The sedative effects of epidural anesthesia without volatile and IV anesthetics and quantification of the degree of epidural anesthesia-induced sedation have not been investigated. In the current study we evaluated the effects of epidural anesthesia on the bispectral index (BIS) during the awake phase and during general anesthesia. After placing the epidural catheter, the patients were randomly allocated to 2 groups receiving either 5 mL of epidural saline (group S) or the same volume of 0.75% ropivacaine (group R). The BIS measurements during the awake phase were performed at 7, 12, 13, 14, 22, and 23 min after the epidural injection. General anesthesia was then induced with propofol and vecuronium and maintained with 0.75% sevoflurane. From approximately 10 min after tracheal intubation, the BIS measurements were made at 1-min intervals for 10 min. The BIS during the awake phase was significantly lower in group R than in group S (P < 0.05). The BIS during general anesthesia was significantly lower in group R than in group S (P < 0.0001). Epidural anesthesia decreased the BIS during the awake phase and during general anesthesia. The decrease of the BIS associated with epidural anesthesia was more prominent during general anesthesia than during the awake phase.

We conclude that forced-air warming can effectively prevent midazolam-induced redistribution hypothermia.

Propofol is widely used for neurosurgical anesthesia; however, its effects on the pial microvasculature are unknown. We therefore evaluated the direct effects of propofol on pial microvessels in rabbits. Pial microcirculation was visualized using a closed cranial window technique in 20 Japanese white rabbits. In the first experiment (n=14), after baseline hemodynamic measurements, the cranial window was superfused with 5 increasing concentrations of propofol (10, 10, 10, 10, 10 mol/L; n=8) or intralipid (at comparable concentrations; n=6) dissolved in artificial cerebrospinal fluid for 7 minutes each. A typical anesthetic concentration of 5 microg/mL corresponds to 10 mol/L. In the second experiment (n=6), phenylephrine 10 mol/L and nitroglycerin 10 mol/L were applied topically for 7 minutes under pentobarbital anesthesia. In the third experiment (n=3), electroencephalogram and bispectral index were measured under pentobarbital anesthesia. Diameters of selected pial arterioles and venules were visualized with a microscope-video capture unit combination and subsequently measured with a digital video analyzer. Topical application of propofol at 10, 10, 10, or 10 mol/L did not alter the diameters of the pial microvessels; however, at 10 mol/L propofol induced dilation in large and small arterioles, along with venular dilation. Intralipid alone did not have any significant effect on vessel diameters. Phenylephrine and nitroglycerin produced pial arteriolar and venular constriction and dilation, respectively. Phenylephrine constricted and nitroglycerin dilated pial arterioles and venules. Pentobarbital did not produce either burst suppression or an isoelectric electroencephalogram. The results confirm our hypothesis: clinically relevant concentrations of propofol, that is, approximately 10 mol/L, do not dilate pial arterioles or venules.

A low dose of JM-1232(-) reduced the shivering threshold in rabbits approximately 0.8 degrees C which is similar to the effects in humans given premedication doses of midazolam. In contrast, a 10-fold larger dose reduced the threshold more than 2.5 degrees C. This is a substantial decrement and might facilitate induction of therapeutic hypothermia.

Urinary bladder temperature appears to be more accurate at high urinary flow rates than at low urinary flow rates for clinical use.