Subject(s)
Airway Management/instrumentation , Airway Management/methods , Intubation, Intratracheal/instrumentation , Intubation, Intratracheal/methods , Laryngoscopes , Adult , Body Mass Index , Female , Hoarseness/etiology , Humans , Male , Pharyngitis/etiology , Postoperative Complications/epidemiology , Treatment FailureABSTRACT
AIM: Ischemic brain damage related to the beach chair position is a matter of concern. The current study was designed to evaluate whether the beach chair position before and during general anesthesia differentially induces changes in cerebral oxygenation as determined by near-infrared spectroscopy (NIRS) in surgical patients. METHODS: We evaluated brain tissue oxygen index (TOI) values using the NIRS monitor NIRO-200TM in the beach chair position the day before and during general anesthesia. Thirty patients with normal preoperative TOI values undergoing shoulder surgery were enrolled. The initial TOI measurement in the supine position after 10 min rest or 10 min after tracheal intubation was followed by measurements after 5 min each in the 30-degree and subsequently 60-degree head-up tilt positions. During general anesthesia, patients were mechanically ventilated to obtain normocapnia under inhalation of 1.5% sevoflurane in 50% oxygen. Mean blood pressure (MAP) was measured non-invasively in the arm at heart level and was maintained above 60 mmHg with phenylephrine. RESULTS: Preoperative TOI values and preoperative MAP were within the normal range in the study population. MAP decreased upon anesthesia but did not further change when the patient was placed in the 30- and 60-degree head-up tilt positions. Heart rate also decreased upon anesthesia. However, TOI values did not change with induction of general anesthesia or placement of the patients in the beach chair position. CONCLUSION: Under general anesthesia, the beach chair position does not alter cerebral oxygenation in patients showing normal preoperative cerebral TOI values.
Subject(s)
Anesthesia, General , Brain/metabolism , Oxygen/metabolism , Patient Positioning , Female , Humans , Male , Middle AgedABSTRACT
BACKGROUND: Ropivacaine is a long-acting local anesthetic with low cardiac toxicity that induces vasoconstriction in vitro and in vivo. Vascular smooth muscle tone is regulated by changes in both intracellular Ca(2+) concentration ([Ca(2+)](i)) and myofilament Ca(2+) sensitivity. Therefore, the aim of this study was to examine the mechanism underlying the increase in [Ca(2+)](i) in ropivacaine-induced vascular contraction. METHODS: Ropivacaine-induced contractile responses and changes in [Ca(2+)](i) were examined using an isometric force transducer and a fluorometer, respectively. RESULTS: Ropivacaine induced a biphasic, concentration-dependent change in [Ca(2+)](i) and contractile response in rat aortic smooth muscles: an increase in [Ca(2+)](i) occurred at lower ropivacaine concentrations (3 x 10(-5) to 3 x 10(-4) M) and a decrease was observed at higher concentrations (10(-3) to 3 x 10(-3) M). Contraction and the [Ca(2+)](i) increase induced by ropivacaine were attenuated significantly by a voltage-dependent Ca(2+) channel antagonist, an inositol 1,4,5-triphosphate receptor antagonist and Ca(2+)-free solution (P < 0.01, n = 6). CONCLUSION: Ropivacaine-induced contraction of rat aortic smooth muscle is, in part, regulated by Ca(2+) influx from the extracellular space and Ca(2+) release from the sarcoplasmic reticulum.
