Forskning
Udskriv Udskriv
Switch language
Rigshospitalet - en del af Københavns Universitetshospital
Udgivet

Acute intramyocardial lipid accumulation in rats does not slow cardiac conduction per se

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

DOI

  1. Reliability of the mean flow index (Mx) for assessing cerebral autoregulation in healthy volunteers

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

  2. Hyperbaric oxygen treatment is associated with a decrease in cytokine levels in patients with necrotizing soft-tissue infection

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

  3. Hypovolemia and reduced hemoglobin mass in patients with heart failure and preserved ejection fraction

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

  1. Oral pre‑treatment with thiocyanate (SCN−) protects against myocardial ischaemia–reperfusion injury in rats

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

  2. Aging suppresses sphingosine-1-phosphate chaperone ApoM in circulation resulting in maladaptive organ repair

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

  3. Effect of menopause and exercise training on plasma apolipoprotein M and sphingosine-1-phosphate

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

Vis graf over relationer

Diabetic patients suffer from both cardiac lipid accumulation and an increased risk of arrhythmias and sudden cardiac death. This correlation suggests a link between diabetes induced cardiac steatosis and electrical abnormalities, however, the underlying mechanism remains unknown. We previously showed that cardiac conduction velocity slows in Zucker diabetic fatty rats and in fructose-fat fed rats, models that both exhibit prominent cardiac steatosis. The aim of this study was to investigate whether acute cardiac lipid accumulation reduces conduction velocity per se. Cardiac lipid accumulation was induced acutely by perfusing isolated rat hearts with palmitate-glucose buffer, or subacutely by fasting rats overnight. Subsequently, longitudinal cardiac conduction velocity was measured in right ventricular tissue strips, and intramyocardial triglyceride and lipid droplet content was determined by thin layer chromatography and BODIPY staining, respectively. Perfusion with palmitate-glucose buffer significantly increased intramyocardial triglyceride levels compared to perfusion with glucose (2.16 ± 0.17 (n = 10) vs. 0.92 ± 0.33 nmol/mg WW (n = 9), P < 0.01), but the number of lipid droplets was very low in both groups. Fasting of rats, however, resulted in both significantly elevated intramyocardial triglyceride levels compared to fed rats (3.27 ± 0.43 (n = 10) vs. 1.45 ± 0.24 nmol/mg WW (n = 10)), as well as a larger volume of lipid droplets (0.60 ± 0.13 (n = 10) vs. 0.21 ± 0.06% (n = 10), P < 0.05). There was no significant difference in longitudinal conduction velocity between palmitate-glucose perfused and control hearts (0.77 ± 0.025 (n = 10) vs. 0.75 m/sec ± 0.029 (n = 9)), or between fed and fasted rats (0.75 ± 0.042 m/sec (n = 10) vs. 0.79 ± 0.047 (n = 10)). In conclusion, intramyocardial lipid accumulation does not slow cardiac longitudinal conduction velocity per se. This is true for both increased intramyocardial triglyceride content, induced by palmitate-glucose perfusion, and increased intramyocardial triglyceride and lipid droplet content, generated by fasting.

OriginalsprogEngelsk
Artikelnummere14049
TidsskriftPhysiological Reports
Vol/bind7
Udgave nummer7
ISSN2051-817X
DOI
StatusUdgivet - apr. 2019

Bibliografisk note

© 2019 The Authors. Physiological Reports published by Wiley Periodicals, Inc. on behalf of The Physiological Society and the American Physiological Society.

ID: 58286520