Anesthesia and analgesia
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Anesthesia and analgesia · Jan 1998
Does the duration of cardiopulmonary bypass or aortic cross-clamp, in the absence of blood and/or blood product administration, influence the IL-6 response to cardiac surgery?
Cardiopulmonary bypass (CPB) induces a systemic inflammatory response characterized by release of proinflammatory cytokines, including interleukin 6 (IL-6). Recent reports suggest that plasma IL-6 is increased after CPB. Previous studies evaluating the influence of duration of CPB and/or aortic cross-clamp time on the release of IL-6 are conflicting. Infusion of blood and blood products during these studies may have influenced plasma concentrations of proinflammatory cytokines by inducing host cell (monocyte) activation and IL-6 release. The purpose of our investigation was to determine, in an environment free from blood and/or blood product administration, the influence of duration of CPB and/or aortic cross-clamp on the magnitude of the IL-6 response in patients undergoing cardiac surgery. We prospectively evaluated plasma IL-6 levels preinduction (T0) and at sternal closure in 16 patients undergoing CPB (coronary artery bypass grafting, n = 9; valvular cardiac surgery, n = 7) to determine whether there is a correlation between the absolute increase in IL-6 and the duration of CPB or aortic cross-clamp time. None of the patients received blood and/or blood products during the study to control for the introduction of additional activated cells and soluble mediators, including IL-6. The results demonstrate that the magnitude of the IL-6 response to CPB is positively correlated with the duration of CPB but not with duration of aortic cross-clamp. It seems that induction of IL-6 release is part of a normal response to CPB and does not depend on activation of host cells during prolonged aortic cross-clamp. The activation or presence of inflammatory cytokines associated with administration of blood and/or blood products could have influenced previously published investigations relating the influence of duration of CPB and/or aortic cross-clamp time to the magnitude of the IL-6 response. ⋯ This study found a positive correlation between the magnitude of the interleukin 6 response to cardiopulmonary bypass and duration of cardiopulmonary bypass (but not duration of aortic cross-clamp) when measurements were made in the absence of blood/blood product transfusion. Future studies evaluating strategies to reduce cytokine responses to cardiopulmonary bypass should therefore control for cardiopulmonary bypass duration.
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Anesthesia and analgesia · Jan 1998
The cerebral and cardiovascular effects of cisatracurium and atracurium in neurosurgical patients.
Drugs for neurosurgical patients should not increase intracranial pressure (ICP) or change cerebral perfusion pressure (CPP) and cerebral blood flow. This double-blind, cross-over study compares the effects of a single (3 x effective dose producing 95% twitch depression) intravenous bolus dose of cisatracurium 0.15 mg/kg with atracurium 0.75 mg/kg on mean red blood cell flow velocity in the middle cerebral artery (CBFV; transcranial Doppler), ICP (intraventricular or intraparenchymal monitor), mean arterial pressure (MAP), CPP (MAP-ICP), and heart rate (HR) every minute during a 15-min study period. Included in the study were 14 sedated and ventilated adult neurosurgical patients. After the cisatracurium bolus, ICP, CPP, CBFV, MAP, and HR did not change, and no histamine related events were observed. After the atracurium bolus, ICP, CPP, CBFV, and MAP decreased. The lowest values of ICP (-16% of baseline), CPP (-5%), CBFV (-8%), and MAP (-7%) were recorded 2-4 min after the atracurium bolus injection. After this transient decrease, MAP and CPP returned to baseline, whereas CBFV and ICP transiently exceeded baseline values. The highest values of CBFV (5%) and ICP (17%) were recorded 9-12 min after the atracurium bolus injection. Five patients showed a typical histamine response after atracurium, with a decrease in MAP and flushing. Excluding these five patients eliminated statistical significance in ICP, CPP, CBFV, and MAP differences. In conclusion, cisatracurium demonstrated fewer cerebral and cardiovascular hemodynamic side effects in sedated adult neurosurgical patients. ⋯ This double-blind study in sedated and mechanically ventilated adult neurosurgical patients demonstrates that an intravenous bolus dose of the neuromuscular blocker cisatracurium results in less cerebral (intracranial pressure, cerebral perfusion pressure, middle cerebral artery blood flow velocity) and cardiovascular (blood pressure) hemodynamic side effects, compared with an equipotent dose of atracurium.
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Anesthesia and analgesia · Jan 1998
The visual analog scale in the immediate postoperative period: intrasubject variability and correlation with a numeric scale.
The visual analog scale (VAS) has been used to assess the efficacy of pain management regimens in patients with acute postoperative pain, but its usefulness has not been confirmed in postoperative pain studies. We studied 60 subjects in the immediate postoperative period. The specific data collected were: VAS scores versus an 11-point numeric pain scale; repeatability in VAS scores over a short time interval; and change in VAS scores from one assessment period to the next versus a verbal report of change in pain. The correlation coefficients for VAS scores with the 11-point pain scale were 0.94, 0.91, and 0.95. The repeatability coefficients were 17.6, 23.0, and 13.5 mm. Of the 56 patients who completed all three assessments, only 16 (29%) had repeatability within 5 mm on all three. Some of the changes in VAS scores between assessments were in the direction opposite the verbally reported changes in pain (31%); however, most (92%) were within 20 mm. There was no correlation between the level of sedation, previous pain experience, anxiety, or anticipated pain with consistency in VAS scores. We conclude that any single VAS score in the immediate postoperative period should be considered to have an imprecision of +/- 20 mm. ⋯ The visual analog scale was developed for assessing chronic pain but is often used in studies of postoperative pain. This study finds that the visual analog scale correlates well with a verbal 11-point scale but that any individual determination has an imprecision of +/- 20 mm.
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Anesthesia and analgesia · Jan 1998
Gabapentin reverses the allodynia produced by the administration of anti-GD2 ganglioside, an immunotherapeutic drug.
Systemically administered, the anti-GD2 antibody produces allodynia demonstrated by decreased mechanical withdrawal threshold. Electrophysiologic recordings indicate a probable neuropathic origin, as small-diameter sensory fibers develop continuous high-frequency discharge after antibody administration. Gabapentin (GBP) is a gamma-aminobutyric acid analog originally synthesized for its anticonvulsant actions. Several open-label clinical studies, as well as a wealth of anecdotal evidence, suggest that GBP may be beneficial for the treatment of neuropathic pain. This study examined the effects of GBP given as a posttreatment after induction of an anti-GD2-associated allodynia. Anti-GD2 (1 mg/kg intravenously [i.v.]) administered to Sprague-Dawley rats reduced the mean withdrawal threshold from 14.71 to 4.95 g (P < 0.001), as measured by using von Frey hairs. This was reversed by GBP in a dose-dependent fashion; the minimal effective dose was between 3 and 30 mg/kg i.v. The maximal percent analgesic effect of GBP was 76% and 93% at doses of 30 and 100 mg/kg, respectively (P < 0.001). With these doses, side effects were minimal and were manifested as slightly decreased spontaneous movement and startle response. No changes were seen in reflex responses to corneal or pinna stimulation, and no motor deficits were observed. These data support the use of GBP as an effective therapy for neuropathic pain. ⋯ After the administration of anti-GD2 antibody, rats display an escape reaction to light touch, increased blood pressure, and aberrant firing in nerve fibers associated with pain transmission. Systemic gabapentin reduced or eliminated the escape response and reversed the hypertension with minimal side effects. This suggests that gabapentin blocked the antibody-associated (neuropathic) pain.
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Anesthesia and analgesia · Jan 1998
Prolonged inhaled NO attenuates hypoxic, but not monocrotaline-induced, pulmonary vascular remodeling in rats.
In concentrations of 10-20 ppm, inhaled nitric oxide (NO) decreases pulmonary artery pressure and attenuates vascular remodeling in pulmonary hypertensive rats. Because NO is potentially toxic, it is important to know whether lower concentrations attenuate vascular remodeling produced by different etiologies. Therefore, we determined the effects of prolonged, small-dose inhaled NO administration on hypoxic and monocrotaline (MCT)-induced pulmonary vascular remodeling. Rats were subjected to normoxia, hypoxia (normobaric 10% oxygen), or hypoxia plus NO in concentrations of 50 ppb, 200 ppb, 2 ppm, 20 ppm, and 100 ppm for 3 wk. A second group of normoxic rats was given MCT (60 mg/kg intraperitoneally) alone or in the presence of 2, 20, and 100 ppm of NO. Subsequently, pulmonary artery smooth muscle thickness and the number of muscular arteries (percentage of total arteries) were determined. Right ventricular hypertrophy was determined by right to left ventricle plus septum weight ratio (RV/LV + S). Pulmonary artery smooth muscle thickness and the percent muscular arteries were increased by hypoxia and MCT. The hypoxic increase in thickness was attenuated by all concentrations of NO, with 100 ppm being greatest, whereas NO had no effect on MCT rats. NO attenuated the increase in percent muscular arteries in hypoxic but not MCT rats. The RV/LV + S was increased by hypoxia and MCT compared with normoxia. Hypoxia-induced RV hypertrophy was decreased by all concentrations of inhaled NO, although attenuation with 50 ppb was less than with 200 ppb, 20 ppm, and 100 ppm. In MCT rats 2 and 100 ppm NO increased RV hypertrophy, whereas 20 ppm had no effect. In conclusion, inhaled NO in concentrations as low as 50 ppb attenuates the pulmonary vascular remodeling and RV hypertrophy secondary to hypoxia. In contrast, concentrations as high as 100 ppm do not attenuate MCT-induced pulmonary remodeling. These results demonstrate that extremely low concentrations of NO may attenuate remodeling but that the effectiveness is dependent on the mechanism inducing pulmonary remodeling. ⋯ The authors determined whether inhaled NO, a selective pulmonary vasodilator, attenuates pulmonary vascular remodeling caused by two models of pulmonary hypertension: chronic hypoxia and monocrotaline injection. Analysis of pulmonary vascular morphology suggests that very low concentrations of NO effectively attenuate hypoxic remodeling but that NO is not effective in monocrotaline-induced pulmonary remodeling.