Tags

Type your tag names separated by a space and hit enter

Propofol impairment of mitochondrial respiration in isolated perfused guinea pig hearts determined by reflectance spectroscopy.
Crit Care Med 2000; 28(1):172-7CC

Abstract

OBJECTIVE

To simultaneously determine the effect of propofol on myocardial oxygenation, mitochondrial function, and whole organ function in an isolated heart model, using optical reflectance spectroscopy.

DESIGN

Controlled laboratory investigation.

SETTING

Research laboratory.

SUBJECTS

Twenty adult guinea pigs.

INTERVENTIONS

Isolated hearts were perfused alternately with a modified oxygenated Krebs-Henseleit buffer and with buffer containing varied concentrations of propofol. Ninety seconds of ischemia were produced during perfusion with each solution studied.

MEASUREMENTS AND MAIN RESULTS

Myoglobin oxygen saturation, cytochrome c and cytochrome a/a3 redox state, and ventricular pressure were continuously measured from isolated guinea pig hearts during a 2-hr period. Myoglobin oxygen saturation increased and both cytochromes became more oxidized in the presence of propofol. During ischemia, myoglobin desaturation and cytochrome reduction were delayed and less complete in the presence of propofol. The mean ischemic time to 50% myoglobin desaturation was, on average, 14.3 secs with buffer perfusion, and increased to 24.5, 27.9, and 41.8 secs, with 50, 100, and 200 microM propofol perfusion, respectively. Ventricular function decreased linearly with increasing propofol concentration. From baseline buffer perfusion, maximal dP/dt per cardiac cycle decreased on average by 30.4%, 40.9%, and 69.4%, with 50, 100, and 200 microM propofol perfusion, respectively.

CONCLUSIONS

Propofol impairs either oxygen utilization or inhibits electron flow along the mitochondrial electron transport chain in the guinea pig cardiomyocyte. Propofol also significantly decreases ventricular performance in the isolated perfused heart. These effects are linearly correlated with propofol concentration in the range studied.

Authors+Show Affiliations

Department of Pediatrics, University of Wisconsin, Madison, USA. kschen@chmc.orgNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

10667518

Citation

Schenkman, K A., and S Yan. "Propofol Impairment of Mitochondrial Respiration in Isolated Perfused Guinea Pig Hearts Determined By Reflectance Spectroscopy." Critical Care Medicine, vol. 28, no. 1, 2000, pp. 172-7.
Schenkman KA, Yan S. Propofol impairment of mitochondrial respiration in isolated perfused guinea pig hearts determined by reflectance spectroscopy. Crit Care Med. 2000;28(1):172-7.
Schenkman, K. A., & Yan, S. (2000). Propofol impairment of mitochondrial respiration in isolated perfused guinea pig hearts determined by reflectance spectroscopy. Critical Care Medicine, 28(1), pp. 172-7.
Schenkman KA, Yan S. Propofol Impairment of Mitochondrial Respiration in Isolated Perfused Guinea Pig Hearts Determined By Reflectance Spectroscopy. Crit Care Med. 2000;28(1):172-7. PubMed PMID: 10667518.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Propofol impairment of mitochondrial respiration in isolated perfused guinea pig hearts determined by reflectance spectroscopy. AU - Schenkman,K A, AU - Yan,S, PY - 2000/2/10/pubmed PY - 2000/2/26/medline PY - 2000/2/10/entrez SP - 172 EP - 7 JF - Critical care medicine JO - Crit. Care Med. VL - 28 IS - 1 N2 - OBJECTIVE: To simultaneously determine the effect of propofol on myocardial oxygenation, mitochondrial function, and whole organ function in an isolated heart model, using optical reflectance spectroscopy. DESIGN: Controlled laboratory investigation. SETTING: Research laboratory. SUBJECTS: Twenty adult guinea pigs. INTERVENTIONS: Isolated hearts were perfused alternately with a modified oxygenated Krebs-Henseleit buffer and with buffer containing varied concentrations of propofol. Ninety seconds of ischemia were produced during perfusion with each solution studied. MEASUREMENTS AND MAIN RESULTS: Myoglobin oxygen saturation, cytochrome c and cytochrome a/a3 redox state, and ventricular pressure were continuously measured from isolated guinea pig hearts during a 2-hr period. Myoglobin oxygen saturation increased and both cytochromes became more oxidized in the presence of propofol. During ischemia, myoglobin desaturation and cytochrome reduction were delayed and less complete in the presence of propofol. The mean ischemic time to 50% myoglobin desaturation was, on average, 14.3 secs with buffer perfusion, and increased to 24.5, 27.9, and 41.8 secs, with 50, 100, and 200 microM propofol perfusion, respectively. Ventricular function decreased linearly with increasing propofol concentration. From baseline buffer perfusion, maximal dP/dt per cardiac cycle decreased on average by 30.4%, 40.9%, and 69.4%, with 50, 100, and 200 microM propofol perfusion, respectively. CONCLUSIONS: Propofol impairs either oxygen utilization or inhibits electron flow along the mitochondrial electron transport chain in the guinea pig cardiomyocyte. Propofol also significantly decreases ventricular performance in the isolated perfused heart. These effects are linearly correlated with propofol concentration in the range studied. SN - 0090-3493 UR - https://www.unboundmedicine.com/medline/citation/10667518/Propofol_impairment_of_mitochondrial_respiration_in_isolated_perfused_guinea_pig_hearts_determined_by_reflectance_spectroscopy_ L2 - http://Insights.ovid.com/pubmed?pmid=10667518 DB - PRIME DP - Unbound Medicine ER -