[Effects of concentration and dosage of lidocaine on preventing the pain on injection of propofol].

Although it is well-known that 2% lidocaine has an effective action for preventing propofol-induced pain, it has been unclear whether or not lidocaine of the concentration below 2% has the effective action similar to 2% lidocaine. One-hundred and thirty-two patients were randomly assigned to one of the six groups according to concentration and dosage of lidocaine administered at the time of the initiation of propofol infusion. Groups I and II received 1 ml and 2 ml of 1% lidocaine, respectively; Groups III and IV were given 1 ml and 2 ml of 0.5% lidocaine, respectively; Group V received 2 ml of 2% lidocaine; Group VI was administered 1 ml of normal saline as a control. There were no significant differences in patients' profiles and alterations of hemodynamics during anesthetic induction among the six groups. Number of patients complaining of a pain during induction was more in Group VI with significance (P < 0.0001) and number of patients complaining of uncomfortableness was also more with significance (P < 0.0001). Incidence of propofol-induced pain and degree of satisfaction with anesthetic induction were similar among the groups receiving lidocaine. Even 0.5% lidocaine may have the same effective action as 2% lidocaine for preventing the pain on injection of propofol.

Volatile anesthetics regulate pulmonary vascular tension through different potassium channel subtypes in isolated rabbit lungs.

BACKGROUND: The effects of volatile anesthetics on subtypes of K(+) channels located on pulmonary vessels remain largely unexplored. METHODS: To investigate whether or not potassium channels play a role in the effect of volatile anesthetic on pulmonary vessels, isolated and perfused rabbit lungs were divided into four groups (n = 7 each): a control group without treatment, a glibenclamide (Glib) group treated with adenosine triphosphate-sensitive K(+) (K(ATP)) channel inhibitor, a 4-aminopyridine (4-AP) group treated with voltage-sensitive K(+) (K(V)) channel inhibitor, and an iberiotoxin (IbTX) group treated with high conductance calcium-activated K(+) (K(Ca)) channel inhibitor. After inhibitor administration and stabilization, two minimum alveolar concentration (MAC) of halothane, enflurane, isoflurane, or 1.8 MAC of sevoflurane were randomly administered for 15 min followed by eight minutes of fresh gas mixture after each agent inhalation. RESULTS: Isoflurane did not change pulmonary vascular tension in the control group but instead constricted the pulmonary vessels when K(V) channels were inhibited with 4-AP; constrictive effects of enflurane and halothane were observed on pulmonary vessels, and were enhanced by K(V) channel inhibition with 4-AP, but they were inhibited by K(Ca) channel inhibition with IbTX; the dilation effect of sevoflurane was observed on pulmonary vessels but was not significantly affected by any of the K(+) channel inhibitors. CONCLUSION: Halothane, enflurane and isoflurane, but not sevoflurane, regulate pulmonary vascular tension through K(V) and/or K(Ca) channels in isolated rabbit lungs.