选取我院择期行腹腔镜结直肠癌根治术的全麻患者60例,年龄42~65岁,男34例,女26例,美国麻醉医师协会(American Society of Anesthesiologists,ASA)分级Ⅰ或Ⅱ级。所有患者术前无严重心脑血管疾病,肝、肾功能正常,无糖尿病、甲状腺功能亢进及凝血功能障碍。排除窦性心动过缓、左束支传导阻滞、麻醉药物过敏,以及严重呼吸疾病史患者。试验经本院医院伦理委员会批准,并与患者签署知情同意书。按随机数字表法将其随机分为对照组和治疗组,每组30例。采用信封装填代码进行分配隐藏。术中若因手术操作不顺导致大量出血或病情危重,病例将被剔除。两组患者年龄、性别比例、体质量等一般资料比较,差异无统计学意义(P>0.05),具有可比性。见表1。
JOSHI GP.Complications of laparoscopy[J].Anesthesiol Clin North Am, 2001,19(1):89-105.
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ALKIRE MT, MCREYNOLDS JR, HAHN EL, et al.Thalamic microinjection of nicotinereverses sevoflurane-induced loss of righting reflex in the rat[J]. Anesthesiology, 2007,107(2):264-272.
Abstract Neuronal nicotinic acetylcholine receptors are both potently inhibited by anesthetics and densely expressed in the thalamus. Brain imaging shows that thalamic activity suppression accompanies anesthetic-induced unconsciousness. Therefore, anesthetic-induced unconsciousness may involve direct antagonism of thalamic nicotinic receptors. The authors test this by separately attempting to block or enhance anesthetic-induced loss of righting in rats using intrathalamic microinjections of nicotine or its antagonist. Rats were implanted with a cannula aimed at the thalamus or control locations. A week later, loss of righting was induced using sevoflurane (1.4 +/- 0.2%). A dose-parameter study (n = 35) first identified an optimal intrathalamic nicotine dose associated with arousal. Subsequently, this dose was used to pinpoint the thalamic site mediating the arousal response (n = 107). Finally, sevoflurane righting dose and response specificity were assessed after blocking nicotinic channels with intrathalamic mecamylamine pretreatment (n = 8) before nicotine challenge. Nicotine (150 microg/0.5 microl over 1 min) was the optimal arousal dose, because lower doses (75 microg) were ineffective and higher doses (300 microg) often caused seizures. Nicotine temporarily restored righting and mobility in animals when microinjections involved the central medial thalamus (P < 0.0001, chi-square). Righting occurred despite continued sevoflurane administration. Intrathalamic mecamylamine pretreatment did not lower the sevoflurane dose associated with loss of righting, but prevented the nicotine arousal response. The reversal of unconsciousness found here with intrathalamic microinfusion of nicotine suggests that suppression of the midline thalamic cholinergic arousal system is part of the mechanism by which anesthetics produce unconsciousness.
HUUPPONENE, MAKSIMOWA, LAPINLAMPIP, et al.Electroencephalogram spindle activity during dexmedetomidine sedation and physiological sleep[J]. Acta Anaesthesiol Scand, 2008, 52(2):289-294.
Background: Dexmedetomidine, a selective α-adrenoceptor agonist, induces a unique, sleep-like state of sedation. The objective of the present work was to study human electroencephalogram (EEG) sleep spindles during dexmedetomidine sedation and compare them with spindles during normal physiological sleep, to test the hypothesis that dexmedetomidine exerts its effects via normal sleep-promoting pathways. Methods: EEG was continuously recorded from a bipolar frontopolar–laterofrontal derivation with Entropy Module (GE Healthcare) during light and deep dexmedetomidine sedation (target-controlled infusions set at 0.5 and 3.265ng/ml) in 11 healthy subjects, and during physiological sleep in 10 healthy control subjects. Sleep spindles were visually scored and quantitatively analyzed for density, duration, amplitude (band-pass filtering) and frequency content (matching pursuit approach), and compared between the two groups. Results: In visual analysis, EEG activity during dexmedetomidine sedation was similar to physiological stage 2 (S2) sleep with slight to moderate amount of slow-wave activity and abundant sleep spindle activity. In quantitative EEG analyses, sleep spindles were similar during dexmedetomidine sedation and normal sleep. No statistically significant differences were found in spindle density, amplitude or frequency content, but the spindles during dexmedetomidine sedation had longer duration (mean 1.1165s, SD 0.1465s) than spindles in normal sleep (mean 0.8865s, SD 0.1465s; =0.0014). Conclusions: Analysis of sleep spindles shows that dexmedetomidine produces a state closely resembling physiological S2 sleep in humans, which gives further support to earlier experimental evidence for activation of normal non-rapid eye movement sleep-promoting pathways by this sedative agent.
FANQ, HUC, YEM, et al.Dexmedetomidine for tracheal extubation in deeply anesthetized adult patients after otologic surgery: acomparison with remifentanil[J]. BMC Anesthesiol, 2015, 15:106.
ABSTRACT Background: Remifentanil and dexmedetomidine are well known to suppress airway reflexes during airway procedures. Smooth tracheal extubation is important after otologic surgery. The purpose of this study is to compare the effectiveness of dexmedetomidine or remifentanil infusion for producing smooth tracheal extubation in deeply anesthetized patients after otologic surgery. Methods: Seventy-four ASA I-II adult patients (18-60 years old) scheduled for elective otologic surgery were randomly assigned to one of three groups: sevoflurane-remifentanil (Group SR, n = 25), sevoflurane-dexmedetomidine (0.5 渭g/kg) (Group SD5, n = 24), or sevoflurane-dexmedetomidine (0.7 渭g/kg) (Group SD7, n = 25). Remifentanil or dexmedetomidine were administered for 10 min at the end of surgery. The primary outcome was the rate of smooth extubation. Respiratory pattern, airway obstruction, hemodynamic and respiratory profiles, time to awake, rescue analgesics in the post-anesthesia care unit (PACU), and postoperative nausea and vomiting (PONV) were also recorded. Results: The rate of smooth tracheal extubation as defined 1 min post-extubation was the same for Groups SR and SD7 (P > 0.05), but the rate of smooth extubation was lower for Group SD5 than for the other two groups (p 0.05), but the mean arterial pressure and heart rate were higher in Group SR at 10 and 15 min after extubation (p 0.05). The need for rescue analgesic in the PACU was more common in Group SR than in both dexmedetomidine groups (P < 0.01). Compared to Group SR, both dexmedetomidine groups had less PONV on postoperative day 1 (p < 0.05). Conclusion: Combined with 1 MAC sevoflurane, dexmedetomidine 0.7 ug/kg and remifentanil provided similar rates for smooth tracheal extubation in spontaneously breathing, anesthetized adults. Dexmedetomidine exhibited opioid-sparing effects postoperatively and was associated with less PONV than remifentanil.
NEGIS, SENI, ARYAV, et al.Dexmedetomidine versus fentanyl as co-adjuvants of balanced anaesthesia technique in renal transplant recipients[J].Middle East J Anaesthesiol, 2014, 22(6):549-557.
Ideal anesthetic technique for renal allograft recipients should provide hemodynamic stability, optimum graft reperfusion and adequate analgesia. Balanced anesthesia is preferred because renal nociception is conducted multi-segmentally and chronically ill ESRD patients have labile psychological profile. Present study compared the efficacy ofdexmedetomidine with fentanyl administered via intravenous and epidural route before induction of general anesthesia.Prospective, double blind randomized study, recruited sixty hemo-dynamically stable ESRD adults, 18-55 years, scheduled for elective live related renal transplantation. Patients randomly received intravenous dexmedetomidine 0.5 渭g/kg followed by epidural dexmedetomidine 0.5 渭g/kg alongwith 5 ml; 0.25% ropivacaine or intravenous fentanyl 1 渭g/kg followed by epiduralfentanyl 1 渭g/kg alongwith 5 ml; 0.25% ropivacaine. All patients received standardized general anaesthesia and continuous epidural ropivacaine 0.25%; 4-8 ml/hr. Preoperative sedation, peri-operative haemodynamics, end tidal anaesthetic agent requirement, peri-operative fluid requirement, need for vasopressors, blood loss and early graft function was assessed.80% patients receiving intravenous dexmedetomidine did not require rescue midazolam for achieving satisfactory sedation before induction of general anaesthesia. Dexmedetomidine significantly reduced propofol and end tidal inhalational agents requirement and need for rescue analgesics. Early renal graft function (onset time of diuresis after declamping, 24 hours urine output and serum creatinine levels) was comparable. There were no adverse sequelae.Dexmedetomidine-based anaesthetic regimen versus fentanyl-based anaesthesia provided appropriate anxiolysis and analgesia for conducting invasive procedures and subsequent epidural administration of these agents reduced anaesthetic requirement and prolonged postoperative analgesia without compromising hemodynamics and respiratory parameters. Further dose finding studies can be conducted in kidney transplant recipients.
BENGGONM, CHENH, APPLEGATER, et al.Effect of dexmedetomidine on brain edema and neurological outcomes in surgicat brain injury in rats[J].Anesth Analg, 2012,115(1):154-159.
BACKGROUND: Surgical brain injury (SBI) is damage to functional brain tissue resulting from neurosurgical manipulations such as sharp dissection, electrocautery, retraction, and direct applied pressure. Brain edema is the major contributor to morbidity with inflammation, necrosis, oxidative stress, and apoptosis likely playing smaller roles. Effective therapies for SBI may improve neurological outcomes and postoperative morbidities associated with brain surgery. Previous studies show an adrenergic correlation to blood-brain barrier control. The alpha-2 receptor agonist dexmedetomidine (DEX) has been shown to improve neurological outcomes in stroke models. We hypothesized that DEX may reduce brain edema and improve neurological outcomes in a rat model of SBI.<br/>METHODS: Male Sprague-Dawley rats (n = 63) weighing 280 to 350 g were randomly assigned to 1 of 4 IP treatment groups: sham IP, vehicle IP, DEX 10 mg/kg, and DEX 30 mg/kg. Treatments were given 30 min before SBI. These treatment groups were repeated to observe the physiologic impact of DEX on mean arterial blood pressure (MAP), heart rate (HR), and blood glucose on SBI naive animals. Rats were also assigned to 4 postinjury IV treatment groups: sham IV, vehicle IV, DEX 10/5, and DEX 30/15 (DEX group doses were 10 and 30 mg/kg/hr, with 5 and 15 mg/kg initial loading doses, respectively). Initial loading doses began 20 min after SBI, followed by 2 h of infusion. SBI animals were subjected to neurological testing 24 h after brain injury by a blinded observer, promptly killed, and brain water content measured via the dry/wet weight method.<br/>RESULTS: All treatment groups showed a significant difference in ipsilateral frontal brain water content and neurological scores when compared with sham animals. However, there was no difference between DEX-treated and vehicle animals. Physiologic monitoring showed treatment with low or high doses of DEX significantly decreased MAP and HR, and briefly increased blood glucose compared with naive or vehicle-treated animals.<br/>CONCLUSIONS: DEX administration did not reduce brain edema or improve neurological function after SBI in this study. The statistical difference in brain water content and neurological scores when comparing sham treatment to vehicle and DEX treatments shows consistent reproduction of this model. Significant changes in MAP, HR, and blood glucose after DEX as compared to vehicle and sham treatments suggest appropriate delivery of drug. (Anesth Analg 2012;115:154-9)
MIZUNOJ, NAKATAY, MORITAS, et al.Predisposing factors and prevention of emergence agitation[J].Masui, 2011, 60(4):425-435.
Agitation during the emergence from general anesthesia is a great post-operative problem that often injures the patients themselves and requires the medical staff to restrain and calm the patients. The predisposing factors for emergence agitation include anesthesia, operation, and patient. Sevoflurane anesthesia results in higher incidence of emergence agitation than halothane, because of the rapid emergence, and its effects on central nervous system inducing convulsion and post-operative behavioral changes. The otorhinolaryngologic and ophthalmologic surgeries, post-operative pain, young age, pre-operative anxiety, no past surgical history, and adjustment disorder of patients are risk factors for emergence agitation. The change from sevoflurane to propofol during anesthesia maintenance is a contributing factor to reduce incidence of emergence agitation. The medications including opioids, midazolam, alpha-2 agonists, ketamine, non-steroidal anti-inflammatory drugs, nitrous oxide, and propofol, and aggressive nerve block such as caudal epidural block for post-operative sedation and analgesia are effective to avoid incidence of emergence agitation. The calm emergence following general anesthesia would decrease the self-injuring behavior, and enhance the parent and caregiver satisfaction in general anesthesia and surgery.
MALVIYAS, VOEPEL-LEWIST, RAMAMURTHI RJ, et al.Clonidine for the prevention of emergence agitation in young children: efficacy and recoveryprofile[J]. Paediatr Anaesth, 2006,16(5):554-559.
Summary Background: Emergence agitation (EA) is a common postoperative problem in young children who have received sevoflurane and isoflurane for general anesthesia. This randomized, double-blinded study evaluated the efficacy of intraoperative clonidine in reducing EA, and describes its recovery profile. Methods: With Institutional Review Board approval and informed consent, children undergoing brief, minimally painful procedures were studied. All children received preemptive analgesia with acetaminophen and ketorolac, sevoflurane for induction, and isoflurane for maintenance of anesthesia. Children received either 2 mug.kg(-1) clonidine or placebo intravenously (i.v.) following induction of anesthesia. Children were observed postoperatively for behavior and side effects, and their parents were telephoned the next day to determine postdischarge recovery characteristics. Results: One hundred and twenty children were included in this study: 59 of whom received clonidine, and 61 placebo; 41% of those in the placebo group exhibited moderate-severe EA compared with only 22% of those in the clonidine group (P < 0.03). Compared with those who received placebo, children who received clonidine awakened more slowly (22 min vs 14 min), had a longer postanesthesia care unit stay (57 min vs 46 min), and experienced sleepiness more frequently after discharge (75% vs 39%; all comparisons significant at P < 0.03). There were no adverse cardiorespiratory events in either group. Conclusions: Findings demonstrate that i.v. clonidine administered after induction of anesthesia significantly reduces the incidence of EA in young children, but is associated with sleepiness postoperatively.
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