摘要:

BackgroundAnesthetic requirements for inhalational agents are decreased during pregnancy, but there are no data regarding requirements for intravenous agents. The quantal dose‐response curves for thiopental were calculated for 70 nonpregnant women having gynecologic surgery and for 70 pregnant women of 7–13 weeks' gestation having elective abortions.MethodsGroups of 10 patients were given 2, 2.4, 2.8, 3.3, 3.8, 4.5, or 5.3 mg/kg thiopental as a bolus dose during a period of 10 s. Two minutes later, patients were asked to open their eyes as a test for hypnosis. Patients who did not open their eyes were given a 10‐s, 50‐Hz, 80‐mA transcutaneous tetanic electrical stimulus to the ulnar nerve as a test for anesthesia. Purposeful movement indicated that there was no anesthesia. Log dose‐response curves for hypnosis and anesthesia were calculated after logit transformation.ResultsIn the nonpregnant women, the median effective doses (ED50s) (95% confidence interval) for hypnosis and anesthesia were 3.1 (2.8–3.4) mg/kg and 4.9 (4.5–5.4) mg/kg, whereas in the pregnant women the corresponding ED50s were 2.6 (2.3–2.8) mg/kg and 4 (3.7–4.4) mg/kg. In the nonpregnant women, the ED95s (95% CI) for hypnosis and anesthesia were 4.4 (3.9–5.4) mg/kg and 6.4 (5.7–7.9) mg/kg, whereas in the pregnant women the corresponding ED95s were 3.7 (3.3–4.5) mg/kg and 5.2 (4.7–6.3) mg/kg. The pregnant to nonpregnant relative median potency (95% CI) ratio for hypnosis was 0.83 (0.67–0.96) and for anesthesia it was 0.82 (0.62–0.94).ConclusionsThe dose of thiopental for hypnosis was 17% less and that for anesthesia was 18% less in pregnant women of 7–13 weeks' gestation compared with that in nonpregnant women.

ISSN:0003-3022    

出版商:OVID    

年代:1997

数据来源: OVID

摘要:

BackgroundAcute respiratory failure may develop in patients with chronic obstructive pulmonary disease because of intrinsic positive end‐expiratory pressure (PEEPi) and increased resistive and elastic loads. Proportional assist ventilation is an experimental mode of partial ventilatory support in which the ventilator generates flow to unload the resistive burden (flow assistance: FA) and volume to unload the elastic burden (volume assistance: VA) proportionally to inspiratory muscle effort, and PEEPi can be counterbalanced by application of external PEEP. The authors assessed effects of proportional assist ventilation and optimal ventilatory settings in patients with chronic obstructive pulmonary disease and acute respiratory failure.MethodsInspiratory muscles and diaphragmatic efforts were evaluated by measurements of esophageal, gastric, and transdiaphragmatic pressures. Minute ventilation and breathing patterns were evaluated by measuring airway pressure and flow. Measurements were performed during spontaneous breathing, continuous positive airway pressure, FA, FA + PEEP, VA, VA + PEEP, FA + VA, and FA + VA + PEEP.ResultsFA + PEEP provided the greatest improvement in minute ventilation (89 +/‐ 3%) and dyspnea (62 +/‐ 2%). The largest reduction in pressure time product per breath of the respiratory muscles and diaphragm (44 +/‐ 3% and 33 +/‐ 2%, respectively) also was observed during FA + PEEP condition. When VA was added to this setting, a reduction in respiratory rate (50 +/‐ 3%), an increase in inspiratory time (102 +/‐ 6%), and a further reduction in pressure time product per minute (65 +/‐ 2% and 64% for the respiratory muscles and diaphragm, respectively) was observed. However, values of pressure time product per liter of minute ventilation during FA + VA + PEEP did not differ with those observed during FA + PEEP condition. Worsening of patient‐ventilator interaction and breathing asynchrony occurred when VA was implemented.ConclusionsApplication of PEEP to counterbalance PEEPi and FA to unload the resistive burden provided the optimal conditions in such patients. Ventilator over‐assistance and patient‐ventilator asynchrony was observed when VA was added to this setting. The clinical use of proportional assist ventilation should be based on continuous measurements of respiratory mechanics.

ISSN:0003-3022    

出版商:OVID    

年代:1997

数据来源: OVID

摘要:

BackgroundIf patients who are more severely ill have greater hospital costs for surgery, then health‐care reimbursements need to be adjusted appropriately so that providers caring for more seriously ill patients are not penalized for incurring higher costs. The authors' goal for this study was to determine if severity of illness, as measured by either the American Society of Anesthesiologists Physical Status (ASA PS) or the comorbidity index developed by Charlson, can predict anesthesia costs, operating room costs, total hospital costs, or length of stay for elective surgery.MethodsThe authors randomly selected 224 inpatients (60% sampling fraction) having either colectomy (n = 30), total knee replacement (n = 100), or laparoscopic cholecystectomy (n = 94) from September 1993 to September 1994. For each surgical procedure, backward‐elimination multiple regression was used to build models to predict (1) total hospital costs, (2) operating room costs, (3) anesthesia costs, and (4) length of stay. Explanatory candidate variables included patient age (years), sex, ASA PS, Charlson comorbidity index (which weighs the number and seriousness of coexisting diseases), and type of insurance (Medicare/Medicaid, managed care, or indemnity). These analyses were repeated for the pooled data of all 224 patients. Costs (not patient charges) were obtained from the hospital cost accounting software.ResultsMean total hospital costs were $3,778 (95% confidence interval +/‐ 299) for laparoscopic cholecystectomy, $13,614 (95% CI +/‐ 3,019) for colectomy, and $18,788 (95% CI +/‐ 573) for knee replacement. The correlation (r) between ASA PS and Charlson comorbidity scores equaled 0.34 (P <.001). No consistent relation was found between hospital costs and either of the two severity‐of‐illness indices. The Charlson comorbidity index (but not the ASA PS) predicted hospital costs only for knee replacement (P =.003). The ASA PS, but not the Charlson index, predicted operating room and anesthesia costs only for colectomy (P <.03).ConclusionsSeverity of illness, as categorized by ASA PS categories 1–3 or by the Charlson comorbidity index, was not a consistent predictor of hospital costs and lengths of stay for three types of elective surgery. Hospital resources for these lower‐risk elective procedures may be expended primarily to manage the consequences of the surgical disease, rather than to manage the patient's coexisting diseases.

ISSN:0003-3022    

出版商:OVID    

年代:1997

数据来源: OVID

摘要:

BackgroundPulse oximetry is considered a standard of care in both the operating room and the postanesthetic care unit, and it is widely used in all critical care settings. Pulse oximeters may fail to provide valid SpO2data in various situations that produce low signal‐to‐noise ratio. Motion artifact is a common cause of oximeter failure and loss of accuracy. This study compares the accuracy and data dropout rates of three current pulse oximeters during standardized motion in healthy volunteers.MethodsTen healthy volunteers were monitored by three different pulse oximeters: Nellcor N‐200, Nellcor N‐3000, and Masimo SET (prototype). Sensors were placed on digits 2, 3, and 4 of the test hand, which was strapped to a mechanical motion table. The opposite hand was used as a stationary control and was monitored with the same pulse oximeters and an arterial cannula. Arterial oxygen saturation was varied from 100% to 75% by changing the inspired oxygen concentration. While SpO sub 2 was both constant and changing, the oximeter sensors were connected before and during motion. Oximeter errors and dropout rates were digitally recorded continuously during each experiment.ResultsIf the oximeter was functioning before motion began, the following are the percentages of time when the instrument displayed an SpO sub 2 value within 7% of control: N‐200 = 76%, N‐3000 = 87%, and Masimo = 99%. When the oximeter sensor was connected after the beginning of motion, the values were N‐200 = 68%, N‐3000 = 47%, and Masimo = 97%. If the alarm threshold was chosen SpO2less than 90%, then the positive predictive values (true alarms/total alarms) are N‐200 = 73%, N‐3000 = 81%, and Masimo = 100%. In general, N‐200 had the greatest SpO2errors and N‐3000 had the highest dropout rates.ConclusionsThe mechanical motions used in this study significantly affected oximeter function, particularly when the sensors were connected during motion, which requires signal acquisition during motion. The error and dropout rate performance of the Masimo was superior to that of the other two instruments during all test conditions. Masimo uses a new paradigm for oximeter signal processing, which appears to represent a significant advance in low signal‐to‐noise performance.

ISSN:0003-3022    

出版商:OVID    

年代:1997

数据来源: OVID

摘要:

BackgroundBrief ischemic periods render the myocardium resistant to infarction from subsequent ischemic insults by a process called ischemic preconditioning. Volatile anesthetics have also been shown to be cardioprotective if administered before ischemia. The effect of preconditioning alone and combined with halothane or isoflurane on hemodynamic recovery and preservation of adenosine triphosphate content in isolated rat hearts was evaluated.MethodsSeven groups of isolated rat hearts (n = 6 each) were perfused in a retrograde manner at constant temperature and pressure. A latex balloon was placed in the left ventricle to obtain isovolumetric contraction. Heart rhythm, coronary flow, left ventricular pressure and its derivative dP/dt (positive and negative), and developed pressure were monitored. The hearts were paced at 300 beats per minute. Each heart was randomly allocated to (1) a time‐control group that received no ischemia, (2) an untreated group that received 25 min of normothermic ischemia only, (3 and 4) an isoflurane group and a halothane group that received 40 min of anesthetic (2.2% and 1.5%, respectively) before ischemia; (5) a preconditioning group that received two 5‐min periods of ischemia separated by 10 min of reperfusion before ischemia; or (6 and 7) a isoflurane + preconditioning group and a halothane + preconditioning group that received anesthetic for 10 min at concentrations of 2.2% or 1.5%, respectively, before two 5‐min periods of ischemia separated by 10 min of reperfusion. All treated groups received 25 min of normothermic ischemia followed by 30 min of reperfusion.ResultsThe time‐control group remained hemodynamically stable for the entire experiment, and the adenosine triphosphate content was 18.3 +/‐ 1.7 (SEM) micro Meter/g at the end of 115 min. The untreated group had depressed recovery after 25 min of normothermic ischemia, and the developed pressure was significantly depressed and recovered only 30 +/‐ 9% (P < 0.001) of its preischemic value. There was also a significant increase in the incidence of ventricular fibrillation (P < 0.001). Adenosine triphosphate content was significantly lower in this group than in all other groups. Five minutes of ischemia in the preconditioning group had little effect on hemodynamics and decreased developed pressure only 6.4%. Halothane depressed developed pressure by 16 +/‐ 5% (P < 0.001), and isoflurane increased coronary flow by 145 +/‐ 9% (P < 0.001) but had no significant hemodynamic effect. The treated groups had significantly better recovery of postischemic function than did the untreated group. In the preconditioning group, developed pressure recovered to 85% of control and dP/dt+ to 87% of control. The addition of halothane or isoflurane to preconditioning did not provide additional functional recovery but did increase the level of adenosine triphosphate preservation (13.1 +/‐ 1.1 and 12.4 +/‐ 1.1 micro Meter/g, respectively).ConclusionsThe results indicate that preconditioning, halothane, and isoflurane provide significant protection against ischemia. The combination of preconditioning and halothane or isoflurane did not improve hemodynamic recovery but did increase preservation of adenosine triphosphate.

ISSN:0003-3022    

出版商:OVID    

年代:1997

数据来源: OVID

摘要:

BackgroundThis study was performed to elucidate and compare the effects of sevoflurane and of isoflurane on the nicotinic acetylcholine receptor of mouse myotubes. The experiments were done with special reference to anesthetic concentrations considerably less than those used for clinical anesthesia.MethodsThe patch‐clamp technique was used to record acetylcholine‐activated currents from the embryonic type of the nicotinic acetylcholine receptor in the outside‐out mode. A piezo‐driven liquid filament switch was used for the ultrafast application of acetylcholine alone or in combination with isoflurane or sevoflurane. In addition, the patches were preexposed to either anesthetic, preceding the activation with acetylcholine.ResultsThe current elicited by acetylcholine was reduced reversibly and in a concentration‐dependent manner by both anesthetics, which were equally effective. Preexposure of the patches to isoflurane or sevoflurane showed an additional inhibition that was present at micromolar concentrations. The time courses of current decay could be fitted by single exponentials for isoflurane. At higher concentrations of sevoflurane, the current decay became biexponential. In contrast to isoflurane, sevoflurane increased the time constants of desensitization when applied in low concentrations.ConclusionAt the nicotinic acetylcholine receptor, isoflurane and sevoflurane act primarily through the same mechanisms: Both affect the open and the closed state of the channels in concentrations equal to and less than those encountered clinically. The kinetics of desensitization, however, are altered in a different manner. Thus there may be several different sites of interaction.

ISSN:0003-3022    

出版商:OVID    

年代:1997

数据来源: OVID

摘要:

BackgroundIschemia‐hypoxia followed by reperfusion and reoxygenation injures cells and organs. Previous studies have indicated that isoflurane may protect organs from ischemia‐reperfusion or hypoxia‐reoxygenation. This study investigated the ability of isoflurane to protect the liver from hypoxia‐reoxygenation injury and the mechanisms of this phenomenon.MethodsThe isolated liver was perfused at a constant pressure of 12 cm H2O with a modified Krebs‐Ringer‐bicarbonate solution saturated with a 95% oxygen/5% carbon dioxide gas mixture. Hypoxic perfusion produced by decreasing the oxygen concentration in the gas mixture to 10% was followed by perfusion at 95% oxygen for 60 min. Viability of the liver was assessed by lactate dehydrogenase release from the liver. Isoflurane at 0.5, 1, and 2 minimum alveolar concentration was administered to assess the effect of isoflurane on hypoxia‐reperfusion injury. To determine the effect of isoflurane on extracellular generation of superoxide in the liver, the reduction of ferricytochrome c with or without superoxide dismutase was measured.ResultsLactate dehydrogenase release was transiently but dramatically increased by reoxygenation and significantly attenuated by 1 and 2 minimum alveolar concentration of isoflurane. Suppression of Kupffer cells with gadolinium chloride also attenuated the lactate dehydrogenase release. Isoflurane significantly reduced the superoxide generation on reperfusion.ConclusionsThe results show that isoflurane protected the liver from an early reoxygenation injury presumably mediated by Kupffer cells. The mechanisms of the inhibitory effects of isoflurane on the injury may involve suppression of extracellular superoxide generation during reoxygenation.

ISSN:0003-3022    

出版商:OVID    

年代:1997

数据来源: OVID

摘要:

BackgroundIn several beating cardiac muscle preparations, a short‐lived increase in twitch tension or amplitude has been observed when they were exposed abruptly to solutions containing halothane or enflurane. As exposure to the anesthetics was continued, the expected negative inotropic effect became evident after the short‐lived increase in twitch. No such increase in twitch has been reported during exposure to isoflurane. It has been hypothesized that this short‐lived increase in twitch is caused by an enhancement of calcium release from the sarcoplasmic reticulum, but other mechanisms have not been excluded.MethodsFreshly isolated, single rat ventricular cells were stimulated to beat at room temperature and abruptly exposed to solutions containing halothane (0.25–0.64 mM), enflurane (0.69–1 mM), or isoflurane (0.31–0.54 mM). During these exposures, twitch amplitude was measured and intracellular calcium concentration was followed using the calcium‐sensitive dye indo‐1. In some experiments, the whole‐cell patch‐clamp technique was used to measure membrane current. In addition, in several cells the sarcoplasmic reticulum calcium content was assessed through the response to brief pulses of caffeine.ResultsBoth the twitch amplitude and the intracellular calcium transient were increased temporarily in cells abruptly exposed to halothane or enflurane. No such behavior was found with isoflurane. After continued exposure to all three agents, both the twitch amplitude and the calcium transient were less than control. During the beats exhibiting an increase in twitch, no alteration in the relation between cell length (twitch amplitude) and the intracellular calcium transient was found compared with control conditions. In addition, the temporary increase in twitch amplitude occurred in cells contracting under voltage‐clamp control when halothane was introduced, and it was not associated with any increase in the calcium current. The sarcoplasmic reticulum calcium content at the time of the halothane‐induced increase in twitch also was not increased.ConclusionsThe short‐lived increase in twitch after abrupt exposure to halothane or enflurane is related to increased intracellular calcium during the beat and not to any changes in myofilament sensitivity to calcium. Because these results eliminate most alternative explanations for this phenomenon, the authors conclude that halothane, and probably also enflurane, increases the fraction of calcium released from the sarcoplasmic reticulum with each heart beat. Isoflurane appears to lack this action.

ISSN:0003-3022    

出版商:OVID    

年代:1997

数据来源: OVID

摘要:

BackgroundHalothane induces negative inotropic and lusitropic effects in myocardium. It has been suggested that halothane potentiates beta‐adrenoceptor stimulation. However, its effects on the inotropic response to alpha‐adrenoceptor stimulation and its effects on the lusitropic effects of alpha‐ and beta‐adrenoceptor stimulation are unknown.MethodsThe effects of halothane (0.5 and 1 minimum alveolar concentration [MAC]) on the inotropic responses induced by phenylephrine (10 sup ‐8 to 10 sup ‐4 M) and isoproterenol (10 sup ‐8 to 10 sup ‐4 M) were studied in rat left ventricular papillary muscles in vitro (in Krebs‐Henseleit solution at 29 degrees Celsius, pH 7.40, with 0.5 mM calcium and stimulation frequency at 12 pulses/min). The lusitropic effects were studied in isotonic (R1) and isometric (R2) conditions.ResultsOne MAC halothane induced a negative inotropic effect (54 +/‐ 3%, P < 0.05), increased R1 (109 +/‐ 3%, P < 0.05), and decreased R2 (88 +/‐ 2%, P < 0.05). In control groups, phenylephrine (137 +/‐ 7%, P > 0.05) and isoproterenol (162 +/‐ 6%, P < 0.05) induced a positive inotropic effect. Halothane did not significantly modify the positive inotropic effect of calcium, suggesting that it did not modify the inotropic reserve of papillary muscles. In contrast, 1 MAC halothane enhanced the positive inotropic effects of phenylephrine (237 +/‐ 19%, P < 0.05) and isoproterenol (205 +/‐ 11%, P < 0.05). Halothane did not modify the lusitropic effect of phenylephrine under high or low load. In contrast, 1 MAC halothane impaired the positive lusitropic effect of isoproterenol under low load (P < 0.05), whereas it did not modify the positive lusitropic effect of isoproterenol under high load.ConclusionsAt clinically relevant concentrations, halothane potentiated the positive inotropic effects of both alpha‐ and beta‐adrenoceptor stimulation. Furthermore, halothane alters the positive lusitropic effect of beta‐adrenoceptor stimulation under low load.

ISSN:0003-3022    

出版商:OVID    

年代:1997

数据来源: OVID

摘要:

BackgroundThe sevoflurane degradation product compound A is nephrotoxic in rats, in which it undergoes extensive metabolism to glutathione and cysteine S‐conjugates. The mechanism of compound A nephrotoxicity in rats is unknown. Compound A nephrotoxicity has not been observed in humans. The authors tested the hypothesis that renal uptake of compound A S‐conjugates and metabolism by renal cysteine conjugate beta‐lyase mediate compound A nephrotoxicity in rats.MethodsCompound A (0–0.3 mmol/kg in initial dose‐response experiments and 0.2 mmol/kg in subsequent inhibitor experiments) was administered to Fischer 344 rats by intraperitoneal injection. Inhibitor experiments consisted of three groups: inhibitor (control), compound A, or inhibitor plus compound A. The inhibitors were probenecid (0.5 mmol/kg, repeated 10 h later), an inhibitor of renal organic anion transport and S‐conjugate uptake; acivicin (10 mg/kg and 5 mg/kg 10 h later), an inhibitor of gamma‐glutamyl transferase, an enzyme that cleaves glutathione conjugates to cysteine conjugates; and aminooxyacetic acid (0.5 mmol/kg and 0.25 mmol/kg 10 h later), an inhibitor of renal cysteine conjugate beta‐lyase. Urine was collected for 24 h and then the animals were killed. Nephrotoxicity was assessed by light microscopic examination and biochemical markers (serum urea nitrogen and creatinine concentration, urine volume and urine excretion of protein, glucose, and alpha‐glutathione‐S‐transferase [alpha GST], a marker of tubular necrosis).ResultsCompound A caused dose‐related nephrotoxicity, as shown by selective proximal tubular cell necrosis at the corticomedullary junction, diuresis, proteinuria, glucosuria, and increased alpha GST excretion. Probenecid pretreatment significantly (P < 0.05) diminished compound A‐induced increases (mean +/‐ SE) in urine excretion of protein (45.5 +/‐ 3.8 mg/24 h vs. 25.9 +/‐ 1.7 mg/24 h), glucose (28.8 +/‐ 6.2 mg/24 h vs. 10.9 +/‐ 3.2 mg/24 h), and alpha GST (6.3 +/‐ 0.8 micro gram/24 h vs. 1.0 +/‐ 0.2 micro gram/24 h) and completely prevented proximal tubular cell necrosis. Aminooxyacetic acid pretreatment significantly diminished compound A‐induced increases in urine volume (19.7 +/‐ 3.5 ml/24 h vs. 9.8 +/‐ 0.8 ml/24 h), protein excretion (37.2 +/‐ 2.7 mg/24 h vs. 22.2 +/‐ 1.8 mg/24 h), and alpha GST excretion (5.8 +/‐ 1.5 vs. 2.3 micro gram/24 h +/‐ 0.8 micro gram/24 h) but did not significantly alter the histologic pattern of injury. In contrast, acivicin pretreatment increased the compound A‐induced histologic and biochemical markers of injury. Compound A‐related increases in urine fluoride excretion, reflecting compound A metabolism, were not substantially altered by any of the inhibitor treatments.ConclusionsIntraperitoneal compound A administration provides a satisfactory model of nephrotoxicity. Aminooxyacetic acid and probenecid significantly diminished histologic and biochemical evidence of compound A nephrotoxicity, whereas acivicin potentiated toxicity. These results suggest that renal uptake of compound A‐glutathione or compound A‐cysteine conjugates and cysteine conjugates metabolism by renal beta‐lyase mediate, in part, compound A nephrotoxicity in rats.

ISSN:0003-3022    

出版商:OVID    

年代:1997

数据来源: OVID