Anesthesia and analgesia
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Anesthesia and analgesia · Oct 1999
Review Comparative StudyExperience with remifentanil in neurosurgical patients.
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Anesthesia and analgesia · Oct 1999
The continuous assessment of cerebrovascular reactivity: a validation of the method in healthy volunteers.
Using transcranial Doppler ultrasonography, we investigated the moving correlation between slow waves in arterial blood pressure (ABP) and blood flow velocity (FV) at different levels of cerebrovascular vasodilation provoked by changing PETCO2. Fourteen healthy volunteers were examined. The FV in middle cerebral arteries, PETCO2, and ABP were recorded during normocapnia, hypercapnia, and hypocapnia. The moving correlation coefficients between ABP and mean FV (FVm) or systolic FV (FVs) during spontaneous fluctuations in ABP were calculated for 3-min epochs and averaged for each investigation, thus yielding the mean index (Mx) and systolic index (Sx). As a reference method, Aaslid's cuff tests were performed to obtain the rate of regulation (RoR). RoR, Mx, and Sx significantly depended on PETCO2 (analysis of variance, P < 0.00001). At high PETCO2, cerebrovascular reactivity was disturbed as reflected in RoR values of < 0.17/s for all volunteers and increased values of Mx (> 0.4 in 86% of volunteers) and Sx (> 0.2 in 79% of volunteers). Overall, there was a reasonably good correlation of both Mx and Sx with RoR (R2 = 0.65 and 0.58, respectively). ⋯ Indices derived from the correlation between spontaneous fluctuations of blood flow velocity wave form and arterial blood pressure may be used for the noninvasive continuous monitoring of cerebrovascular reactivity.
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Anesthesia and analgesia · Oct 1999
Comparative StudyThe effect of a sciatic nerve block on the development of inflammation in carrageenan injected rats.
Neurogenic inflammation may participate in postoperative inflammatory pain. We evaluated, in the rat, the influence of a short and prolonged sciatic nerve block on carrageenan-induced inflammation, the time course of which may be compared to postoperative inflammation. A catheter was placed on the right sciatic nerve and injected with 0.5% bupivacaine with epinephrine (0.2 mL): one injection in the Short Block Group, and four injections performed at 90-min intervals in the Prolonged Block Group. In all groups, the two hind paws were then injected with carrageenan. The development of inflammation was evaluated in both hind paws by measurement of paw circumference (PC) before, and 1, 2, 3, 4, 6, and 24 h after carrageenan injection. Temperature of both hind paws was evaluated at the same time points. The vocalization threshold to paw pressure test (VTPP) of both hind paws was evaluated at 6, 8, 10, 12, and 24 h after carrageenan injection. The left hind paw was used for the Control Group. A Sham Group had a catheter placed on the sciatic nerve and injected with normal saline. Inflammation developed in the Control Group with a maximum increase of PC (32%) and temperature (14%) 4 h after carrageenan injection and a maximal reduction of VTPP (44%) at 6 h, reflecting mechanical allodynia. A similar evolution was observed in the Sham Group. In the Short Block Group, the nerve block did not influence the PC, the paw temperature, or the VTPP when compared with the Control Group. In the Prolonged Block Group, when compared with the Control Group, the increased PC was reduced throughout the 24 h (P < 0.0001). The maximal increase in PC at 4 h was limited to 23%, as compared with the precarrageenan value. This effect on PC did not persist at 24 h. Paw temperature was increased (P = 0.07) throughout the study in the Prolonged Block Group, as compared with the Control Group. The VTPP reduction was still limited in the Prolonged Block Group at 24 h, as compared with the Control Group (P < 0.0001). We conclude that a prolonged sciatic nerve block limits carrageenan-induced increase in PC and, subsequently, mechanical allodynia at 24 h in rats. ⋯ Our study has shown that a prolonged (6 h) but not a short sciatic nerve block (90 min) can limit edema and related pain after carrageenan-induced inflammation in rat.
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Anesthesia and analgesia · Oct 1999
Comparative StudyMouse strain modestly influences minimum alveolar anesthetic concentration and convulsivity of inhaled compounds.
In this study, we measured the minimum alveolar anesthetic concentration (MAC) in several mouse strains, including strains used in the construction of genetically engineered mice. This is important because defined genetic modifications are used increasingly to test mechanisms of inhaled anesthetic action, and background variability in MAC can potentially influence the interpretation of these studies. We investigated the effect of strain on MAC for desflurane, isoflurane, halothane, ethanol, the experimental anesthetic 1-chloro-1,2,2-trifluorocyclobutane, and convulsive 50% effective dose (the dose required to produce convulsions in 50% of animals) of the nonimmobilizer 1,2-dichlorohexafluorocyclobutane. These drugs were studied in eight inbred strains, including both laboratory and wild mouse strains (129/J, 129/SvJ, 129/Ola Hsd, C57BL/6NHsd, C57BL/6J, DBA/2J, Spret/Ei, and Cast/Ei), one hybrid strain (B6129F2/J, derived from the C57BL/6J and 129/J strains), and one outbred strain (CD-1). To test our ability to detect effects in a genetically modified mouse, we compared these data with those for a mouse lacking the gamma (neuronal) isoform of the protein kinase C gene (PKCgamma). We also assessed whether amputating the tail tip of mice (a standard method of obtaining tissue for genetic analysis) increased MAC (e.g., by sensitization of the spinal cord). MAC and convulsant 50% effective dose values differed modestly among strains, with a range of 17% to 39% from the lowest to highest values for MAC using conventional anesthetics, and up to 48% using the experimental anesthetic 1-chloro-1,2,2-trifluorocyclobutane. Convulsivity to the nonimmobilizer varied by 47%. Amputating the tail tip did not affect MAC. PKCgamma knockout mice had significantly higher MAC values than control animals for isoflurane, but not for halothane or desflurane, which implies that protein phosphorylation by PKCgamma can alter sensitivity to isoflurane. ⋯ Anesthetic potency differs by modest amounts among inbred, outbred, wild, and laboratory mouse strains. Absence of the neural form of protein kinase C increases minimum alveolar anesthetic concentration for isoflurane, indicating that protein phosphorylation by the gamma-isoform of protein kinase C (PKCgamma) can influence the potency of this anesthetic.