Loss of cardiac contractility and severe morphologic changes by acutely lowering the pH of the perfusion medium: protection by fatty acids

Hülsmann, W.C.; Dewit, L; Schneydenberg, C; Verkleij, A.J.

doi:10.1016/0304-4165(90)90016-p

Cited by 16 publications

(9 citation statements)

References 5 publications

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“…Fluorescence rapidly increases when the pH of the medium is lowered to 7.0 or less. indicative of decreased flow in affected areas, as may have been expected from previous investigations in which either respiratory acidosis was effected in working hearts [6,14] or metabolic acidosis in Langendorff hearts [1,7]. The heterogeneous pattern of fluorescence increase by acidosis, induced by changing the pH of the medium from 7.5 to 7.0 during Langendorff perfusion in thc present work (Fig.…”

Section: Discussionsupporting

confidence: 84%

“…Our previous experience [7], that albumin-bound oleate can prevent the strong decrease of flow by changing the pH of the perfusion medium from 7.5 to 7.0, led us to use another fatty acid, octanoate, in the present study. This fatty acid as well as acetate has been shown by others to protect the energy state of glucose-perfused working rat hearts after respiratory acidosis [6].…”

Section: Octanoate Addition and Nadh Fluorescencementioning

confidence: 99%

“…Lowering of the pH of the perfusion medium results in loss of high affinity binding of Ca 2 + to membranes [3][4][5]. This results in a brief period of positive inotropy, accompanied by an increase of flow rate, followed by progressive decline of inotropy and flow so that ischemia follows [1,6,7]. This phenomenon may be delayed by fatty acids [6,7], which are known to have vasodilatory properties (compare ref.…”

Section: Introductionmentioning

confidence: 99%

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Imminent ischemia in normal and hypertrophic Langendorff rat hearts; effects of fatty acids and superoxyde dismutase monitored by NADH suraface fluorescence

Hülsmann

Ashruf

Bruining

et al. 1993

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Diseas

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Hypertrophic hearts contain areas of hypoperfusion which can be visualized by increased NADH surface fluorescence during in vitro perfusion without oxygen-carrying particles under constant pressure and pacing. By contrast, fluorescence remained low when non-hypertrophic hearts were used instead. When during perfusion of normal hearts the pH of the medium was lowered from 7.5 to 7.0, areas of high fluorescence appeared in a few minutes. The high fluorescent areas under conditions of cardiac hypertrophy or pH 7.0 perfusion could be reduced by addition of superoxide dismutase. It indicates that oxygen free radicals interfere with proper flow regulation in areas of low pH. Fluorescence in hypertrophic hearts also diminished during addition of albumin-bound oleate to the standard, glucose-containing, medium. This is in agreement with our earlier finding of fatty acid protection from acidosis-initiated loss of capillary flow (Biochim. Biophys. Acta, 1033 (1990) 214-218). In contrast to low concentrations of free fatty acids, high concentrations interfere with tissue oxygenation. This has been illustrated by the use of 1 mM octanoate, which after a few min caused the appearance of high fluorescent areas. We conclude that decompensation of flow in hypoperfused areas of heart, as occurs in hypertrophy, may be stimulated by acidosis and oxygen free radicals.

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Section: Discussionsupporting

confidence: 84%

Section: Octanoate Addition and Nadh Fluorescencementioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Imminent ischemia in normal and hypertrophic Langendorff rat hearts; effects of fatty acids and superoxyde dismutase monitored by NADH suraface fluorescence

Hülsmann

Ashruf

Bruining

et al. 1993

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Diseas

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“…It is probably not the smooth muscle alpha-adrenergic receptor or guanylate cyclase of smooth muscle cells, as judged by prompt reactions upon vasoxin or nitroprusside addition [3]. The observed effect of fatty acids on delaying imminent ischemia, as induced by acidosis [5], is probably located in endothelial cells, the most likely source of 02-in preischemia [3,23,26]. Our experience that fatty acid and carnitine are both needed to improve force of the paced latissimus dorsi muscle [1], suggests that fatty acids must be activated in order to be effective.…”

Section: Discussionmentioning

confidence: 97%

“…This enzyme was probably involved in the production of oxygen free radicals in the interstitium, as the rapid loss of cardiac function due to hypoperfusion, could acutely be diminished by superoxide dismutase (SOD) administration. As we have observed that fatty acids are vasodilators [4] and delay acidosis-induced loss of vascular flow [5], we decided to investigate fatty acid metabolism in vascular cells.…”

Section: Introductionmentioning

confidence: 99%

Carnitine requirement of vascular endothelial and smooth muscle cells in imminent ischemia

Hülsmann

Dubelaar²

1992

Mol Cell Biochem

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Vascular endothelial and -smooth muscle cells have been shown to use fatty acids as substrates for oxidative phosphorylation. Endothelial cells are more vulnerable to oxidative stress than muscle cells and are prone to loose carnitine early during hypoperfusion. This has been suggested by two observations. The first is that incubation of isolated endothelial cells in a low carnitine medium leads to oleate oxidation, dependent upon carnitine addition, whereas smooth muscle cells do not depend on carnitine addition during in vitro incubation, although aminocarnitine, a specific inner-membrane carnitine palmitoyltransferase inhibitor, inhibits fatty acid oxidation. The second observation is that rat hearts labeled in vivo with 14C-carnitine loose, as paced Langendorff heart, only 4% of their carnitine in 20 min perfusion, following 60 min global ischemia. The carnitine released had a much higher specific radioactivity than the carnitine that was not released. It indicates compartmentation of carnitine in heart. As earlier and presently discussed work shows endothelial vulnerability, it is to be expected that this cell type may become carnitine deficient during pacing and ischemia. Endothelial incompetence in flow regulation could be delayed by the presence of carnitine and fatty acids in pre-ischemia. It is speculated how activated fatty acids could protect endothelium.

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Carnitine requirement of vascular endothelial and smooth muscle cells in imminent ischemia

Hülsmann

Dubelaar²

1992

Lipid Metabolism in the Healthy and Disease Heart

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Loss of cardiac contractility and severe morphologic changes by acutely lowering the pH of the perfusion medium: protection by fatty acids

Cited by 16 publications

References 5 publications

Imminent ischemia in normal and hypertrophic Langendorff rat hearts; effects of fatty acids and superoxyde dismutase monitored by NADH suraface fluorescence

Imminent ischemia in normal and hypertrophic Langendorff rat hearts; effects of fatty acids and superoxyde dismutase monitored by NADH suraface fluorescence

Carnitine requirement of vascular endothelial and smooth muscle cells in imminent ischemia

Carnitine requirement of vascular endothelial and smooth muscle cells in imminent ischemia

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