The effects of sevoflurane on isolated gravid human myometrium

The volatile anaesthetic agents are known to influence uterine muscle tone. All of the agents studied to date have been found to produce uterine relaxation. This property has been used to produce therapeutic uterine relaxation for difficult obstetric deliveries and the Ex Utero Intrapartum Treatment (EXIT) procedure. This study describes the effects of sevoflurane on isolated human myometrium at concentrations of 0.1, 0.25, 0.5, 0.75, 1.0, 1.5, 2.5 and 3.5 MAC. Sevoflurane produces dose-dependent depression of uterine muscle contractility with an ED50 of 0.94 MAC. Frequency of contraction was increased at concentrations of 2.5 MAC and greater. At concentrations of 3.5 MAC and above, uterine activity was virtually abolished.     

Inhibitory effects of desflurane and sevoflurane on oxytocin-induced contractions of isolated pregnant human myometrium

BACKGROUND: In this study, we investigated the inhibitory effects of desflurane and sevoflurane on oxytocin-induced contractions of isolated human myometrium. METHODS: Following delivery of the infant and placenta, a small segment of myometrium was excised from the upper incisional surface of the lower uterine segment and 20 strips, randomly assigned into two groups (n = 10), were obtained from 20 non-laboring term parturients. The study protocol consisted of a 60-min period of spontaneous contractions, control recording with oxytocin 2 x 10(9) m (10-min period), washout interval of 10 min, volatile administration (three times per 15-min period) of 0.5, 1 and 2 minimum alveolar concentration (MAC), response to oxytocin (10-min period), a further washout interval (10-min period) and subsequent control recording with oxytocin without anesthetics. RESULTS: After oxytocin administration, the frequency and amplitude of contractions increased (P < 0.05) and the duration decreased (P < 0.05). The frequency and amplitude of contractions induced with oxytocin decreased significantly at 0.5, 1 and 2 MAC of desflurane and sevoflurane (P < 0.05). The amplitude of contractions was significantly different at 1 MAC between the two groups (P < 0.05). The duration of contractions at 2 MAC decreased in both groups (P < 0.05). CONCLUSIONS: Desflurane and sevoflurane at 0.5, 1 and 2 MAC inhibit the frequency and amplitude of myometrial contractions induced with oxytocin in a dose-dependent manner. However, desflurane inhibits the amplitude less than sevoflurane at 1 MAC. We suggest that 0.5 MAC of both agents and 1 MAC of desflurane may be safely used in the presence of oxytocin following delivery of the infant and placenta during Cesarean section without fear of uterine atony and hemorrhage.     

Inhibitory effects of desflurane and sevoflurane on contractions of isolated gravid rat myometrium under oxytocin stimulation

BACKGROUND: We studied the inhibitory effects of desflurane and sevoflurane on oxytocin-induced contractions of isolated gravid rat myometrium. METHODS: Twenty strips were obtained from rats and these were randomly assigned into two groups. The effects of desflurane and sevoflurane were evaluated by treating strips with oxytocin alone 2x10-9 M or with oxytocin after desflurane and sevoflurane at 0.5, 1, and 2 MAC. RESULTS: Oxytocin significantly increased the amplitude and duration of contractions (P< 0.05), but it did not increase the frequency. The duration (84%, 79%), amplitude (90%, 84%) and frequency (88%, 75%) were inhibited at 2 MAC of desflurane and sevoflurane, respectively. CONCLUSION: These results suggest that the in vitro application of desflurane and sevoflurane similarly inhibit oxytocin-induced myometrial contractions of gravid rat in a dose-dependent manner.     

The effects of volatile anesthetics on spontaneous contractility of isolated human pregnant uterine muscle: a comparison among sevoflurane, desflurane, isoflurane, and halothane

We examined the effects of equianesthetic concentrations of sevoflurane, desflurane, isoflurane, and halothane on the spontaneous contractility of isolated human pregnant uterine muscles. We also determined if their action was related to potassium channels. Uterine specimens were obtained from normal full-term pregnant women undergoing elective lower-segment cesarean delivery. Longitudinal muscle strips were mounted vertically in tissue chambers. Their isometric tension was recorded while they were exposed to 0.5-3 minimum alveolar concentration (MAC) of volatile anesthetics in the absence and presence of the high conductance calcium-activated potassium channel blocker, tetraethylammonium, or the adenosine triphosphate-sensitive potassium channel (K(ATP))-blocker, glibenclamide. The anesthetics examined produced a dose-dependent depression of contractility. The inhibitory potency of sevoflurane and desflurane was comparable to, whereas that of isoflurane was smaller than, that of halothane: concentrations causing 50% inhibition of the contractile amplitude (ED(50)) were 1.72, 1.44, 2.35, and 1.66 MAC (P < 0.05), respectively. Tetraethylammonium and glibenclamide did not affect the uterine response to the anesthetics, except for glibenclamide, which attenuated the response to isoflurane. These results indicate that the volatile anesthetics have inhibitory effects on the contractility of the human uterus. The inhibitory effect of isoflurane may in part be mediated through activation of K(ATP) channels.     

The direct depressant effects of desflurane and sevoflurane on spontaneous contractions of isolated gravid rat myometrium

Our purpose was to investigate the direct depressant effects of desflurane and sevoflurane at 0.5, 1 and 2 minimum alveolar concentrations (MAC) on spontaneous contractions of isolated gravid rat myometrium. Ten gravid, albino Wistar rats, weighing 240-310 g and at 19-20 days' gestation were used. Sixty myometrial strips were obtained from 10 rats, and randomly assigned into six groups of 10. After obtaining spontaneous myometrial contractions in de Jalon solution for 45 min, 0.5, 1 or 2 MAC of desflurane or sevoflurane were continuously bubbled in the bath for 15 min and myometrial contractions evaluated during the last 10 min. Desflurane 0.5 MAC did not affect duration or amplitude of spontaneous contractions, but frequency was significantly decreased (P < 0.05). Duration, amplitude and frequency were all significantly decreased by desflurane 1 and 2 MAC (P < 0.05). Sevoflurane did not affect duration, amplitude or frequency at 0.5 MAC, but amplitude and frequency were significantly decreased at 1 MAC and all were significantly decreased at 2 MAC (P < 0.05). The frequency of contractions was decreased 21.2% with 1 MAC desflurane versus 17.1% with 1 MAC sevoflurane. The amplitude and frequency of contractions were decreased 48.2% and 48.7% with 2 MAC desflurane versus 58.9% and 49.3% with 2 MAC sevoflurane, respectively. We suggest that due to tocolytic activity, desflurane and sevoflurane can be useful in non-obstetric surgery during pregnancy.     

Sevoflurane increases lumbar cerebrospinal fluid pressure in normocapnic patients undergoing transsphenoidal hypophysectomy.

BACKGROUND: The data on the effect of sevoflurane on intracranial pressure in humans are still limited and inconclusive. The authors hypothesized that sevoflurane would increase intracranial pressure as compared to propofoL METHODS: In 20 patients with no evidence of mass effect undergoing transsphenoidal hypophysectomy, anesthesia was induced with intravenous fentanyl and propofol and maintained with 70% nitrous oxide in oxygen and a continuous propofol infusion, 100 microg x kg(-1) x min(-1). The authors assigned patients to two groups randomized to receive only continued propofol infusion (n = 10) or sevoflurane (n = 10) for 20 min. During the 20-min study period, each patient in the sevoflurane group received, in random order, two concentrations (0.5 times the minimum alveolar concentration [MAC] and 1.0 MAC end-tidal) of sevoflurane for 10 min each. The authors continuously monitored lumbar cerebrospinal fluid (CSF) pressure, blood pressure, heart rate, and anesthetic concentrations. RESULTS: Lumbar CSF pressure increased by 2+/-2 mmHg (mean+/-SD) with both 0.5 MAC and 1 MAC of sevoflurane. Cerebral perfusion pressure decreased by 11+/-5 mmHg with 0.5 MAC and by 15+/-4 mmHg with 1.0 MAC of sevoflurane. Systolic blood pressure decreased with both concentrations of sevoflurane. To maintain blood pressure within predetermined limits (within+/-20% of baseline value), phenylephrine was administered to 5 of 10 patients in the sevoflurane group (range = 50-300 microg) and no patients in the propofol group. Lumbar CSF pressure, cerebral perfusion pressure, and systolic blood pressure did not change in the propofol group. CONCLUSIONS: Sevoflurane, at 0.5 and 1.0 MAC, increases lumbar CSF pressure. The changes produced by 1.0 MAC sevoflurane did not differ from those observed in a previous study with 1.0 MAC isoflurane or desflurane.     

Influence of volatile anesthetics on myocardial contractility in vivo: desflurane versus isoflurane

The direct effects of desflurane on myocardial contractility in vivo have not been characterized. Therefore, the purpose of this investigation was to systematically examine the effects of desflurane on myocardial contractile function and compare these actions to equianesthetic concentrations of isoflurane in chronically instrumented dogs. Contractility was evaluated using an established index of inotropic state, the preload recruitable stroke work (PRSW) versus end-diastolic segment length (EDL) relationship. Since autonomic nervous system tone may influence the hemodynamic effects of the volatile anesthetics in vivo, experiments were performed in the presence of pharmacologic blockade of the autonomic nervous system. Two groups of experiments were performed with seven dogs instrumented for measurement of aortic and left ventricular pressure, the maximum rate of increase of left ventricular pressure (dP/dt), subendocardial segment length, coronary blood flow velocity, and cardiac output. After autonomic nervous system blockade, ventricular pressure-segment length loops were generated using preload reduction via partial inferior vena caval occlusion. The PRSW versus EDL relation was calculated from the pressure-length loops. Dogs were then anesthetized with 1.0 or 1.5 MAC desflurane or isoflurane in a random fashion, and measurements were repeated after 30 min of equilibration at each anesthetic concentration. The PRSW versus EDL slope reflected similar changes in contractile state when desflurane or isoflurane was administered (53 +/- 4 during control to 26 +/- 4 erg.cm-2 x 10(-3).mm-1 at 1.5 MAC desflurane, and 57 +/- 5 during control to 31 +/- 3 erg.cm-2 x 10(-2).mm-1 at 1.5 MAC isoflurane). In conclusion, desflurane and isoflurane produced equivalent direct decreases in myocardial contractility.     

Desflurane increases intracranial pressure more and sevoflurane less than isoflurane in pigs subjected to intracranial hypertension

Desflurane and sevoflurane may have advantages over isoflurane in neuroanesthesia, but this is still under debate. A porcine model with experimental intracranial hypertension was used for paired comparison of desflurane, sevoflurane, and isoflurane with respect to the effects on cerebral blood flow (CBF), cerebrovascular resistance (CVR), and intracranial pressure (ICP). The agents, given in sequence to each of six pigs, were compared at 0.5 and 1.0 minimal alveolar concentrations (MAC) and three mean arterial blood pressure (MAP) levels (50, 70, and 90 mm Hg) at normocapnia and one MAP level (70 mm Hg) at hypocapnia. MAC for each agent had been previously determined in a standardized manner for comparison reliability. CBF was measured with Xe. MAP was lowered by inflation of a balloon catheter in the inferior caval vein and raised by inflation of a balloon catheter in the descending aorta. ICP was measured intraparenchymally. Two Fogarty catheters positioned extradurally were inflated to a baseline ICP of 20 to 22 mm Hg at 0.2 MAC of each agent. CBF and ICP with the three agents at normocapnia and MAP 70 and 90 mm Hg at both 0.5 and 1.0 MAC were as follows (P < 0.05): desflurane > isoflurane > sevoflurane. None of the agents abolished CO2 reactivity. High-dose desflurane resulted in a higher CBF at hypocapnia than corresponding doses of sevoflurane or isoflurane, but there were no significant differences between the agents in ICP at hypocapnia. The present study showed that desflurane increased ICP more and sevoflurane less than isoflurane during normoventilation, but the differences disappeared with hyperventilation.     

Acute desflurane or sevoflurane exposure on a previously stabilized atracurium-induced neuromuscular block

BACKGROUND AND OBJECTIVE: The aim of this prospective study was to compare the effect of the administration of desflurane or sevoflurane to a fixed neuromuscular block. METHODS: After written consent, 12 patients were anaesthetized with propofol and sufentanil. Atracurium was administered via a continuous infusion in order to obtain 85% twitch depression of the control value assessed by repeated accelerometric stimulation at the adductor pollicis. Once stabilized over the course of 30 min, propofol was discontinued and either desflurane (n = 6) or sevoflurane (n = 6) was delivered at 1 MAC in a mixture of 50% O(2) in air. Study parameters were the magnitude and the time of twitch height variations. Results are presented in mean +/- SD. RESULT: Exposure to halogenated agents led to a significant reduction in twitch height with similar magnitude between the two agents. However, interaction with desflurane showed an initial and transient rise (35 +/- 22%) in twitch height before subsequent depression occurred. The time to reach 50% of the signal depression in the desflurane group was significantly delayed (25 +/- 7 vs. 11 +/- 4 min in the sevoflurane group; P < 0.01). CONCLUSIONS: On a stable neuromuscular block elicited by continuous infusion of atracurium, the abrupt administration of desflurane or sevoflurane reduces the accelerometric responses of the adductor pollicis in a similar way. This potentiating effect is produced faster after sevoflurane than after desflurane. With desflurane, a biphasic effect (of a transient and moderate increase followed by depression of the signal) was recorded.     

Beneficial effects of sevoflurane and desflurane against myocardial reperfusion injury after cardioplegic arrest

PURPOSE: To determine whether sevoflurane or desflurane offer additional protective effects against myocardial reperfusion injury after protecting the heart against the ischemic injury by cardioplegic arrest. METHODS: Isolated rat hearts in a Langendorff-preparation (n = 9) were arrested by infusion of HTK cardioplegic solution and subjected to 30 min global ischemia followed by 60 min reperfusion (controls). An additional 18 hearts were subjected to the same protocol, and sevoflurane (n = 9) or desflurane (n = 9) was added to the perfusion medium during the first 30 min of reperfusion in a concentration corresponding to 1.5 MAC in rats. Left ventricular (LV) developed pressure and creatine kinase (CK) release were determined as indices of myocardial performance and cellular injury, respectively. RESULTS: The LV developed pressure recovered to 46+/-7% of baseline in controls. Functional recovery during reperfusion was improved by inhalational anesthetics to 67+/-3% (sevoflurane, P<0.05) and 61+/-5% of baseline (desflurane, P<0.05), respectively. Peak CK release during early reperfusion was reduced from 52+/-11 U x min(-1) x g(-1) in controls to 34+/-7 and 26+/-7 U x min(-1) x g(-1) in sevoflurane and desflurane treated hearts, respectively. The CK release during the first 30 min of reperfusion was reduced from 312+/-41 U x g(-1) in control hearts to 195+/-40 and 206+/-37 U x g(-1) in sevoflurane and desflurane treated hearts. CONCLUSION: After ischemic protection by cardioplegia, sevoflurane and desflurane given during the early reperfusion period offer additional protection against myocardial reperfusion injury.     

Effect of sevoflurane on diaphragmatic contractility in dogs.

The effect of sevoflurane on diaphragmatic contractility was investigated in 12 anesthetized, mechanically ventilated dogs with the thorax opened. Animals were divided into two groups of six each: the sevoflurane and time control groups. We assessed contractility by the transdiaphragmatic pressure (Pdi) during supramaximal stimulation of the phrenic nerve at frequencies of 0.5, 10, 20, 50, and 100 Hz under quasiisometric conditions. The integrated electrical activity (Edi) of the crural and costal parts of the diaphragm (Edi cru, Edi cost) was also measured. In the sevoflurane group, diaphragmatic contractility was determined during three levels of anesthesia, specifically 0, 1.0, and 1.5 minimum alveolar anesthetic concentration (MAC). Measurements were made at the start of the stimulation (initial) and at the end of the 2-s period (2-s). Increasing the depth of sevoflurane anesthesia did not cause any significant differences in Pdi and Edi at 0.5-, 10-, and 20-Hz stimulation. By contrast, at 50- and 100-Hz stimulation, initial Pdi during 1.0 and 1.5 MAC sevoflurane exposure decreased significantly compared with the 0 MAC value (P less than 0.05). In addition, there was a statistical difference in 2-s Pdi between 1.0 and 1.5 MAC at 100-Hz stimulation (P less than 0.05). The Edi cru showed similar changes in Pdi at both measurements, whereas there was no remarkable change in Edi cost. There was no significant change either in Pdi or in Edi with respect to time in the time control group. We conclude from these results that sevoflurane impairs diaphragmatic contractility through its inhibitory effect on neuromuscular transmission, predominantly of the crural part.     

Protective effects of volatile agents against methacholine-induced bronchoconstriction in rats

BACKGROUND: The protective properties of common volatile agents against generalized lung constriction have previously been addressed only via estimations of parameters that combine airway and tissue mechanics. Their effectiveness in preventing airway constriction have not been compared systematically. Therefore, the authors investigated the abilities of halothane, isoflurane, sevoflurane, and desflurane to provide protection against airway constriction induced by methacholine. METHODS: Low-frequency pulmonary impedance data were collected in open-chest rats under baseline conditions and during three consecutive intravenous infusions of methacholine (32 microg x kg(-1) x min(-1)) while the animals were anesthetized with intravenous pentobarbital (control group). Methacholine challenges were performed in four other groups of rats, first during intravenous anesthesia and then repeated during the inhalation of halothane, isoflurane, sevoflurane, or desflurane at concentrations of 1 and 2 minimum alveolar concentration (MAC). Airway resistance and inertance, parenchymal damping, and elastance were estimated from the impedance data by model fitting. RESULTS: The methacholine-induced increases in airway resistance during intravenous pentobarbital anesthesia (204 +/- 53%) were markedly and significantly (P < 0.005) reduced by 1-MAC doses of halothane (80 +/- 48%), isoflurane (112 +/- 59%), sevoflurane (68 +/- 34%), and desflurane (96 +/- 34%), with no significant difference between the gases applied. Increasing the concentration to 2 MAC did not lead to any significant further protection against the increase in airway resistance. CONCLUSIONS: These data demonstrate that isoflurane, sevoflurane, and desflurane are as effective as the widely accepted halothane in protecting against methacholine-induced airway constriction.     

Cerebral blood flow at 0.5 and 1.0 minimal alveolar concentrations of desflurane or sevoflurane compared with isoflurane in normoventilated pigs

Whether desflurane and sevoflurane have clinical advantages over isoflurane in neuroanesthesia is much debated. A porcine model was used for comparison of desflurane and sevoflurane with isoflurane with respect to their cerebrovascular effects. The minimal alveolar concentration (MAC) of each of the three agents was first determined in a standardized manner in six domestic juvenile pigs to enhance comparison reliability. Six other pigs were then anesthetized with isoflurane, desflurane, and sevoflurane, given in sequence to each pig in an even crosswise order with the first agent also used to maintain anesthesia during surgical preparation. Cerebral blood flow (CBF) was calculated from the clearance curve of intraarterially injected 133Xe. The mean arterial pressure (MAP) was invasively monitored. The estimated cerebrovascular resistance (CVRe) was calculated by dividing MAP with CBF, thereby approximating the cerebral perfusion pressure with MAP. For both MAC levels, the trend for CBF was desflurane > isoflurane > sevoflurane, and the trend for MAP and CVRe was sevoflurane > isoflurane > desflurane. Statistical comparison of desflurane and sevoflurane with isoflurane with respect to CBF and MAP revealed two statistically significant differences-namely, that CBF at 1.0 MAC desflurane was 17% higher than CBF at 1.0 MAC isoflurane (P =.0025) and that MAP at 1.0 MAC sevoflurane was 16% higher than MAP at 1.0 MAC isoflurane (P =.011). Consequently, in this study at normocapnia, these agents did not seem to differ much in their cerebral vasodilating effects at lower doses. At higher doses, however, desflurane, in contrast to sevoflurane, was found to induce more cerebral vasodilation than isoflurane.     

The recovery of cognitive function after general anesthesia in elderly patients: a comparison of desflurane and sevoflurane.

We evaluated the cognitive recovery profiles in elderly patients after general anesthesia with desflurane or sevoflurane. After IRB approval, 70 ASA physical status I-III consenting elderly patients (> or =65 yr old) undergoing total knee or hip replacement procedures were randomly assigned to one of two general anesthetic groups. Propofol and fentanyl were administered for induction of anesthesia, followed by either desflurane 2%-4% or sevoflurane 1%-1.5% with nitrous oxide 65% in oxygen. The desflurane (2.5 +/- 0.6 MAC. h) and sevoflurane (2.7 +/- 0.5 MAC. h) concentrations were adjusted to maintain comparable depths of hypnosis using the electroencephalogram bispectral index monitor. The Mini-Mental State (MMS) test was used to assess cognitive function preoperatively and postoperatively at 1, 3, 6, and 24-h intervals. The use of desflurane was associated with a more rapid emergence from anesthesia (6.3 +/- 2.4 min versus 8.0 +/- 2.8 min) and a shorter length of stay in the postanesthesia care unit (213 +/- 66 min versus 241 +/- 87 min). However, there were no significant differences between the Desflurane and the Sevoflurane groups when the MMS scores were compared preoperatively, and postoperatively at 1, 3, 6, and 24 h. Compared with the preoperative (baseline) MMS scores, the values were significantly decreased at 1 h postoperatively (27.8 +/- 1.7 versus 29.5 +/- 0.5 in the Desflurane group, and 27.4 +/- 1.7 versus 29.2 +/- 1.0 in the Sevoflurane group, respectively). However, the MMS scores returned to preoperative baseline levels within 6 h after surgery. At 1 h and 3 h after surgery, 51% and 11% (versus 57% and 9%) of patients in the Desflurane (versus Sevoflurane) Group experienced cognitive impairment. In conclusion, desflurane is associated with a faster early recovery than sevoflurane after general anesthesia in elderly patients. However, recovery of cognitive function was similar after desflurane and sevoflurane-based anesthesia. IMPLICATIONS: Desflurane was associated with a faster early recovery than sevoflurane after general anesthesia in elderly patients. However, recovery of cognitive function was similar with both volatile anesthetics.     

Cerebral blood flow velocity in children anaesthetized with desflurane

BACKGROUND: Desflurane allows for rapid emergence and changes in depth of anaesthesia which makes it especially suitable for neuroanaesthesia. This study was designed to determine the effects of different desflurane concentrations on cerebral blood flow velocity (CBFV) in healthy children. METHODS: Twenty children, aged 1-7 years undergoing urological surgery were studied. Anaesthesia was induced with sevoflurane in oxygen. After tracheal intubation, sevoflurane was discontinued and ventilation with desflurane in air/oxygen was initiated and normoventilation maintained. A caudal block was performed. The patients were randomized to receive three different desflurane concentrations (0.5, 1.0 and 1.5 MAC). Fifteen minutes were allowed to reach steady-state at which time CBFV was measured by transcranial Doppler sonography. Mean arterial pressure (MAP) and heart rate (HR) were simultaneously recorded at 1-min intervals. RESULTS: Cerebral blood flow velocity increased from 0.5 to 1.0 MAC (P < 0.05), but not from 1.0 to 1.5 MAC. HR increased from 0.5 to 1.0 (P < 0.001) and from 1.0 to 1.5 MAC (P < 0.001), whereas the MAP decreased only from 0.5 to 1.0 MAC (P < 0.001). CONCLUSIONS: Desflurane in concentrations of 1.0 and 1.5 MAC in children increases CBFV significantly when compared with 0.5 MAC. These changes were associated with a significant increase in HR and decrease in MAP.     

末梢灌注指数监测地氟醚诱发患者交感神经兴奋的评价

目的 评价末梢灌注指数(TPI)监测地氟醚诱发的患者交感神经兴奋作用.方法 择期全麻患者48例,年龄25～60岁,ASA Ⅰ或Ⅱ级,随机分为3组(n=16):七氟醚组(Ⅰ组)、地氟醚组(Ⅱ组)和地氟醚+异丙酚组(Ⅲ组).气管插管后Ⅰ组和Ⅱ组地氟醚或七氟醚呼气末浓度依次快速达到0.5 MAC、1.0 MAC和1.5 MAC,并在每个水平维持5 min.Ⅲ组在气管插管后靶控输注异丙酚.血浆靶浓度至1μg/ml,地氟醚呼气末浓度依次快速达到0.5 MAC、1.0 MAC,并在每个水平维持5 min.分别在给予咪达唑仑后5 min(T0)、麻醉诱导后3 min(T1)、插管后即刻(T2)、呼气末浓度达到0.5 MAC(T3)、0.5 MAC后5 min(T4)、1.0 MAC(T5)、1.0MAC后5min(T6)、1.5MAC(T7)、1.5MAC后5min(T8)时记录心率(HR)、平均动脉压(MAP)、TPI、脑电双频谱指数,并在T0、T1、T2、T5、T7时测定血浆肾素活性和血管紧张素Ⅱ水平.结果 与T4时比较,Ⅱ组T5时,IPI降低(P<0.05);与T7时比较,Ⅱ组T4～6、T8时HR、MAP降低,T3～6、T8时TPI降低(P<0.05);与Ⅰ组比较,Ⅱ组T7时HR、MAP升高,TPI降低(P<0.05);Ⅱ组T5和T7时TPI出现变化最大值的时间短于HR、MAP;ATPI与△HR、AMAP呈负相关(r=-0.593,P<0.05;r=-0.591,P<0.05);与Ⅰ组比较,Ⅱ组血浆肾素活性和AT-Ⅱ浓度升高(P<0.05).结论 TPI可灵敏地反映地氟醚诱发的患者交感神经兴奋.     

Haemodynamic changes during halothane, sevoflurane and desflurane anaesthesia in dogs before and after the induction of severe heart failure

BACKGROUND AND OBJECTIVE: The effects of desflurane and sevoflurane on the failing myocardium are still uncertain. We investigated the effects of different concentrations of sevoflurane, desflurane and halothane in dogs with pacing induced chronic heart failure. METHODS: Global (left ventricular pressure, left ventricular dP/dt, Konigsbergtransducer) and regional myocardial function (systolic segment length shortening, ultrasonic crystals) were measured in chronically instrumented dogs with tachycardia induced severe congestive heart failure. Measurements were performed in healthy dogs and after induction of heart failure in the awake state and during anaesthesia with 0.75, 1.0, 1.25 and 1.75 minimum alveolar concentration (MAC) of halothane, sevoflurane or desflurane. RESULTS: The anaesthetics reduced dP/dtmax in a dose-dependent manner in healthy dogs (dP/dtmax decreased to 43-53% of awake values at 1.75 MAC). Chronic rapid left ventricular pacing increased heart rate and left ventricular end-diastolic pressure and decreased mean arterial pressure, left ventricular systolic pressure and dP/dtmax. The reduction in contractility was similar in the failing myocardium (to 41-50% of awake values at 1.75 MAC). Segmental shortening was reduced during anaesthesia by 50-62% after pacing compared with 22-44% in normal hearts. While there were similar effects of the different anaesthetics on diastolic function in healthy dogs, after induction of heart failure a more pronounced increase of the time constant of isovolumic relaxation and a greater decrease of dP/dtmin was observed with sevoflurane than with desflurane, indicating a stronger depression of diastolic function. CONCLUSIONS: While the negative inotropic effects of sevoflurane and desflurane were similar in normal and in the failing myocardium in vivo, desflurane led to a better preservation of diastolic function in the failing myocardium.     

The minimum alveolar concentration (MAC) and hemodynamic effects of halothane, isoflurane, and sevoflurane in newborn swine

To determine the minimum alveolar concentration (MAC) and hemodynamic responses to halothane, isoflurane, and sevoflurane in newborn swine, 36 fasting swine 4-10 days of age were anesthetized with one of the three volatile anesthetics in 100% oxygen. MAC was determined for each swine. Carotid artery and internal jugular catheters were inserted and each swine was allowed to recover for 48 h. After recovery, heart rate (HR), systemic systolic arterial pressure (SAP), and cardiac index (CI) were measured awake and then at 0.5, 1.0, and 1.5 MAC of the designated anesthetic in random sequence. The (mean +/- SD) MAC for halothane was 0.90 +/- 0.12%; the MAC for isoflurane was 1.48 +/- 0.21%; and the MAC for sevoflurane was 2.12 +/- 0.39%. Awake (mean +/- SD) measurements of HR, SAP, and CI did not differ significantly among the three groups. Compared to the awake HR, the mean HR decreased 35% at 1.5 MAC halothane (P less than 0.001), 19% at 1.5 MAC isoflurane (P less than 0.005), and 31% at 1.5 MAC sevoflurane (P less than 0.005). Compared to awake SAP, mean SAP measurements decreased 46% at 1.5 MAC halothane (P less than 0.001), 43% at 1.5 MAC isoflurane (P less than 0.001), and 36% at 1.5 MAC sevoflurane (P less than 0.005). Mean SAP at 1.0 and 1.5 MAC halothane and isoflurane were significantly less than those measured at equipotent concentrations of sevoflurane (P less than 0.005). Compared to awake CI, mean CI measurements decreased 53% at 1.5 MAC halothane (P less than 0.001) and 43% at 1.5 MAC isoflurane (P less than 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of the Physical Properties of Isoflurane, Sevoflurane, and Desflurane on Pulmonary Resistance in a Laboratory Lung Model

Background: Airway resistance depends not only on an airway's geometry but also on flow rate, and gas density and viscosity. A recent study showed that at clinically relevant concentrations, the mixtures of volatile agents with air and oxygen and oxygen-nitrogen affected the density of the mixture. The goal of the current study was to investigate the effect of different minimum alveolar concentrations (MACs) of three commonly used volatile agents, isoflurane, sevoflurane, and desflurane, on the measurements of airway resistance.

Methods: A two-chamber fixed-resistance test lung was connected to an anesthesia machine using the volume control mode of ventilation. Pulmonary resistance was calculated at baseline (25% oxygen in air); at 1.0, 1.5, and 2.0 MAC; and also at the same concentrations, 1.2% and 4%, of isoflurane, sevoflurane, and desflurane mixtures with 25% oxygen in air. The analysis of variance test for repeated measures and probabilities for post hoc Tukey and least significant difference tests were used.

Results: Isoflurane affected pulmonary resistance only at 2 MAC. Sevoflurane caused a significant increase of pulmonary resistance at 1.5 and 2 MAC, whereas desflurane caused the greatest increase in pulmonary resistance at all MAC values used. At 1.2% concentration, no difference from the baseline resistance was observed, whereas at 4%, the three agents produced similar increases of pulmonary resistance.     

The effect of desflurane and sevoflurane on cerebral oximetry under steady-state conditions

We studied the effect of sevoflurane and desflurane on regional cerebral oxygenation (rSO2). Twenty-two patients undergoing abdominal hysterectomy received sevoflurane and desflurane for 15 min each and 30 min apart under steady-state conditions in a randomized, crossover manner to maintain a bispectral index (BIS) of 40-50. In another 22 patients undergoing the same anesthesia and surgery BIS was maintained at 20-30. During the 15-min administration of each anesthetic at steady-state conditions rSO2, BIS, inspired and end-tidal anesthetic concentrations, end-tidal CO2, Spo2, systolic and diastolic blood pressures, and heart rate were recorded every 3 min. The rSO2 did not differ between sevoflurane and desflurane when BIS values were maintained between 40-50 or 20-30. The MAC(BIS) values required to maintain BIS at 40-50 and at 20-30 were 1.0 versus 1.2 (P = 0.004) and 1.6 versus 1.8 (P < 0.001) for desflurane and sevoflurane respectively. Higher rSO2 values were obtained by 1.6 MAC (71 +/- 13) than by 1 MAC of desflurane (66 +/- 10; P < 0.001) and by 1.8 MAC (72 +/- 11) than by 1.2 MAC of sevoflurane (66 +/- 13; P < 0.001). In conclusion, equipotent concentrations of desflurane or sevoflurane in terms of BIS are associated with similar rSO2 values, but larger anesthetic concentrations of both anesthetics increased the rSO2 values.