrax while masking potential inotropic effects. Although lethal toxin produced myocardial depression, this only occurred at high doses, and its relevance to in vivo findings is unclear.

In vivo heat shock preconditioning mitigates calcium overload during ischaemia/reperfusion in the isolated, perfused rat heart

2004 ◽  
Vol 449 (6) ◽  
pp. 518-525 ◽  
Author(s):  
Orsolya Szenczi ◽  
Péter Kemecsei ◽  
Zsuzsanna Miklós ◽  
László Ligeti ◽  
Luc H. E. H. Snoeckx ◽  
...  
Keyword(s):  
Heat Shock ◽  
Rat Heart ◽  
Calcium Overload ◽  
Perfused Rat Heart ◽  
Isolated Perfused Rat Heart ◽  
Ischaemia Reperfusion

Cloning of the rat P2u receptor and its potential role in coronary vasodilation

1996 ◽  
Vol 270 (2) ◽  
pp. C570-C577 ◽  
Author(s):  
S. Godecke ◽  
U. K. Decking ◽  
A. Godecke ◽  
J. Schrader
Keyword(s):  
Blood Vessels ◽  
Rat Heart ◽  
Receptor Gene ◽  
Coding Region ◽  
Rat Hearts ◽  
Perfused Rat Hearts ◽  
Coronary Blood Vessels ◽  
The Brain ◽  
Isolated Perfused Rat Hearts

We cloned and sequenced the cDNA as well as the genomic DNA of the P2u receptor gene from the rat. The coding region of the gene is not interrupted by introns. P2u is expressed in a variety of rat organs with pronounced differences of expression intensities. Highest expression was found in liver and testis, while no expression could be detected in the brain. High P2u expression was found in primary microvascular endothelial cells from the rat heart, but not in cardiac myocytes. By in situ analysis, we localized P2u expression in epithelial cells of esophagus and bronchi. Functional analysis revealed that, in isolated perfused rat hearts, the P2u ligands UTP and ATP induce a pronounced vasodilation of coronary blood vessels. In contrast, UMP and uridine, the degradative products of UTP, act as potent vasoconstrictors. Our experiments suggest that, in the rat heart, endothelial P2u receptors are involved in the ATP/UTP-mediated vasodilation of coronary blood vessels.

The effect of calcium on cardiac phosphorylase activation, contractile force and cyclic AMP in euthyroid and hyperthyroid rat hearts

1976 ◽  
Vol 54 (4) ◽  
pp. 590-595 ◽  
Author(s):  
Elizabeth J. Hartley ◽  
John H. McNeill
Keyword(s):  
Enzyme Activity ◽  
Thyroid Hormone ◽  
Cyclic Amp ◽  
Positive Inotropic Effect ◽  
Contractile Force ◽  
Inotropic Effect ◽  
Chronotropic Effect ◽  
Rat Hearts ◽  
Perfused Rat Hearts ◽  
Isolated Perfused Rat Hearts

Calcium chloride injected into isolated perfused rat hearts produced a positive inotropic effect and increased the levels of phosphorylase a (EC 2.4.1.1). The increase in enzyme activity lagged behind the inotropic effect. Pretreatment of animals with thyroid hormone enhanced the ability of noradrenaline to activate phosphorylase but did not affect the inotropic or phosphorylase activating effect of calcium. Thyroid hormone pretreatment did enhance the chronotropic effect of calcium. Calcium did not affect the cardiac levels of cyclic AMP. It is concluded that calcium can activate phosphorylase by a mechanism other than cyclic AMP and that the enhancement of adrenergic amine-induced phosphorylase activation by thyroid hormone is not a calcium mediated event.

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