ISSN:0003-3022    

出版商:OVID    

年代:1997

数据来源: OVID

ISSN:0003-3022    

出版商:OVID    

年代:1997

数据来源: OVID

摘要:

Background:The safety of low‐flow sevoflurane anesthesia, during which CF2= C(CF3)‐O‐CH2F (compound A) is formed by sevoflurane degradation, in humans has been questioned because compound A is nephrotoxic in rats. Several reports have evaluated renal function after closed‐circuit or low‐flow sevoflurane anesthesia, using blood urea nitrogen (BUN) and serum creatinine as markers. However, these are not the more sensitive tests for detecting renal damage. This study assessed the effects of low‐flow sevoflurane anesthesia on renal function using not only BUN and serum creatinine but also creatinine clearance and urinary excretion of kidney‐specific enzymes, and it compared these values with those obtained in high‐flow sevoflurane anesthesia and low‐flow isoflurane anesthesia.Methods:Forty‐eight patients with gastric cancer undergoing gastrectomy were studied. Patients were randomized to receive sevoflurane anesthesia with fresh gas flow of 1 l/min (low‐flow sevoflurane group; n = 16) or 6–10 l/min (high‐flow sevoflurane group; n = 16) or isoflurane anesthesia with a fresh gas flow of 1 l/min (low‐flow isoflurane group; n = 16). In all groups, the carrier gas was oxygen/nitrous oxide in the ratio adjusted to ensure a fractional concentration of oxygen in inspired gas (FiO2) of more than 0.3. Fresh Baralyme was used in the low‐flow sevoflurane and low‐flow isoflurane groups. Glass balls were used instead in the high‐flow sevoflurane group, with the fresh gas flow rate adjusted to eliminate rebreathing. The compound A concentration was measured by gas chromatography. Gas samples taken from the inspiratory limb of the circle system at 1‐h intervals were analyzed. Blood samples were obtained before and on days 1, 2, and 3 after anesthesia to measure BUN and serum creatinine. Twenty‐four‐hour urine samples were collected before anesthesia and for each 24‐h period from 0 to 72 h after anesthesia to measure creatinine, N‐acetyl‐beta‐D‐glucosaminidase, and alanine aminopeptidase.Results:The average inspired concentration of compound A was 20 +/‐ 7.8 ppm (mean +/‐ SD), and the average duration of exposure to this concentration was 6.11 +/‐ 1.77 h in the low‐flow sevoflurane group. Postanesthesia BUN and serum creatinine concentrations decreased, creatinine clearance increased, and urinary N‐acetyl‐beta‐D‐glucosaminidase and alanine aminopeptidase excretion increased in all groups compared with preanesthesia values, but there were no significant differences between the low‐flow sevoflurane, high‐flow sevoflurane, and low‐flow isoflurane groups for any renal function parameter at any time after anesthesia.Conclusions:The only difference between the low‐flow and high‐flow sevoflurane groups was compound A formation, and postanesthesia laboratory data showed no significant effects of compound A formation during sevoflurane anesthesia on renal function. No significant effects on renal function were observed in either the low‐flow or high‐flow sevoflurane groups compared with the low‐flow isoflurane group.

ISSN:0003-3022    

出版商:OVID    

年代:1997

数据来源: OVID

摘要:

Background:Carbon dioxide absorbents degrade sevoflurane, particularly at low gas flow rates, to fluoromethyl‐2,2‐difluoro‐1‐(trifluoromethyl)vinyl ether (compound A). Compound A causes renal proximal tubular injury in rats but has had no effect on blood urea nitrogen (BUN) or creatinine concentrations in patients. This investigation compared the effects of low‐flow sevoflurane and isoflurane on renal tubular function in surgical patients using conventional (BUN and creatinine) and finer indices of renal injury, specifically those biomarkers sensitive for compound A toxicity in rats (glucosuria, proteinuria, and enzymuria [N‐acetyl‐beta‐D‐glucosaminidase (NAG) and alpha‐glutathione‐S‐transferase (alpha GST)]).Methods:Consenting patients with normal preoperative renal function at two institutions were randomized to receive sevoflurane (n = 36) or isoflurane (n = 37) in oxygen and air. Total gas flow was 1 l/min, opioid doses were minimized, and barium hydroxide lime was used to maximize anesthetic degradation. Inspiratory and expiratory compound A concentrations were quantified every 30–60 min. Blood and urine were obtained before and 24–72 h after anesthesia for laboratory evaluation.Results:Sevoflurane and isoflurane groups were similar with respect to age, weight, sex, American Society of Anesthesiologists status, anesthetic duration (3.7 or 3.9 h), and anesthetic exposure (3.6 or 3 minimum alveolar concentration [MAC]‐hour). Maximum inspired compound A concentration (mean +/‐ standard deviation) was 27 +/‐ 13 ppm (range, 10–67 ppm). Areas under the inspired and expired compound A concentration versus time curves (AUC) were 79 +/‐ 54‐ppm‐h (range, 10–223 ppm‐h) and 53 +/‐ 40 ppm‐h (range, 6–159 ppm‐h), respectively. There was no significant difference between anesthetic groups in postoperative serum creatinine or BUN, or urinary excretion of protein, glucose, NAG, proximal tubular alpha GST, or distal tubular pi GST. There was no significant correlation between compound A exposure (AUC) and protein, glucose, NAG, alpha GST, or pi GST excretion. Postoperative alanine and aspartate aminotransferase concentrations were not different between the anesthetic groups, and there were no significant correlations between compound A exposure and alanine or aspartate aminotransferase concentrations.Conclusions:The renal tubular and hepatic effects of low‐flow sevoflurane and isoflurane were similar as assessed using both conventional measures of hepatic and renal function and more sensitive biochemical markers of renal tubular cell necrosis. Moderate duration low‐flow sevoflurane anesthesia, during which compound A formation occurs, appears to be as safe as low‐flow isoflurane anesthesia.

ISSN:0003-3022    

出版商:OVID    

年代:1997

数据来源: OVID

摘要:

Background:Enhancement of hypoxic pulmonary vasoconstriction (HPV) in nonventilated lung areas by almitrine increases the respiratory response to inhaled nitric oxide (NO) in patients with acute respiratory distress syndrome (ARDS). Therefore the authors hypothesized that inhibition of HPV in nonventilated lung areas decreases the respiratory effects of NO.Methods:Eleven patients with severe ARDS treated by venovenous extracorporeal lung assist were studied. Patients' lungs were ventilated at a fraction of inspired oxygen (FIO2) of 1.0. By varying extracorporeal blood flow, mixed venous oxygen tension (PO2; partial oxygen pressure in mixed venous blood [Pv with barO2]) was adjusted randomly to four levels (means, 47, 54, 64 and 84 mmHg). Extracorporeal gas flow was adjusted to prevent changes in mixed venous carbon dioxide tension [Pv with barCO2]). Hemodynamic and gas exchange variables were measured at each level before, during, and after 15 ppm NO.Results:Increasing Pv with barO2from 47 to 84 mmHg resulted in a progressive decrease in lung perfusion pressure (PAP‐PAWP; P < 0.05) and pulmonary vascular resistance index (PVRI; P < 0.05) and in an increase in intrapulmonary shunt (Q with dotS/Q with dotT; P < 0.05). Pv with barCO2and cardiac index did not change. Whereas the NO‐induced reduction in PAP‐PAWP was smaller at high Pv with barO2, NO‐induced decrease in Q with dotS/Q with dotTwas independent of baseline Pv with barO2. In response to NO, arterial PO2increased more and arterial oxygen saturation increased less at high compared with low Pv with barO2.Conclusion:In patients with ARDS, HPV in nonventilated lung areas modifies the hemodynamic and respiratory response to NO. The stronger the HPV in nonventilated lung areas the more pronounced is the NO‐induced decrease in PAP‐PAWP. In contrast, the NO‐induced decrease in Q with dot S /Q with dot T is independent of Pv with barO2over a wide range of Pv with barO2levels. The effect of NO on the arterial oxygen tension varies with the level of Pv with barO2by virtue of its location on the oxygen dissociation curve.

ISSN:0003-3022    

出版商:OVID    

年代:1997

数据来源: OVID

摘要:

Background:Preclinical studies have emphasized that persistent small afferent input will induce a state of central facilitation that can be regulated by systemically administered lidocaine. The authors extended these preclinical studies to human volunteers by examining the concentration‐dependent effects of intravenous lidocaine on acute sensory thresholds and facilitated processing induced by intradermal capsaicin.Methods:Fifteen healthy persons received a lidocaine or a placebo infusion. A computer‐controlled infusion pump targeted sequential stepwise increases in plasma lidocaine concentration steps of 1, 2, and 3 micro gram/ml. At each plasma concentration, neurosensory testing (thermal and von Frey hair test stimulation) were performed. After completing the tests at the 3 micro gram/ml plasma lidocaine level, intradermal capsaicin was injected into the volar aspect of the left forearm, and the flare response and hyperalgesia to von Frey hair stimulation, stroking, and heat was assessed.Results:The continuous infusion of lidocaine and placebo had no significant effect on any stimulus threshold. Although intravenous lidocaine resulted in a decrease in all secondary hyperalgesia responses, this was only significant for heat hyperalgesia. Intravenous lidocaine resulted in a significant decrease in the flare response induced by intradermal capsaicin.Conclusions:These studies suggest that the facilitated state induced by persistent small afferent input human pain models may predict the activity of agents that affect components of nociceptive processing that are different from those associated with the pain state evoked by “acute” thermal or mechanical stimuli. Such insight may be valuable in the efficient development of novel analgesics for both neuropathic and post‐tissue‐injury pain states.

ISSN:0003-3022    

出版商:OVID    

年代:1997

数据来源: OVID

摘要:

Background:Xenon, an inert gas with anesthetic properties (minimum alveolar concentration [MAC] = 71%), has an extremely low blood:gas partition coefficient (0.14). Therefore, we predicted that xenon would provide more rapid emergence from anesthesia than does N2O + isoflurane or N2O + sevoflurane of equivalent MAC.Methods:Thirty American Society of Anesthsiologists class I or II patients undergoing total abdominal hysterectomy were randomly assigned to receive 60% xenon, 60% N2O + 0.5% isoflurane, or 60% N2O + 0.7% sevoflurane (all concentrations are end‐tidal: n = 10 per group). After placement of an epidural catheter, anesthesia was induced with standardized doses of midazolam, thiopental, and fentanyl. Thirty minutes later, xenon, N2O + isoflurane, or N2O + sevoflurane was started as previously assigned. These regimens were supplemented with epidural anesthesia with mepivacaine so that the mean arterial pressure and heart rate were controlled within 20% of the preoperative values. At the end of operation lasting approximately 2 h, all inhalational anesthetics were discontinued, and the patients were allowed to awaken while breathing spontaneously on an 8 l/min inflow of oxygen. A blinded investigator recorded the time until the patient opened her eyes on command (T1), was judged ready for extubation (T2), could correctly state her name, her date of birth, and the name of the hospital (T3), and could count backward from 10 to 1 in less than 15 s (T4).Results:Emergence times from xenon anesthesia were: T1, 3.4 +/‐ 0.9 min; T2, 3.6 +/‐ 1 min; T3, 5.2 +/‐ 1.4 min; and T4, 6.0 +/‐ 1.6 min (mean +/‐ SD). These were one half to one third of those from N2O + sevoflurane (T1, 6.0 +/‐ 1.7 min; T4, 10.5 +/‐ 2.5 min) or N2O + isoflurane (T1, 7.0 +/‐ 1.9 min; T4, 14.3 +/‐ 2.8 min) anesthesia. The three groups did not differ in terms of patient demographics, the duration of anesthesia, the amount of epidural mepivacaine administered, or the postoperative pain rating. No patient could recalls intraoperative events.Conclusions:Emergence from xenon anesthesia is two or three times faster than that from equal‐MAC N2O + isoflurane or N2O + sevoflurane anesthesia.

ISSN:0003-3022    

出版商:OVID    

年代:1997

数据来源: OVID

摘要:

Background:Intradermal injection of capsaicin produces brief pain followed by hyperalgesia and allodynia in humans, and the latter effects are mediated by spinal N‐methyl‐D‐aspartate mechanisms. Amitriptyline recently was shown to antagonize N‐methyl‐D‐aspartate receptors, and in this study, the authors sought to determine the effect of amitriptyline alone and with the opioid alfentanil on hyperalgesia and allodynia produced by intradermal injection of capsaicin.Methods:Forty‐six healthy volunteers in the general clinical research center received repeated intradermal injections of capsaicin (100 micro gram) alone or before and after systemic injection of 4 mg midazolam, 25 mg amitriptyline, alfentanil by computer‐controlled infusion, or amitriptyline plus alfentanil. Acute pain and areas of mechanical hyperalgesia and allodynia were determined at specified intervals. Blood was obtained for alfentanil and amitriptyline assay.Results:Capsaicin injection produced acute pain followed by hyperalgesia and allodynia. Alfentanil reduced these pain responses in a plasma‐concentration‐dependent manner, and reduction in hyperalgesia and allodynia correlated with reduction in acute pain. Amitriptyline alone had no effect and did not potentiate alfentanil. Alfentanil produced concentration‐dependent nausea, an effect diminished by amitriptyline.Discussion:These data correspond with previous studies in volunteers demonstrating reduction in hyperalgesia and allodynia after intradermal injection of capsaicin by systemically administered opioids, and they suggest that this reduction may be secondary to reduced nociceptive input by acute analgesia. These data do not support the use of acute systemic administration of amitriptyline for acute pain, hyperalgesia, and allodynia, although the roles of chronic treatment and spinal administration are being investigated.

ISSN:0003-3022    

出版商:OVID    

年代:1997

数据来源: OVID

摘要:

Background:Effect of local anesthetic concentration and volume on the spread and density of epidural anesthesia is unclear. This study was performed to delineate effects of a threefold difference in concentration and volume of 2‐chloroprocaine on epidural anesthesia.Methods:Twelve healthy volunteers underwent lumbar epidural anesthesia with 300 mg of 2‐chloroprocaine as a 3% (10 ml) and a 1% (30 ml) solution in a randomized, double‐blind, balanced, crossover fashion. Sensory block was assessed with pinprick, touch (calibrated plastic filament), cold, and electrical stimulation. Motor block was assessed at the quadriceps and gastrocnemius muscles with isometric force dynamometry. Differences between solutions were assessed with repeated measures analysis of variance followed by post hoc testing.Results:The number of dermatomes blocked to pinprick, touch, and cold was significantly greater with the 1% concentration (2 dermatomes greater than the 3% concentration on average, P < 0.05). Similar intensity of sensory block to electrical stimulation developed at the hip and knee and was unaffected by concentration of 2‐chloroprocaine. Similar intensity of motor block developed at the quadriceps with both concentrations.Conclusions:Intensity of sensory and motor block from epidural anesthesia with 2‐chloroprocaine appears to depend primarily on total milligram dose.

ISSN:0003-3022    

出版商:OVID    

年代:1997

数据来源: OVID

摘要:

Background:After tracheal intubation, lung resistance and therefore respiratory system resistance (Rrs) routinely increase, sometimes to the point of clinical bronchospasm. Volatile anesthetics generally have been considered to be effective bronchodilators, although there are few human data comparing the efficacy of available agents. This study compared the bronchodilating efficacy of four anesthetic maintenance regimens: 1.1 minimum alveolar concentration (MAC) end‐tidal sevoflurane, isoflurane or halothane, and thiopental/nitrous oxide.Methods:Sixty‐six patients underwent tracheal intubation after administration of 2 micro gram/kg fentanyl, 5 mg/kg thiopental, and 1 mg/kg succinylcholine. Vecuronium or pancuronium (0.1 mg/kg) was then given to ensure paralysis during the rest of the study. Postintubation R sub rs was measured using the isovolume technique. Maintenance anesthesia was then randomized to thiopental 0.25 mg [center dot] kg sup ‐1 [center dot] min sup ‐1 plus 50% nitrous oxide, or 1.1 MAC end‐tidal isoflurane, halothane, or sevoflurane. The Rrswas measured after 5 and 10 min of maintenance anesthesia. Data were expressed as means +/‐ SD.Results:Maintenance with thiopental/nitrous oxide failed to decrease Rrs, whereas all three volatile anesthetics significantly decreased Rrsat 5 min with little further improvement at 10 min. Sevoflurane decreased Rrsmore than either halothane or isoflurane (P < 0.05; 58 +/‐ 14% of the postintubation Rrsvs. 69 +/‐ 20% and 75 +/‐ 13%, respectively).Conclusions:After tracheal intubation in persons without asthma, sevoflurane decreased Rrsas much or more than isoflurane or halothane did during a 10‐min exposure at 1.1 MAC.

ISSN:0003-3022    

出版商:OVID    

年代:1997

数据来源: OVID