Anesthesiology
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Depression of myocardial contractility associated with the volatile anesthetics is well established clinically and experimentally. The molecular mechanisms underlying this effect, however, have not been completely characterized. Whereas the Ca2+ release channel of cardiac sarcoplasmic reticulum (SR) has been implicated as a potential target contributing to anesthetic-induced myocardial depression, the effect of the volatile anesthetics on this protein have not been characterized at the isolated, single-channel level. The authors sought to identify changes in channel gating and conductance resulting from exposure to halothane, enflurane, and isoflurane that would contribute to the associated negative inotropy, as well as to explain the observation that isoflurane causes less contractile depression than either halothane or enflurane. ⋯ Halothane and enflurane gate the Ca2+ release channel into the open state without altering the channel conductance. An increase in the duration of open events results from halothane and enflurane, but does not occur in the presence of isoflurane. Activation of the SR Ca2+ release channel would lead to loss of SR stores of Ca2+ into the cytoplasm, which is rapidly mobilized to the extracellular space. A net depletion of Ca2+ available for excitation-contraction coupling would result. The observation that isoflurane does not alter gating of this channel contributes to the understanding of the molecular mechanisms by which isoflurane depresses myocardial contractility less than halothane and enflurane.
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The alpha 2-adrenergic agonist, dexmedetomidine, alters hemodynamics by diminishing sympathetic and/or augmenting parasympathetic neurogenic tone to the heart and peripheral vasculature. However, the specific actions of dexmedetomidine on baroreceptor function are unknown. The purpose of the current investigation was to determine baroreceptor function during an anesthetic state produced by halothane and a similar anesthetic state produced by halothane after dexmedetomidine pretreatment. ⋯ The results indicate that dexmedetomidine alone does not alter baroreflex sensitivity. In addition, possibly through an anesthetic-sparing action, dexmedetomidine preserves baroreflex responses during halothane anesthesia. Such a preservation of the baroreceptor reflex by dexmedetomidine might provide an important mechanism for maintenance of cardiovascular stability by retaining buffer reflexes during general anesthesia.
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A decrease in myocardial perfusion pressure may reduce myocardial blood flow. However, it may not significantly affect myocardial perfusion when in presence of a concurrent coronary artery vasodilation. However, the effects of propofol in coronary arteries are not well determined. In this study, the effects of propofol on porcine coronary artery responses to vasoactive agents that operate through voltage- and receptor-mediated calcium mechanisms were investigated. ⋯ Propofol possesses vasodilator effect and attenuates the effects of vasoconstrictor agents in porcine coronary artery. Further, an antagonism of calcium channels may be responsible for these effects of propofol.
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Left ventricular diastolic function is known to be impaired in patients with coronary artery disease and patients with valvular aortic stenosis. Phenylephrine is frequently administered as an intravenous bolus in these patients perioperatively to increase coronary perfusion pressure. Although this is common practice, there is no information about the effect of phenylephrine bolus administration on left ventricular filling dynamics. ⋯ Phenylephrine bolus administration causes an alteration of left ventricular filling in coronary artery disease patients that seems to be more marked than that seen in normal subjects. In patients with aortic stenosis no deleterious effects were observed in response to phenylephrine.