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CARDIOVASCULAR ANESTHESIA

Propofol Inhibits Ca²⁺ Transients but Not Contraction in Intact Beating Guinea Pig Hearts

Yuri Nakae, MD^*, Satoshi Fujita, MD, PhD, and Akiyoshi Namiki, MD, PhD^*

*Department of Anesthesiology, Sapporo Medical University School of Medicine; and Department of Anesthesia, Hokkaido Keiaikai Minami 1-jyo Hospital, Sapporo, Japan

Address correspondence and reprint requests to Yuri Nakae, MD, Department of Anesthesiology, Sapporo Medical University School of Medicine, South-1, West-16, Chuo-ku, Sapporo 060-8543, Japan. Address e-mail to yurinaka{at}sapmed.ac.jp

We investigated whether propofol inhibits Ca²⁺ transients and left ventricular pressure (LVP) in intact beating guinea pig hearts at clinical concentrations and whether an inhibition of Ca²⁺ transients by propofol results from an impairment of sarcolemmal or of sarcoplasmic reticulum (SR) function. By using a Langendorff’s preparation, transmural left ventricular phasic intracellular Ca²⁺ concentration ([Ca²⁺]_i) was measured by the fluorescence ratio of indo-1 emission at 385 nm and 456 nm and was calibrated to Ca²⁺ transients (in nM). The Ca²⁺ transients during each contraction were defined as available [Ca²⁺]_i. Sixty hearts were perfused with modified Krebs-Ringer’s solution containing lipid vehicle and propofol (1 and 10 µM) in the absence and presence of ryanodine, thapsigargin, and nifedipine, while developed LVP and available [Ca²⁺]_i were recorded. Propofol (10 µM) decreased available [Ca²⁺]_i by 11.0% ± 1.3% without decreasing developed LVP (% of control, P < 0.05). Propofol (10 µM) caused a leftward shift in the curve of developed LVP as a function of available [Ca²⁺]_i. Propofol (10 µM) with nifedipine (1 µM), but not with ryanodine (1 µM) or thapsigargin (1 µM), decreased available [Ca²⁺]_i by 15.5% ± 1.7% (P < 0.05). Propofol decreases available [Ca²⁺]_i without decreasing cardiac contraction, and it enhances myofilament Ca²⁺ sensitivity in intact beating hearts at clinical concentrations. The inhibition of available [Ca²⁺]_i by propofol may be mainly mediated by an impairment of sarcoplasmic reticulum Ca²⁺ handling rather than the sarcolemmal L-type Ca²⁺ current.

Implications: This is the first study of the effects of propofol on intracellular Ca²⁺ concentration and myofilament Ca²⁺ sensitivity under physiologic conditions in intact isolated beating guinea pig hearts.

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