Impaired fatty acid oxidation in propofol infusion syndrome

Wolf, Andrew; Weir, Patricia; Segar, Philip; Stone, Janet; Shield, Julian

doi:10.1016/s0140-6736(00)04064-2

Cited by 349 publications

(255 citation statements)

References 5 publications

Supporting

Mentioning

226

Contrasting

Unclassified

Order By: Relevance

“…PRIS resembles mitochondrial cytopathies and acquired carnitine deficiency [5,6] . Malonyl-carnitine, C5-acylcarnitine, creatine kinase, troponin T (TnT) and myoglobin levels are increased in pediatric PRIS, which is consistent with impaired fatty acid oxidation due to a reduction of the mitochondrial entry of long-chain acylcarnitine esters and the failure of the respiratory chain.…”

Section: Introductionmentioning

confidence: 99%

Lipid metabolism disturbances and AMPK activation in prolonged propofol-sedated rabbits under mechanical ventilation

et al. 2011

View full text Add to dashboard Cite

Aim: To explore the mechanisms underlying the propofol infusion syndrome (PRIS), a potentially fatal complication during prolonged propofol infusion. Methods: Male rabbits under mechanical ventilation through endotracheal intubation were divided into 3 groups (n=6 for each) that were sedated with 1% propofol (Group P), isoflurane (Group I) or isoflurane while receiving 10% intralipid (Group II), respectively. Blood biochemical parameters were collected at 0, 6, 12, 18, 24, and 30-36 h after the initiation of treatments. The hearts were removed out immediately after the experiments, and the level of tumor necrosis factor (TNF)-α in the hearts were studied using immunohistochemistry. AMP-activated protein kinase (AMPK) and phospho-AMPK in the hearts were assessed using Western blotting. Results: The mortality rate was 50% in Group P, and 0% in Groups I and II. The serum lipids and liver function indices in Group P were significantly increased, but moderately increased in Group II. Significant decreases in these indices were found in Groups I. All the groups showed dramatically increased release of creatine kinase (CK). Intense positive staining of TNF-α was found in all the heart samples in Group P, but only weak and neglectful staining was found in the hearts from Group II and Group I, respectively. AMPK phosphorylation was significantly increased in the hearts of Group P. Conclusion: Continuous infusion of large dose of propofol in rabbits undergoing prolonged mechanical ventilation causes hyperlipidemia, liver dysfunction, increased CK levels, AMPK activation and myocardial injury. The imbalance between energy demand and utilization may contribute to PRIS.

show abstract

Section: Introductionmentioning

confidence: 99%

Lipid metabolism disturbances and AMPK activation in prolonged propofol-sedated rabbits under mechanical ventilation

et al. 2011

View full text Add to dashboard Cite

show abstract

“…1 Standardized approach for analyzing disturbances in acid-base physiology. AG anion gap, HCO 3 − bicarbonate, K + potassium ions, Na + sodium ions, Cl − chloride ions, BUN blood urea nitrogen, ABD acid-base disorders, GI gastrointestinal tract, EABV effective arterial blood volume, CDA chloride depletion alkalosis, RTA renal tubular acidosis, fK + e fractional K + excretion, N normal, I increased, D decreased oxidation, leading to PRIS, and inhibits the level of mitochondrial oxidative phosphorylation and lipid metabolism [46,47].…”

Section: Pathophysiologymentioning

confidence: 99%

Drug-induced acid-base disorders

et al. 2014

View full text Add to dashboard Cite

The incidence of acid-base disorders (ABDs) is high, especially in hospitalized patients. ABDs are often indicators for severe systemic disorders. In everyday clinical practice, analysis of ABDs must be performed in a standardized manner. Highly sensitive diagnostic tools to distinguish the various ABDs include the anion gap and the serum osmolar gap. Drug-induced ABDs can be classified into five different categories in terms of their pathophysiology: (1) metabolic acidosis caused by acid overload, which may occur through accumulation of acids by endogenous (e.g., lactic acidosis by biguanides, propofol-related syndrome) or exogenous (e.g., glycol-dependant drugs, such as diazepam or salicylates) mechanisms or by decreased renal acid excretion (e.g., distal renal tubular acidosis by amphotericin B, nonsteroidal antiinflammatory drugs, vitamin D); (2) base loss: proximal renal tubular acidosis by drugs (e.g., ifosfamide, aminoglycosides, carbonic anhydrase inhibitors, antiretrovirals, oxaliplatin or cisplatin) in the context of Fanconi syndrome; (3) alkalosis resulting from acid and/or chloride loss by renal (e.g., diuretics, penicillins, aminoglycosides) or extrarenal (e.g., laxative drugs) mechanisms; (4) exogenous bicarbonate loads: milk-alkali syndrome, overshoot alkalosis after bicarbonate therapy or citrate administration; and (5) respiratory acidosis or alkalosis resulting from drug-induced depression of the respiratory center or neuromuscular impairment (e.g

show abstract

“…(17) tavşanlarda yaptığı çalışmada; bizim çalışmamızın sonuçlarıyla benzer olarak, yüksek doz propofol infüzyonunun laktat seviyelerinde artmaya ve metabolik asidoza neden olduğunu göstermişlerdir. Yayımlanan vaka raporlarında (19)(20)(21)(22) insanlarda propofol infüzyonuna başlandıktan sonra diğer biyokimyasal belirtilerin yokluğunda erken dönemde gelişen laktat artışına bağlı metabolik asidozun PRİS'nun habercisi olabileceği belirtilmiştir. Ayrıca kritik olarak hasta olmayan ve kısa süre-li fakat yüksek doz propofol infüzyonu yapılan hastalarda erken dönemde ve beklenmeyen metabolik asidoz geliştiği-ne dair çok sayıda vaka raporu mevcuttur (23)(24)(25)(26)(27).…”

Section: Bulgularunclassified

Mekanik Ventilatördeki Tavşanlarda Propofol İnfüzyonu İle Oluşan Metabolik ve Biokimyasal Değişikliklerde L-Karnitin Tedavisinin Etkileri

Yılbaş¹,

Ayhan²,

Akbay³

et al. 2011

tybdd

View full text Add to dashboard Cite

Amaç: Uzun süreli propofol infüzyonuna bağlı, vücutta artan lipid yükünün karnitin eksikliğine neden olabileceği düşünülmektedir. Çalışmamızda; tavşanlarda yüksek doz propofol infüzyonu sırasın-da karnitin verilmesinin etkilerinin incelenmesi amaçlanmıştır. Gereç ve Yöntem: Etik komite iznini takiben; 20 adet, 2500-3500 g, 3-4 aylık, erkek, Yeni Zelanda cinsi tavşan çalışmaya dahil edildi. Ksilazin ve atropinle premedikasyon yapılan tavşanlara; ketaminle anestezi indüksiyonu sonrası trakeostomi açıldı ve ventilatöre bağ-landı. Grup P (n:5)'e 20 mg/kg/saat dozunda, %2'lik propofol infüz-yonu; Grup PK (n:5)'ya 20 mg/kg/saat dozunda, %2'lik propofol ve eş zamanlı olarak 100 mg/kg L-karnitin infüzyonu, Grup S (n:5)'ye 4 lt/dk %100 oksijen içerisinde, %1,5'lik sevofluran, Grup SK (n:5)'ya ise sevofluranla birlikte 100 mg/kg L-karnitin infüzyonu uygulandı. Sedasyon seviyeleri 30 dk'da bir değerlendirildi. Tüm vital bulguları 15 dk'da bir takip edildi. Arteriyel kan gazı analizi 2 saat arayla, diğer tüm serum biyokimya testleri için ise 12 saat arayla kan alındı. Gruplara uygulanan anestezi yöntemine hayvanlar ölene kadar veya 24 saat süresince devam edildi. 24 saat sonunda ölmeyen tavşan-lara; yüksek doz ketaminle (60 mg/kg) ötenazi yapıldı. Bulgular: Tüm gruplar ağırlık, vital parametreler, arteriyel kan gazı ile bakılan tüm parametreler, yaşam süreleri, karaciğer enzimleri, laktat dehidrogenaz, serum elektrolitleri, kreatin kinaz, böbrek fonksiyon testleri açısından benzerdi (p>0,05). Bununla birlikte ölüm veya ötenazi öncesinde amilaz değerlerinin; Grup PK'da; Grup P'ye göre daha düşük; miyoglobin ve CK-MB değerlerinin ÖZET SUMMARYObjective: Increased lipid mass in the body secondary to long term and high doses of propofol infusion may cause carnitine deficiency. In this study; we aimed to investigate the effects of carnitine, given for treatment purposes and have not been analyzed before, during high doses of propofol infusion in rabbits. Materials and Methods: Following ethical committee approval; 2500-3500 grams weight, 3-4 months-old, healthy, male, white 20 New Zealand rabbits were included in the study. The rabbits were premedicated with xsilazine and atropine. After the preparation period including tracheostomy, monitorization, catheterization of the ear arteries and veins and urinary vesical; basal blood samples for biochemical and metabolic parameters included in the study were taken and rabbits were divided into 4 groups, 5 rabbits in each, randomly (Group P, Group PC, Group S, Group SC). For sedation 20 mg/kg/h propofol infusion was given to Group P, 20 mg/kg/h propofol and 100 mg/kg L-carnitine infusions were given simultaneously to Group PC, sevoflurane for sedation was given to Group S, sevoflurane and L-carnitine infusion were given simultaneously to Group SC. Their sedation levels were evaluated every 30 minutes and their vital signs were reported every 15 minutes. Every 2 hours arterial blood gases analysis and every 12 hours electrolytes and metabolic parameters were repeated. Euthanasia with high...

show abstract

Impaired fatty acid oxidation in propofol infusion syndrome

Cited by 349 publications

References 5 publications

Lipid metabolism disturbances and AMPK activation in prolonged propofol-sedated rabbits under mechanical ventilation

Lipid metabolism disturbances and AMPK activation in prolonged propofol-sedated rabbits under mechanical ventilation

Drug-induced acid-base disorders

Mekanik Ventilatördeki Tavşanlarda Propofol İnfüzyonu İle Oluşan Metabolik ve Biokimyasal Değişikliklerde L-Karnitin Tedavisinin Etkileri

Contact Info

Product

Resources

About