ABSTRACT
Objective To evaluate the effects of a single preoperative dose of gabapentin on buprenorphine patient controlled intravenous analgesia after modified radical mastectorny. Methods Sixty female patients,ASA physical starus Ⅰ and Ⅱ undergoing modified radical mastectomy under general anesthesia were divided into two groups of 30 each group by random digits table to receive either gabapentin 1200 mg (gabapentin group) or a matching placebo (control group), administered orally 2 h before the induction of anesthesia. Subjects received patient controlled intravenous buprenorphi(n)e analgesia during thepostoperative period. Fifty-three patients finished this study, 28 cases in control group,25 cases in gabapentin group. Postoperative pain (static and dynamic),postoperative nausea and vomiting,anxiety,sedation were assessed by pain visual analogue scale(VAS), four-point ordinal scale, anxiety visual analogue scale, Ramsay sedation scale respectively. Postoperative buprenorphine consumption and time to first patient controlled analgesia were observed. Results Postoperative VAS (static and dynamic) was lower in gabapentin group than that in control group (P ＜0.05). Postoperative buprenorphine consumption was (506.1 ±37.9)μg , time to first patient controlled analgesia was (21.1 ±2.3)min,incidence rate of postoperative nausea and vomiting was 40.0% (10/25), antemetic rate was 12.0% (3/25), grade of anxiety was (28.5 ± 12.1) scores in gabapentin group, (699.8 ± 87.8)μ g, (4.3 ±0.8) min,64.3% (18/28),32.1%(9/28) and (66.3±15.7) scores in control group respectively. There were significant differences between two groups (P ＜ 0.05). Conclusion A single preoperative oral dose of gabapentin 1200 mg can effectively attenuate postoperative pain,reduce the consumption of buprenorphine,decrease the incidence rate of postoperative nausea and vomiting,improve patients' anxiety in patients undergoing modified radical mastectomy under general anesthesia.
ABSTRACT
BACKGROUND: Neuron-specific enolase, γtype isoenzyme that is specially present in the cytoplasm of neurons and neuroendocrine cells, is considered as a sensitive predictor for neuronal damage.OBJECTIVE: To observe the changes of serum neuron-specific enolase in patients with transient brain ischemic attack, so as to explore its relationship with the degree of neuronal damage.DESIGN: Case-control observation.SETTING: Department of Neurology, Jinan No. 4 People's Hospital.PARTICIPANTS: A total of 29 patients who were hospitalized in the Department of Neurology, Jinan No. 4 People's Hospital, due to transient brain ischemic attack (all called for emergent medical treatment within the onset of 6 hours) between March 2002 and May 2004 were enrolled in this study. There were 18 males and 11 females with the average age of(60.36t11.67) years. According to the duration of neural functional deficits, all subjects were divided into two groups, namely, transient-symptom group (≤ 6 hours) of 19 cases and lasting-symptom group (＞ 6 hours)of 10 cases. At the same time, 25 healthy controls, 15 males and 10 females with the average age of (62.34±9.65) years, rere selected from those who came for routine health examination.METHODS: Fasting elbow venous blood of 1 mL was collected only once from the subjects in control group; the same amount of blood was collected from the patients in transient ischemic attack group immediately after hospitalization, and at days 2, 3, 4 and 5. Roche Elecsys 2010 automatic analyzer was used to detect serum neuron-specific enolase. Neuronal damage was assessed with neurological deficit scale (defined as practical recovery if scores were reduced by 90%-100%; remarkable improvement if scores were reduced by 46%-89%; improvement if scores were reduced by 18%-45%; ineffective if scores were reduced by less than 17% or even the disease aggravated).MAIN OUTCOME MEASURES: The daily changes of serum neuronspecific enolase.RESULTS: All the54 subjects remained in the final result analysis. [1]Comparison of neuron-specific enolase density: It was significantly higher in transient brain ischemic attack group than in control group [(23.53±12.35) vs(14.29±6.83) μg/L, t=2.678, P ＜ 0.01]. [2] Curve of neuron-specific enolase changes during the acute stage: It began to increase at the early stage,reached the peak level on the next day, and gradually declined to the normal level in 4-5 days. [3] The level of serum neuron-specific enolase in the two groups with various durations of neurological deficit symptoms: It was obviously higher in transient-symptom group than in control group [(19.24±8.95)vs (14.29±6.83) μg/L, t=1.893, P ＜ 0.05], and higher in lasting-symptom group than in control group [(28.87±13.15) vs (14.29±6.83) μg/L, t=4.367,P ＜ 0.001]. [4] The level of neuron-specific enolase was positively correlated with the duration of neuronal damage (r=0.815, P＜0.01).CONCLUSION: Serum neuron-specific enolase increases within a short term after transient brain ischemic attack and reaches the peak level at around 24-36 hours, suggesting that the detection of serum neuron-specific enolase has a guiding value in assessing the severity of transient brain ischemic attack.