Anesthesia and analgesia
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Anesthesia and analgesia · Jun 2000
Absorbents differ enormously in their capacity to produce compound A and carbon monoxide.
Concern persists regarding the production of carbon monoxide (CO) and Compound A from the action of carbon dioxide (CO(2)) absorbents on desflurane and sevoflurane, respectively. We tested the capacity of eight different absorbents with various base compositions to produce CO and Compound A. We delivered desflurane through desiccated absorbents, and sevoflurane through desiccated and moist absorbents, then measured the resulting concentrations of CO from the former and Compound A from the latter. We also tested the CO(2) absorbing capacity of each absorbent by using a model anesthetic system. We found that the presence of potassium hydroxide (KOH) and sodium hydroxide (NaOH) increased the production of CO from calcium hydroxide (Ca[OH](2)) but did not consistently affect production of Compound A. However, the effect of KOH versus NaOH was not consistent in its impact on CO production. Furthermore, the effect of KOH versus NaOH versus Ca(OH)(2) was inconsistent in its impact on Compound A production. Two absorbents (Amsorb) [Armstrong Medica, Ltd, Coleraine, Northern Ireland], composed of Ca(OH)(2) plus 0.7% polyvinylpyrrolidine, calcium chloride, and calcium sulfate; and lithium hydroxide) produced dramatically lower concentrations of both CO and Compound A. Both produced minimal to no CO and only small concentrations of Compound A. The presence of polyvinylpyrrolidine, calcium chloride, and calcium sulfate in Amsorb appears to have suppressed the production of toxic products. All absorbents had an adequate CO(2) absorbing capacity greatest with lithium hydroxide. ⋯ Production of the toxic substances, carbon monoxide and Compound A, from anesthetic degradation by carbon dioxide absorbents, might be minimized by the use of one of two specific absorbents, Amsorb (Armstrong Medica, Ltd., Coleraine, Northern Ireland) (calcium hydroxide which also includes 0.7% polyvinylpyrrolidine, calcium chloride, and calcium sulfate) or lithium hydroxide.
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Anesthesia and analgesia · Jun 2000
Propofol inhibits Ca(2+) transients but not contraction in intact beating guinea pig hearts.
We investigated whether propofol inhibits Ca(2+) transients and left ventricular pressure (LVP) in intact beating guinea pig hearts at clinical concentrations and whether an inhibition of Ca(2+) 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 Ca(2+) concentration ([Ca(2+)](i)) was measured by the fluorescence ratio of indo-1 emission at 385 nm and 456 nm and was calibrated to Ca(2+) transients (in nM). The Ca(2+) transients during each contraction were defined as available [Ca(2+)](i). Sixty hearts were perfused with modified Krebs-Ringer's solution containing lipid vehicle and propofol (1 and 10 microM) in the absence and presence of ryanodine, thapsigargin, and nifedipine, while developed LVP and available [Ca(2+)](i) were recorded. Propofol (10 microM) decreased available [Ca(2+)](i) by 11.0% +/- 1.3% without decreasing developed LVP (% of control, P < 0.05). Propofol (10 microM) caused a leftward shift in the curve of developed LVP as a function of available [Ca(2+)](i). Propofol (10 microM) with nifedipine (1 microM), but not with ryanodine (1 microM) or thapsigargin (1 microM), decreased available [Ca(2+)](i) by 15.5% +/- 1.7% (P < 0.05). Propofol decreases available [Ca(2+)](i) without decreasing cardiac contraction, and it enhances myofilament Ca(2+) sensitivity in intact beating hearts at clinical concentrations. The inhibition of available [Ca(2+)](i) by propofol may be mainly mediated by an impairment of sarcoplasmic reticulum Ca(2+) handling rather than the sarcolemmal L-type Ca(2+) current. ⋯ This is the first study of the effects of propofol on intracellular Ca(2+) concentration and myofilament Ca(2+) sensitivity under physiologic conditions in intact isolated beating guinea pig hearts.