Effects of excess free fatty acids on mechanical and metabolic function in normal and ischemic myocardium in swine.

Liedtke, A. J.; Nellis, S. H.; Neely, James R.

doi:10.1161/01.res.43.4.652

Cited by 278 publications

(103 citation statements)

References 28 publications

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“…The mechanism behind altered left ventricular function remains to be established. Elevated plasma free fatty acids together with reduced cardiac glycogen subsequent to prolonged exercise38 39 have been postulated to result in impaired myocardial performance5 38 However, the fourfold increase in free fatty acids in this study was apparently too low to be responsible for the altered left ventricular function.…”

Section: +33mentioning

confidence: 52%

Evidence of impaired left ventricular performance after an uninterrupted competitive 24 hour run.

Niemelä¹,

Palatsi²,

Ikäheimo³

et al. 1984

Circulation

102

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ALTHOUGH the response of the human heart to exercise has been studied extensively, little information is available on the effects of utterly exhaustive exercise on cardiac performance in man. Marathon running is growing in popularity, however, and thousands of runners, more or less well trained, are taking part in various ultramarathon races (i.e., distances greater than the marathon) all over the world each year. It is well recognized that ultramarathon running is not without risk. In addition to casualties caused by exhaustion, heat stroke, renal failure, and sudden cardiac death," repeated hemoptysis and pulmonary edema due to left ventricular failure has been reported in two welltrained athletes during a 90 km run.5 However, subsequent clinical investigations in these athletes, including cardiac catheterization, revealed no apparent cardiac abnormalities, and it was postulated that some as yet unknown factor (or factors) could lie behind these observations. We had a unique opportunity to make echocardiographic and biochemical measurements on welltrained ultramarathon runners in connection with a competitive 24 hr run. Our results indicate a deleterious effect of such severe prolonged exercise on left ventricular performance. Methods

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Section: +33mentioning

confidence: 52%

Evidence of impaired left ventricular performance after an uninterrupted competitive 24 hour run.

Niemelä¹,

Palatsi²,

Ikäheimo³

et al. 1984

Circulation

102

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“…Inhibition of carnitine acyltransferase I with POCA may enhance the accumulation of another amphiphile, acyl CoA, in ischemic myocardium. However, the magnitude of the increase of acyl CoA with ischemia is much smaller than that of long-chain acylcarnitine (42,43). Acyl CoA is confined, almost exclusively, to the mitochondria (44) and is therefore unlikely to impact directly on the sarcolemma particularly early after the onset of ischemia.…”

Section: Discussionmentioning

confidence: 98%

Prophylaxis of early ventricular fibrillation by inhibition of acylcarnitine accumulation

Corr¹,

Creer²,

Yamada³

1989

Journal of Critical Care

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“…Mitochondrial P-oxidation of fatty acids is blocked during ischaemia resulting in accumulation of acyl-CoA in mitochondria and of acyl carnitines in the cytosol (Idell-Wenger et al, 1978;Liedtke et al, 1978; 'Present address (and correspondence): Syntex Research Centre, Research Park, Riccarton, Edinburgh EH 14 4AS 2Present address: Preclinical Research, Sandoz, CH-4002, Basle, Switzerland. Neely & Feuvray, 1981;Knabb et al, 1986).…”

Section: Introductionmentioning

confidence: 99%

Direct activation of Ca²⁺ channels by palmitoyl carnitine, a putative endogenous ligand

Spedding¹,

Mir²

1987

British J Pharmacology

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Palmitoyl carnitine, a lipid metabolite which accumulates in cytoplasmic membranes during ischaemia, has been shown to resemble the Ca2+ channel activator, Bay K 8644, in K+‐depolarized smooth muscle. Palmitoyl carnitine caused concentration‐dependent (1–1000 μmol l−1) augmentations in the sensitivity to Ca2+ of K+‐depolarized taenia preparations from the guinea‐pig caecum. The (±)‐isomer was equieffective with the (–)‐isomer, whereas carnitine was ineffective and palmitic acid relaxed the tissues. The shift to the left of Ca2+ concentration‐response curves induced by palmitoyl carnitine (100 μmol l−1) was additive with that of Bay K 8644 (1 μmol l−1). The interactions of palmitoyl carnitine with the different classes of calcium‐antagonist were similar to those seen with Bay K 8644. Schild plots of the calcium‐antagonist effects of nifedipine were shifted to the right following preincubation of the taenia with palmitoyl carnitine (30–300 μmol l−1). The inhibitory effects of verapamil were especially sensitive to palmitoyl carnitine (100 μmol l−1). Whereas the potency of diltiazem as a calcium‐antagonist was reduced by palmitoyl carnitine (100 μmol l−1), the inhibitory effects of the lipophilic class III calcium‐antagonists, cinnarizine and flunarizine, were entirely resistant to palmitoyl carnitine (100 μmol l−1). Although palmitoyl carnitine has detergent properties in high concentrations and lyses red blood cells, these effects were not Ca2+‐dependent, nor were they modified by calcium‐antagonists. Other detergents did not have selective interactions with Ca2+ channels. Palmitoyl carnitine inhibited [3H]‐nitrendipine, [3H]‐verapamil and [3H]‐diltiazem binding to rat cortical membranes with IC50 values (μmol l−1) of 120 ± 1, 95 ± 17 and 120 ± 15 μmol l−1 respectively. The inhibition showed little temperature‐dependence, in contrast to that of Bay K 8644, except for a small reduction in the IC50 value for [3H]‐verapamil binding at 37°C (42 ± 5 μmol l−1). Palmitoyl carnitine interacted selectively with the Ca2+ channel, in that effects on ligand binding to α‐adrenoceptors, β‐adrenoceptors and 5‐HT1A receptors occurred only at 5–10 fold higher concentrations. It is concluded that palmitoyl carnitine, at concentrations which have previously been shown to occur in the cytoplasm during myocardial ischaemia, may interact directly with Ca2+ channels and may therefore be considered as an endogenous modulator of channel function. The site of action differs from that of other agents.

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Effects of excess free fatty acids on mechanical and metabolic function in normal and ischemic myocardium in swine.

Cited by 278 publications

References 28 publications

Evidence of impaired left ventricular performance after an uninterrupted competitive 24 hour run.

Evidence of impaired left ventricular performance after an uninterrupted competitive 24 hour run.

Prophylaxis of early ventricular fibrillation by inhibition of acylcarnitine accumulation

Direct activation of Ca²⁺ channels by palmitoyl carnitine, a putative endogenous ligand

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Effects of excess free fatty acids on mechanical and metabolic function in normal and ischemic myocardium in swine.

Cited by 278 publications

References 28 publications

Evidence of impaired left ventricular performance after an uninterrupted competitive 24 hour run.

Evidence of impaired left ventricular performance after an uninterrupted competitive 24 hour run.

Prophylaxis of early ventricular fibrillation by inhibition of acylcarnitine accumulation

Direct activation of Ca2+ channels by palmitoyl carnitine, a putative endogenous ligand

Contact Info

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Direct activation of Ca²⁺ channels by palmitoyl carnitine, a putative endogenous ligand