We mapped molecular gas toward the supernova remnant W44 in the HCO + J = 1-0 line with the Nobeyama Radio Observatory 45 m telescope and in the CO J = 3-2 line with the Atacama Submillimeter Telescope Experiment 10 m telescope. High-velocity emission wings were detected in both lines over the area where the radio shell of W44 overlaps the molecular cloud in the plane of the sky. We found that the average velocity distributions of the wing emission can be fitted by a uniform expansion model. The best-fit expansion velocities are 12.2±0.3 km s −1 and 13.2±0.2 km s −1 in HCO + and CO, respectively. The non-wing CO J = 3-2 component is also fitted by the same model with an expansion velocity of 4.7 ± 0.1 km s −1 . This component might be dominated by a post shock higher-density region where the shock velocity had slowed down. The kinetic energy of shocked molecular gas is estimated to be (3.5±1.3) × 10 49 erg. Adding this and the energy of the previously identified HI shell, we concluded that (1.2±0.2) × 10 50 erg has been converted into gas kinetic energy from the initial baryonic energy of the W44 supernova. We also found ultra-high-velocity CO J = 3-2 wing emission with a velocity width of ∼ 100 km s −1 at (l, b) = (+34. • 73, −0. • 47). The origin of this extremely high-velocity wing is a mystery.

To help clarify the mechanisms by which volatile anaesthetics act on neuronal Ca2+ channel currents (IBa), the effects of isoflurane were studied on IBa in rat dorsal root ganglion (DRG) cells. Voltage-dependent IBa were pharmacologically subdivided into L-, N- and P/Q-types, and toxin-resistant IBa. At clinically relevant concentrations, isoflurane inhibited the L-, N- and P/Q-types, but not toxin-resistant IBa. The IC50 values for the L-, N- and P/Q-types were 0.7%, 1.3% and 3.0%, respectively (concentrations equivalent to 0.35, 0.68 and 1.46 mmol litre-1 in the aqueous phase). Isoflurane also produced initial transient augmentation of the N-type IBa. Isoflurane shifted the mid-point of the steady-state inactivation curve for the L-, N- and P/Q-type IBa towards negative potentials, and prolonged the time constant of current reactivation. We conclude that isoflurane inhibited L-, N- and P/Q-type IBa in rat DRG neurones by enhancing current inactivation and prolonging recovery time after inactivation. Transient augmentation of the N-type IBa may also form part of the overall actions of isoflurane in DRG neurones.

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Arterial blood pressure (ABP) and heart rate were recorded at one-minute intervals during several stages of intubation in the fiberscope group and the laryngoscope group, to determine if fiberoptic nasotracheal intubation would result in fewer hemodynamic and catecholamine responses than when intubation was performed with a Macintosh laryngoscope. Blood samples were also taken to measure plasma catecholamine concentration immediately after intubation with the fiberscope. The mean ABP in the laryngoscope group was slightly greater than that of the fiberscope group for 4 min after intubation. Heart rates at 2 min and 4 min after intubation in the laryngoscope group were significantly greater than those for the fiberscope group. Even immediately after intubation, the mean plasma levels of epinephrine and norepinephrine were unchanged in the fiberscope group. Arterial oxygen saturation (Sp(O)(2)) was maintained within normal range during both of intubation procedures, although the time required for intubation was longer than in the laryngoscope group. Other cardiovascular complications were more common in the laryngoscope group than in the fiberscope group. These results suggest that fiberoptic intubation results in less severe stress than does laryngoscopic intubation. Fiberoptic intubation should therefore be used not only in patients with difficult airway, hypertension, ischemic heart disease, or cerebrovascular atherosclerosis, but also it is recommended for all patients for whom nasotracheal intubation is indicated.

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