Anesthesia and analgesia
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Anesthesia and analgesia · Nov 2001
A simple apparatus for accelerating recovery from inhaled volatile anesthetics.
Hyperpnea increases anesthetic elimination but is difficult to implement with current anesthetic circuits without decreasing arterial PCO2. To circumvent this, we modified a standard resuscitation bag to maintain isocapnia during hyperpnea without rebreathing by passively matching inspired PCO2 to minute ventilation. We evaluated the feasibility of using this apparatus to accelerate recovery from anesthesia in a pilot study in four isoflurane-anesthetized dogs. The apparatus was easy to use, and all dogs tolerated being ventilated with it. Under our experimental conditions, isocapnic hyperpnea reduced the time to extubation by 62%, from an average of 17.5 to 6.6 min (P = 0.012), but not time from extubation to standing unaided. This apparatus may provide a practical means of applying isocapnic hyperpnea to shorten recovery time from volatile anesthetics. ⋯ A simple modification to a standard resuscitation bag allows one to increase ventilation without decreasing blood carbon dioxide levels. In dogs, we confirmed that this circuit can be used to accelerate the elimination of and recovery from volatile anesthetics.
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Anesthesia and analgesia · Nov 2001
Resuscitation with Hextend decreases endogenous circulating heparin activity and accelerates clot initiation after hemorrhage in the rabbit.
Hemorrhagic shock can result in a hypercoagulable state and has been associated with both hemorrhagic and thrombotic complications in the perioperative period. The author hypothesized that hemorrhage and resuscitation could result in a hypercoagulable state via changes in the heparin-antithrombin III anticoagulant mechanism in rabbits. Rabbits sedated with ketamine underwent sham operation (n = 8) or hemorrhage (25 mL/kg blood shed) for 60 min, followed by resuscitation with an equal volume of 5% human albumin (n = 8) or Hextend (n = 8). Coagulation analysis with the Thrombelastograph analyzer and determination of endogenous heparin and antithrombin III activity were performed on arterial blood samples obtained before hemorrhage and 30 min after resuscitation. The reaction time significantly decreased by 34% after hemorrhage and resuscitation with Hextend, whereas no other significant changes in Thrombelastograph variables were noted. Antithrombin III activity was significantly less in the Albumin (83% +/- 8% of control, mean +/- SD) and Hextend (88% +/- 8%) Resuscitated groups compared with the Sham-Operated animals. Of interest, only the Hextend-Resuscitated animals demonstrated a significant decrease in heparin activity (53.4 +/- 13.6 mU/mL before hemorrhage, 42.3 +/- 5.6 mU/mL after resuscitation). A Hextend)-mediated decrease of both heparin and antithrombin III activity may explain the acceleration of clot initiation compared with albumin administration after hemorrhage in the rabbit. ⋯ Hemorrhage may result in a hypercoagulable state after resuscitation. Decreases in both endogenous heparin and antithrombin III activity after hemorrhage and Hextend resuscitation in rabbits resulted in a significantly decreased time to clot coagulation analysis initiation without a significant change in the rate of clot formation or final clot strength.
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Anesthesia and analgesia · Nov 2001
Oxygen and glucose deprivation-induced neuronal apoptosis is attenuated by halothane and isoflurane.
Both in vitro and in vivo evidence supports the reduction of early ischemic, both global and focal, brain injury by volatile anesthetics. However, the protection afforded by volatile anesthetics in later neuronal death, i.e., apoptosis, caused by global ischemia has not been investigated. We induced oxygen and glucose deprivation in neuronal cortical cell cultures prepared from newborn rats on in vitro Days 10-14. This hypoxic (PO2 <50 mm Hg) condition was maintained continuously (30, 60, and 90 min). In a separate experiment, the neuronal cell cultures were exposed to isoflurane (1.13%, 2.3%, or 3.3%) or halothane (1.7%, 3.4%, or 5.1%) before oxygen and glucose deprivation, with continued exposure to isoflurane or halothane during oxygen and glucose deprivation. After 48 h, neuronal apoptosis was assessed with terminal deoxynucleotidyl transferase-mediated in situ nick-end labeling and DNA gel electrophoresis. Oxygen and glucose deprivation (30, 60, and 90 min) caused significant apoptosis of cerebral cortical cultured neurons. However, pretreatment and continued treatment during the period of oxygen and glucose deprivation with halothane or isoflurane resulted in a concentration-dependent attenuation of oxygen and glucose deprivation-induced neuronal apoptosis. ⋯ This is the first investigation to evaluate the effect of volatile anesthetics on oxygen and glucose deprivation-induced neuronal apoptosis. Oxygen and glucose deprivation-induced neuronal apoptosis can be decreased by prior and continued administration of halothane or isoflurane.