腹腔镜胃癌根治术后镇痛中地佐辛应用的有效性及对患者血流动力学的影响

摘要 目的：探讨腹腔镜胃癌根治术后镇痛中地佐辛应用的有效性及对患者血流动力学的影响。方法：选取2018年10月~2019年5月我院收治的需接受腹腔镜下胃癌根治术治疗患者120例,按照数字表法将其随机分为两组,对照组应用布托菲诺进行术后镇痛,研究组应用布托菲诺联合地佐辛进行术后镇痛,分析两组患者镇痛效果、炎症反应以及术后血流动力学改变情况,对比两组患者镇痛安全性。结果：研究组术后24 h、48 h疼痛视觉模拟评分（VisualAnalogueScale/Score,VAS）评分评分低于对照组（P＜0.05）,研究组术后6 h、12 h布氏舒适评分（Brinell Comfort Score,BCS）评分低于对照组（P＜0.05）;研究组术后24 h、48 h的白细胞介素-6（interleukin-6,IL-6）低于对照组（P＜0.05）,研究组术后24 h、48 h 的IL-2高于对照组（P＜0.05）;研究组术后6 h、12 h、24 h的简易精神状态量表（MMSE）评分高于对照组（P＜0.05）,研究组术前以及术后48 h与对照组无明显差异（P＞0.05）;研究组舒张压（diastolic blood pressure,DBP）、收缩压（systolic blood pressure ,SBP）以及心率（heart rate,HR）水平在麻醉前、气管拔管后5 min以及10 min时变化无明显差异（P＞0.05）,对照组HR、SBP以及DBP水平在气管拔管后5 min以及10 min时高于麻醉前（P＜0.05）,研究组气管拔管后5 min以及10 min时HR、SBP以及DBP水平低于对照组（P＜0.05）;研究组不良反应低于对照组（P＜0.05）。结论：在对腹腔镜胃癌根治术患者术后进行镇痛干预时,在布托菲诺的基础上联合使用地佐辛可有效降低对患者血流动力学的影响,提高镇痛效果,降低患者应激反应,且具有较高的安全性。     

多模式镇痛在全膝关节置换术中的疗效评价

目的：探讨联合关节周围注射镇痛药物和持续静脉镇痛的多模式镇痛对全膝关节置换术（total knee arthroplasty,TKA）患者功能恢复的疗效。方法：60例拟行单侧TKA的患者完全随机分为实验组（28例）和对照组（28例）。所有患者术前48 h开始服用塞来昔布（西乐葆）200 mg/次,每天2次。实验组患者术中膝关节周围注射镇痛药物,术后给予持续静脉镇痛（continuous intravenousanalgesia,CIA）。对照组患者没有运用关节周围注射药物,仅给予术后CIA。记录术后CIA用量、各时间点静止视觉模拟疼痛评分（rest visual analogue score,RVAS）、被动活动视觉模拟疼痛评分（passive visual analogue score,PVAS）和膝关节活动度（range of mo-tion,ROM）,同时观察药物的毒副作用。结果：（1）实验组术后24、48 h内PCA的用量均显著低于对照组（P〈0.05）。（2）实验组术后4、8、12、24、48 h的RVAS和24、48 h的PVAS均显著低于对照组（P〈0.05）;术后72 h两组间RVAS和PVAS的差异均无统计学差异（P〉0.05）。（3）实验组术后第1、2、3 d的ROM均显著高于对照组（P〈0.05）,术后第l、2 w两组ROM之间的差异无统计学意义（P〉0.05）;实验组术后主动屈膝到90？所需的天数显著低于对照组（P〈0.05）。（4）实验组中恶心、呕吐和追加药物的发生率均显著低于对照组（P〈0.05）,未发现伤口感染、延期愈合及组织坏死等并发症。结论：联合使用关节周围注射镇痛药物和持续静脉镇痛的多模式镇痛方案,可以有效的缓解TKA患者术后早期的疼痛,促进患者膝关节的功能恢复,减少了单一用药所产生的不良反应。该方案安全有效、操作简单,是一种值得推广的TKA术后镇痛方法。     

右美托咪定复合舒芬太尼自控镇痛对剖宫产产妇应激反应和炎症介质的影响

目的:探讨右美托咪定复合舒芬太尼自控镇痛对剖宫产产妇应激反应和炎症介质的影响。方法:选取2017年4月～2019年4月期间在我院行剖宫产术的产妇105例,根据乱数表法将患者分为研究组(n=53)和对照组(n=52),其中对照组采用舒芬太尼自控镇痛方案,研究组采用右美托咪定复合舒芬太尼自控镇痛方案,比较两组视觉疼痛模拟评分(VAS)、Ramsay镇静评分、应激反应和炎症介质指标,记录两组术后48 h内自控镇痛泵使用情况、镇痛期间不良反应发生情况。结果:两组术后2 h、12 h、24 h、48 h VAS评分均呈下降趋势,且研究组术后2 h、12 h、24 h、48 h VAS评分低于对照组(P0.05),研究组术后2 h、12 h、24 h、48 h Ramsay镇静评分高于对照组(P0.05)。两组术后48h血清皮质醇(Cor)、肿瘤坏死因子-α(TNF-α)、甲肾上腺素(NE)、C反应蛋白(CRP)、内皮素-1(ET-1)、白介素-10(IL-10)水平均升高,但研究组低于对照组(P0.05)。研究组术后48 h内舒芬太尼用量、镇痛泵按压次数均少于对照组(P0.05)。两组不良反应发生率比较无差异(P0.05)。结论:采用右美托咪定复合舒芬太尼自控镇痛方案可有效减轻剖宫产产妇应激反应并降低其炎症介质水平,同时还可减少舒芬太尼用量和镇痛泵按压次数,用药安全性较好,临床应用价值较高。     

Pre-emptive morphine treatment abolishes nerve injury-induced lysophospholipid synthesis in mass spectrometrical analysis

We have previously demonstrated that lysophosphatidic acid (LPA) production in the spinal cord following partial sciatic nerve injury (SCNI) and its signaling initiate neuropathic pain. In order to examine whether LPA production depends on the intense nociceptive signal, we have attempted to see suppression by pre-emptive treatment with centrally administered morphine, which mainly inhibits nociceptive signal at the level of spinal cord. In the present study, we developed a quantitative mass spectrometry assay to simultaneously analyze several species of lysophosphatidyl choline (LPC). The levels of 16:0-, 18:0- and 18:1-LPC in the spinal cord and dorsal root were maximally increased at 75 min after SCNI and then declined, as LPC is converted to LPA by autotaxin (ATX). In atx(+/-)-mice, on the other hand, these levels were similar to wild-type mice at 75 min, but maximal at 120 min, suggesting that this difference is partly due to the low conversion of LPC to LPA in atx(+/-)-mice. When morphine was centrally administered before SCNI, the injury-induced increase of LPC was completely abolished. These results suggest that LPC (or LPA) is produced by injury-induced nociceptive signal, which is effectively and pre-emptively suppressed by central morphine, possibly through known descending anti-nociceptive pathways.     

New approach for graded compression spinal cord injuries in Rhesus macaque: method feasibility and preliminary observations

Background Current models of spinal cord injury (SCI) have been ineffective for translational research. Primate blunt SCI, which more closely resembles human injury, could be a promising model to fill this gap. Methods Graded compression SCI was produced by inflating at T9 an epidural balloon as a function of spinal canal dimensions in a non‐uniform group of monkeys. Results Sham injury and cord compression by canal invasion of 50–75% produced minimal morpho‐functional alterations, if at all. Canal invasion of 90–100% resulted in proportional functional deficits. Unexpectedly, these animals showed spontaneous gradual recovery over a 12‐week period achieving quadruped walking, although with persistent absence of foot grasping reflex. Histopathology revealed predominance of central cord damage that correlated with functional status. Conclusions Our preliminary results suggest that this model could potentially be a useful addition to translational work, but requires further validation by including animals with permanent injuries and expansion of replicates.     

The relation of emotions to placebo responses

The hypothesis put forth is that expectations of treatment effects reduce negative emotions and thereby reduce symptoms, e.g. pain. Negative emotions increase pain, and it is hypothesized that placebos reduce pain by reducing negative emotions, i.e. feelings of nervousness, fear and anxiety. Placebo analgesia has been shown to be mediated via opioid activity, and relaxation increases opioid activity. The placebo acquires its relaxing effect due to verbal information that pain will be reduced, or due to associations between the placebo and the reduction in pain after effective treatment. Thus, the placebo signals that unpleasantness will be less after administration of the placebo. This involves negative reinforcement which is due to activation of a dopaminergic system that has been found to be activated during placebo analgesia and is involved in positive emotions. The nocebo effect of increased pain is, consistent with this model, because of increased fear and anxiety. The new aspect of the presented model is the hypothesis that expectations reduce negative emotions, and that negative reinforcement that involves the dopaminergic reinforcement system should be a contributor to placebo responses.     

Effects of melatonin and antagonists of MT1 and MT2 receptors on somatic pain induced within the fixed circadian rhythm

We studied behavioral pain-related reactions (PRRs) induced in mice by subcutaneous injections of 5% formalin within different phases of the fixed circadian illumination rhythm under conditions of administration of exogenous melatonin and of blocking of MT1 and MT2 melatonin receptors. It was demonstrated that modulation of experimentally induced somatic pain depends considerably on the phase of the preset circadian rhythm. In the norm, the duration of PRRs in the middle of the dark phase was 30% smaller than that in the middle of the light phase. Administration of exogenous melatonin in the middle of the light phase decreased the duration of episodes of noxious behavior by 43%, on average. Injections of melatonin within the dark phase resulted in no significant changes in the duration of PRRs. In the dark phase, the blockade of MT1 receptors by luzindole led to an increase in the duration of PRRs by 45%, as compared with the norm, while in the light phase we observed no significant alterations of this duration under conditions of blocking of the above-mentioned receptors. The blockade of MT2 receptors by prazocine in the middle of dark and light phases increased the durations of PRRs by 92 and 28%, respectively. Our data indicate that the analgesic effect of melatonin depends significantly on the level of this hormone in the organism; in turn, such a level is determined by the illumination conditions. The antinoxious effect of melatonin is mediated by MT receptors, in particular by MT2 receptors. Neirofiziologiya/Neurophysiology, Vol. 39, No. 3, pp. 255–259, May–June, 2007.     

Combination of pharmacological analgesics and microwave irradiation of an acupuncture point for suppression of visceral pain in mice: Role of the opioid and serotonergic cerebral systems

We studied suppression of pain-related reactions induced in mice by i.p. injection of 0.08 ml of a 2% solution of acetic acid using pharmacological analgesics (analgin and tramadol) combined with low-intensity microwave irradiation of an acupuncture point (AP) E-36 (frequency 30 to 300 GHz and power rate density 3·10⁻⁹ W/cm²). The respective effects were also observed under conditions of suppression of the functions of opioid and serotonergic cerebral systems using injections of, respectively, naloxone and DL-p-chlorophenylalanine (p-CPA). We found that antinociceptive effects provided by analgesics used in a 50% mean single dose in the combination with microwave irradiation of the AP were significantly more intense than those induced by isolated injection of analgesics used in both 50% and full mean single doses and isolated microwave irradiation of the AP E-36. After injections of naloxone, analgesic effects caused by the combined action of analgin and microwave irradiation of the AP were considerably smaller. At the same time, after injection of p-CPA, analgesic effects, provided by the combination of injection of pharmacological agents and microwave irradiation of the AP, weakened in the case of use of both analgesics. This was manifested in a significant increase in the total duration of pain-related behavioral reactions. Therefore, the studied analgesic effects observed in the examined animal groups are realized due to the involvement of the opioid and serotonergic cerebral systems. Neirofiziologiya/Neurophysiology, Vol. 39, No. 6, pp. 468–477, November–December, 2007.     

不同浓度罗哌卡因术后自控镇痛的临床观察

目的：比较三种不同浓度罗哌卡因的术后自控镇痛效果、运动阻滞及不良反应。方法：选择63例择期妇科手术病人．ASAⅠ～Ⅱ级,随机分为0．15％罗哌卡因（A组）、0．20％罗哌卡因（B组）和0．25％罗哌卡因（C组）,均复合5ng／L芬太尼,以持续剂量4ml／11,PCA剂量4ml,锁定时间30min硬膜外自控镇痛,观察各组镇痛效果、运动阻滞情况及不良反应发生率。结果：术后6、12、24h和48hVAS评分,A组显著高于B、C组;C组Bromage评分显著高于A、B组;镇静及并发症的发生率差异无显著性意义。结论：三组均适合妇科手术的术后镇痛,其中0．2％罗哌卡因术后镇痛效果好,无明显运动阻滞,病人更加舒适。     

Protective role of microRNA-374 against myocardial ischemia-reperfusion injury in mice following thoracic epidural anesthesia by downregulating dystrobrevin alpha-mediated Notch1 axis

Ischemia-reperfusion (I/R) injury often leads to myocardial apoptosis and necrosis. Studies have demonstrated the role microRNAs (miRs) played in myocardial I/R injury. Thus, we established a myocardial I/R injury model and a thoracic epidural anesthesia (TEA) model in mice to explore whether microRNA-374 (miR-374) affects myocardial I/R injury. We collected myocardial tissues to evaluate whether TEA exerts a protection effect on myocardial tissues. In addition, the levels of miR-374, dystrobrevin alpha (DTNA), and the statue of the Notch1 axis were detected. Subsequently, cardiomyocytes extracted from TEA mice were treated to regulate their levels of miR-374 and DTNA. After that, cell viability, cell cycle distribution, and apoptosis of cardiomyocytes were assessed. This was followed by the detection of the myocardial infarction area. The mice models of myocardial I/R injury were associated with poorly expressed miR-374 and highly expressed DTNA. TEA was found to protect myocardial tissues against myocardial I/R injury by elevating miR-374 and reducing DTNA. Dual-luciferase reporter assay validated that DTNA was the target gene of miR-374. Cardiomyocytes with overexpressed miR-374 were shown to have downregulated DTNA levels and blocked Notch1 axis. Overexpressed miR-374 was also found to promote the viability and inhibit the apoptosis of cardiomyocytes, as well as to increase the number of cells arrested in the S phase. In accordance with this, the myocardial infarction area was decreased with the upregulated miR-347 and downregulated DTNA. Collectively, these results demonstrated that, by inhibiting the activity of DTNA-mediated Notch1 axis, miR-374 could protect against myocardial I/R injury in mice after TEA.