Influence of Dietary Linoleic Acid on Cardiac Function and Prostaglandin Release and on the Effects of Isoprenaline in the Isolated Rat Heart

Hoffmann, Pavel; Mentz, P; Ke, Blass; Förster, W

doi:10.1097/00005344-198209000-00004

Cited by 26 publications

(12 citation statements)

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“…They both caused slowly developing decreases in heart rate to approx 70% of baseline values during the 60-min treatment; however, depending on neuroendocrine status and venous return, this decrease in rate may not affect cardiac output. A similar negative chronotropic effect of linoleic acid has been noted in hearts from rats fed a diet enriched with the fatty acid (32). Previous work in our lab showed that linoleic acid and 12,13-EOA decrease mitochondrial membrane potential in rabbit renal cortical mitochondria, possibly as a result of their uncoupling capabilities (25), and Xiao et al demonstrated that linoleic acid can suppress voltage-activated Na + current in rat ventricular myocytes (26).…”

Section: Discussionsupporting

confidence: 73%

“…Previous studies using isolated heart preparations and cell culture models have suggested that linoleic acid has direct effects on cardiac function (26,27,(29)(30)(31). The Langendorff-perfused heart, which has been used previously to examine cardiac effects of linoleic acid, is an excellent model for such studies because direct effects on ventricular function can be examined in the absence of neurohumoral control (9,10,29,32,33). We selected the Langendorff-perfused heart for our experiments because of its advantages as an in vitro model, the ability to compare observed effects of linoleic acid to published data, and the ability to compare effects of the 12,13-metabolites with those of the parent fatty acid.…”

Section: Discussionmentioning

confidence: 99%

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Linoleic acid metabolites act to increase contractility in isolated rat heart

et al. 2002

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Previous in vivo studies in dogs suggest that the 9,10-monoepoxide of linoleic acid (9,10-cis-epoxyoctadecenoic acid [9,10-EOA]) has toxic cardiovascular effects that result in death at higher doses. More recent work with rabbit renal proximal tubule cells suggests that the 12,13-metabolites of linoleic acid are more toxic than the 9,10-isomers. Thus, in the current study, we tested the hypothesis that 12,13-EOA and 12,13-dihydroxyoctadecadienoic acid (12,13-DHOA) have direct adverse effects on the heart. Langendorff-perfused rat hearts were exposed to 30 microM linoleic acid, 30 microM 12,13-EOA, or 30 microM 12,13-DHOA for 60 min followed by a 30-min recovery period. As indicated by peak left intraventricular pressure and/or +dP/dt(max), all three of the agents elicited moderate increases in contractile function that peaked within 10 20 min. The effects of linoleic acid and 12,13-EOA returned to control values during the remainder of the 60-min exposure, whereas the positive inotropic response to 12,13-DHOA was maintained until washout. Sustained arrhythmias and negative inotropic actions were not observed with any of the three compounds. Subsequently, the monoepoxides were infused into conscious rats (35 mg/kg/h) while blood pressure, heart rate, and EKG were monitored for 24 h using biotelemetry techniques. The only effect observed was a slight decline in blood pressure. Thus, current data suggest that linoleic acid and its oxidative metabolites do not have direct cardiotoxic effects during acute exposure.

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Section: Discussionsupporting

confidence: 73%

Section: Discussionmentioning

confidence: 99%

Linoleic acid metabolites act to increase contractility in isolated rat heart

et al. 2002

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“…Diminished inotropic responsiveness to isoprenaline has been demonstrated in isolated perfused hearts of rats fed a linoleic acid-rich diet compared with a linoleic aciddeficient diet [17,181 and in rats fed sunflower oil (polyunsaturated fats) compared with coconut oil (saturated fats) supplemented diets [2]. Similar results were obtained using other inotropic agents acting via cyclic AMP-dependent mechanisms (forskolin, IBMX, dibutyryl cyclic AMP) but not with agents acting via cyclic AMP-independent (calcium, phenylephrine) mechanisms [2].…”

Section: Discussionmentioning

confidence: 99%

Effects of Dietary Lipid Modification on Adrenoceptor-Mediated Cardiovascular Responsiveness and Baroreflex Sensitivity in Normotensive Subjects

et al. 1997

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To examine the effects of short-term dietary lipid modification on alpha- and beta-adrenoceptor-mediated cardiovascular responsiveness, 19 normal volunteers consumed either a high-fat or a low-fat diet for 2 weeks in an open, randomized, crossover study of 6 weeks' duration. Diets were balanced for sodium and potassium content. Adrenoceptor-mediated cardiovascular responsiveness was assessed by measuring blood pressure and heart rate responses to incremental infusions of phenylephrine and isoprenaline. Baroreflexes were studied by examining heart rate responses to phenylephrine and to the Valsalva manoeuvre. Total plasma cholesterol and low-density lipoprotein cholesterol levels both fell significantly (by 22% and 26%, respectively), on the low-fat compared with the high-fat diet, as did resting supine blood pressures and heart rate (by 6 mmHg systolic and 3 mmHg diastolic, and 5 beats/min). These changes were accompanied by a significant reduction in the systolic blood pressure response to isoprenaline. Blood pressure responses to phenylephrine and baroreflex sensitivity did not change. These results suggest that dietary fat intake alters cardiac beta-adrenergic reactivity without significant effects on vascular alpha-adrenoceptor mediated responses or baroreflexes.

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“…In particular, the level of ara chidonic acid in cardiac membranes does not increase when a linoleic acid supplement is provided. When one considers the frequently proposed role of linoleic and arachidonic acids in the production of prostaglandins, and the numerous suggestions in the litera ture that altered levels of membrane 20:4 may be responsible for a wide variety of induced effects [17][18][19][20][21][22], it is prudent to note that the majority of these suggestions have arisen from experiments in a single animal species, namely, the rat.…”

Section: Discussionmentioning

confidence: 99%

Changes in Fatty Acid Composition of the Cardiac Phospholipids of the Cotton-Eared Marmoset (<i>Callithrix jacchus</i>) after Feeding Different Lipid Supplements

McIntosh

et al. 1985

Ann Nutr Metab

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After feeding marmosets different lipid supplements for 6 months, the distribution of phospholipid classes and the fatty acid composition of phosphatidylcholine (PC), phosphatidylethanolamine (PE) and diphosphatidylglycerol (DPG) were determined in their cardiac membranes. Supplementing the diet with linoleic-acid-rich sunflower seed oil raised the level of 18:2, n-6 in both PC and PE, but did not change the level significantly in DPG. When 18:2, n-6 was increased, the level of arachidonic acid (20:4, n-6) was significantly decreased in PC and PE. No arachidonic acid was present in DPG. Supplementing the diet with mutton fat did not markedly increase the level of saturated fats, nor did it markedly reduce the level of arachidonic acid in any phospholipid component. No dietary treatment altered the distribution of the major phospholipid classes.

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Influence of Dietary Linoleic Acid on Cardiac Function and Prostaglandin Release and on the Effects of Isoprenaline in the Isolated Rat Heart

Cited by 26 publications

References 0 publications

Linoleic acid metabolites act to increase contractility in isolated rat heart

Linoleic acid metabolites act to increase contractility in isolated rat heart

Effects of Dietary Lipid Modification on Adrenoceptor-Mediated Cardiovascular Responsiveness and Baroreflex Sensitivity in Normotensive Subjects

Changes in Fatty Acid Composition of the Cardiac Phospholipids of the Cotton-Eared Marmoset (<i>Callithrix jacchus</i>) after Feeding Different Lipid Supplements

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