Time Characteristics of Shoulder Pain after Laparoscopic Surgery.

OBJECTIVE: To explore the time characteristics of shoulder pain after laparoscopic gynecological operation. METHODS: We conducted prospective clinical observations and literature review. We studied 442 cases of laparoscopic gynecological surgery. We used a visual analogue scale to evaluate the pain of patients at different time points after operation. We searched the English literature of shoulder pain after gynecological laparoscopic surgery. The observation time points of these studies included 12-24 hours or the first day after surgery, and at least one time point before this time point. RESULTS: The total incidence of shoulder pain was 68%. More than 90% of patients begin to feel shoulder pain on the first day after surgery, not on the day of surgery. 26 articles observed the severity of postlaparoscopic shoulder pain (PLSP) at different time points, of which 17 articles found that the intensity of the shoulder pain peaked at 12-24 hours or the first day after operation. DISCUSSION: The occurrence of PLSP presents obvious time characteristics. The incidence and severity of PLSP peaked on the first day or 12-24 hours after operation. To prevent and treat PLSP better, clinicians should make a more in-depth study according to the time characteristics of PLSP.

Effects of sevoflurane exposure during different stages of pregnancy on the brain development of rat offspring.

OBJECTIVE: This study explored the effects of sevoflurane exposure during different stages of pregnancy on the brain development of offspring. METHODS: Thirty-six pregnant SD rats were randomly divided into 4 groups: control, sevoflurane exposure in early (S1) pregnancy, sevoflurane exposure in middle (S2) pregnancy, and sevoflurane exposure in late (S3) pregnancy. After natural birth, the learning and memory capacity of offspring rats was analyzed using the Morris water maze experiment. The hippocampi of offspring rats were collected. The levels of interleukin (IL)-1ß, IL-6, and tumor necrosis factor (TNF)-α in the hippocampus were measured by ELISA. Additionally, the Nissl bodies in the hippocampus were analyzed using Nissl staining. Immunohistochemistry was used to examine the expression of BDNF and CPEB2 in the hippocampus of offspring. Proteins related to the NR4A1/NF-κB pathway were analyzed using western blotting. RESULTS: The memory and learning capacity of offspring rats was significantly reduced in the S1 and S2 groups compared to the control group (p < 0.05), while there was no obvious difference between the control and S3 groups (p > 0.05). The level of IL-1ß was significantly increased (p < 0.05) in the S1 group compared with the control group. Sevoflurane anesthesia received in early and middle pregnancy could significantly affect the formation of Nissl bodies in the hippocampi of offspring rats. In addition, the expression of BDNF and CPEB2 in the hippocampi of offspring rats was greatly decreased in the S1 group compared with the control group (p < 0.05). The expression of NR4A1 in the hippocampi of rat offspring was significantly decreased in the S1 and S2 groups compared with the control group (p < 0.05). The expression of proteins related to the NF-κB pathway was increased in the S1 group compared to the control group (p < 0.05). CONCLUSIONS: The neurotoxic effect of maternal sevoflurane anesthesia on the brain development of offspring is higher when the exposure occurs in early pregnancy than in late pregnancy, and its mechanism might involve the NR4A1/NF-κB pathway to increase the secretion of inflammatory cytokines.

Erythropoietin protects propofol induced neuronal injury in developing rats by regulating TLR4/NF-κB signaling pathway abstract.

OBJECTIVE: To explore the protective effect of erythropoietin on propofol induced neuronal injury in developing rats by regulating TLR4/NF-κB signaling pathway. METHOD: Rats were divided into normal control group (Control), propofol group (PPF), erythropoietin group (EPO), propofol + erythropoietin group (P + E), propofol + TAK-242 group (P + T), and propofol + EPO + LPS group (P + E+L) (n = 12). The pathology of hippocampal neurons was observed. The inflammatory factors were detected by ELISA. The expression of TLR4/NF-κB pathway-related proteins were detected by Western blot. RESULTS: Compared with the PPF group, the percentage of apoptotic cells in the hippocampal CA1 area of the erythropoietin treatment groups were greatly decreased while the percentage of positive cells in the hippocampus were remarkably increased(p < 0.05). The production of inflammatory factors and the expressions of TLR4/NF-κB pathway-related proteins were greatly improved in treatment groups (p < 0.05). Compared with P + E group, the percentage of apoptotic cells in CA1 area of the P + E+L group was significantly increased and the percentage of positive cells was remarkably reduced(p < 0.05), the levels of interleukin-1ß(IL-1ß), interleukin-6(IL-6), interleukin-8(IL-8) and tumor necrosis factor-α(TNF-α) were significantly increased and interleukin-4(IL-4) and interleukin-10(IL-10) was notably reduced(p < 0.05). The protein expression of TLR4 and p-P65 was significantly increased, while the protein expression of p-IκBαwas significantly decreased (p < 0.05). CONCLUSION: Erythropoietin has a protective effect on propofol induced neuropathic injury propofol in rats, and its mechanism is relevant to the regulation of TLR4/NF-κB signaling pathway.

Effect of Remifentanil Combined Anesthesia on Cytokines and Oxidative Stress in Patients undergoing Laparoscopic Surgery for Colon Cancer.

OBJECTIVE: To investigate the effect of remifentanil combined anesthesia on serum cytokines and oxidative stress indices in patients undergoing laparoscopic surgery for colon cancer. STUDY DESIGN: Experimental study. PLACE AND DURATION OF STUDY: Department of Anesthesiology, Yuhuangding Hospital Affiliated to Qingdao University, Yantai, China, from May 2016 to March 2018. METHODOLOGY: A total of 154 patients undergoing laparoscopic surgery for colon cancer were randomly divided into control group and observation group, with 77 cases in each group. Control group received fentanyl combined anesthesia, and observation group received remifentanil combined anesthesia. Levels of serum cytokines IL-8, IL-6, CRP, TNF- α and the levels of oxidative stress indices SOD, MDA, CAT, and GSH on the first day after operation were compared. Occurrence of adverse reactions during anesthesia recovery was observed and recorded in both groups. RESULTS: On the first day after surgery, levels of serum cytokines IL-8, IL-6, CRP, TNF- α and MDA in the observation group were lower than those in the control group (all p<0.001); levels of serum SOD, GSH, and CAT in the observation group were higher than those in the control group (all p<0.001). The frequency of adverse reactions such as nausea and vomiting, chills, restlessness, cough, and tachycardia in the observation group was lower than that in the control group (p=0.029, 0.016, 0.009, 0.025, and 0.003, respectively). CONCLUSION: Compared with fentanyl combined anesthesia, the remifentanil combined anesthesia can significantly reduce serum levels of cytokines IL-8, IL-6, CRP, TNF- α and oxidative stress level, and is, therefore, more secure for patients undergoing laparoscopic surgery for colon cancer.

miR-34a Inhibitor May Effectively Protect against Sevoflurane-Induced Hippocampal Apoptosis through the Wnt/ß-Catenin Pathway by Targeting Wnt1.

PURPOSE: Research has shown that sevoflurane-induced toxicity causes neurodegeneration in the developing brain. miR-34a has been found to negatively regulate ketamine-induced hippocampal apoptosis and memory impairment. However, the role of miR-34a in sevoflurane-induced hippocampal neurodegeneration remains largely unclear. MATERIALS AND METHODS: C57/BL6 mice (7-day-old) inhaled 2.3% sevoflurane for 2 h/day over 3 consecutive days. miR-34a expression was reduced through intracerebroventricular injection with miR-34a interference lentivirus vector (LV-anti-miR-34a) into mouse hippocampus after anesthesia on the first day of exposure. Hippocampal apoptosis was detected by TUNEL assay and flow cytometry analysis. Spatial memory ability was evaluated by the Morris water maze test. The interaction between miR-34a and Wnt1 was confirmed by luciferase reporter assay, RNA immunoprecipitation, Western blot, and immunofluorescence staining. The effects of miR-34a on protein levels of B-cell lymphoma 2 (Bcl-2), bcl-2-like protein 4 (Bax), and Wnt/ß-catenin pathway-related proteins were evaluated using Western blot analysis. RESULTS: Sevoflurane upregulated hippocampal miR-34a, and miR-34a inhibitor attenuated sevoflurane-induced hippocampal apoptosis and memory impairment. miR-34a negatively regulated Wnt1 expression by targeting miR-34a in hippocampal neurons. Moreover, forced expression of Wnt1 markedly undermined miR-34a-mediated enhancement of sevoflurane-induced apoptosis of hippocampal neurons, while Wnt1 silencing greatly restored anti-miR-34a-mediated repression of sevoflurane-induced apoptosis of hippocampal neurons. Increased expression of miR-34a inhibited the Wnt/ß-catenin pathway in hippocampal neurons exposed to sevoflurane, while anti-miR-34a exerted the opposite effects. CONCLUSION: miR-34a inhibitor may effectively protect against sevoflurane-induced hippocampal apoptosis via activation of the Wnt/ß-catenin pathway by targeting Wnt1.

Andrographolide protects mouse astrocytes against hypoxia injury by promoting autophagy and S100B expression

Andrographolide (ANDRO) has been studied for its immunomodulation, anti-inflammatory, and neuroprotection effects. Because brain hypoxia is the most common factor of secondary brain injury after traumatic brain injury, we studied the role and possible mechanism of ANDRO in this process using hypoxia-injured astrocytes. Mouse cortical astrocytes C8-D1A (astrocyte type I clone from C57/BL6 strains) were subjected to 3 and 21% of O2 for various times (0-12 h) to establish an astrocyte hypoxia injury model in vitro. After hypoxia and ANDRO administration, the changes in cell viability and apoptosis were assessed using CCK-8 and flow cytometry. Expression changes in apoptosis-related proteins, autophagy-related proteins, main factors of JNK pathway, ATG5, and S100B were determined by western blot. Hypoxia remarkably damaged C8-D1A cells evidenced by reduction of cell viability and induction of apoptosis. Hypoxia also induced autophagy and overproduction of S100B. ANDRO reduced cell apoptosis and promoted cell autophagy and S100B expression. After ANDRO administration, autophagy-related proteins, S-100B, JNK pathway proteins, and ATG5 were all upregulated, while autophagy-related proteins and s100b were downregulated when the jnk pathway was inhibited or ATG5 was knocked down. ANDRO conferred a survival advantage to hypoxia-injured astrocytes by reducing cell apoptosis and promoting autophagy and s100b expression. Furthermore, the promotion of autophagy and s100b expression by ANDRO was via activation of jnk pathway and regulation of ATG5.

Intraoperative use of dexmedetomidine promotes postoperative sleep and recovery following radical mastectomy under general anesthesia.

Postoperative sleep disturbance and fatigue following radical mastectomy were high risks for prolonged convalescence in patients with breast cancer. The present study was designed to observe the effect of intraoperative use of dexmedetomidine on postoperative sleep, fatigue and recovery following radical mastectomy under general anesthesia. Forty-seven patients were randomized into two groups that were maintained with propofol/remifentanil/Ringer's solution (Control group), or propofol/remifentanil/Dexmedetomidine (DEX group) for surgery under general anesthesia. During the first night following surgery, patients receiving dexmedetomine spent more time sleeping when compared with those form the Control group. During the first week following operation, when compared with the Control group, patients from the DEX group had a higher score of global 40-item recovery questionnaire on day 3 following operation, and lower 9-question fatigue severity scores on day 3 and day 7 following operation. In conclusion, intraoperative use of dexmedetomidine is sufficient to improve postoperative sleep disorder, promote postoperative recovery. The adverse effect of dexmedetomidine on sleep disturbance might be contributed to its recovery-promoting effect.

Effects of andrographolide on postoperative cognitive dysfunction and the association with NF-κB/MAPK pathway.

The present study investigated the effects of andrographolide on postoperative cognitive dysfunction (POCD) in aged rats to gain insight of the underlying mechanism, which may provide theoretical basis for the clinical application of andrographolide to prevent POCD in older patients. Thirty aged male rats were randomly assigned to 3 groups: Control, model and andrographolide groups. The Morris water maze test was used to examine the spatial memory and learning ability of the rats postoperatively. The histological alterations of neuronal cells in the hippocampus were visualized by H&E staining. The serum levels of neuron-specific enolase (NSE), human soluble protein-100ß (S-100ß) and the inflammation factors of interluekin (IL)-1ß, IL-6 and TNF-α involved in the nuclear factor κB (NF-κB)/mitogen-activated protein kinase (MAPK) signaling pathway were detected by ELISA. The NF-κB/MAPK signaling pathway-associated proteins in rat serum were detected by western blotting. Following andrographolide treatment, the rats significantly gained learning ability after surgery. Is it ameliorated hippocampal neuronal injury in rats following surgery. Andrographolide decreased NSE, S-100ß, and the inflammation factors, IL-6, IL-1ß and TNF-α in serum. Andrographolide reduced NF-κB/MAPK pathway-associated protein expression. Andrographolide ameliorated POCD in aged rats following surgery. The underlying mechanism may be associated with the downregulation the inflammatory factors and NF-κB/MAPK-associated protein expression.

THE INVESTIGATION OF EFFECT OF FLURBIPROFEN AXETIL ON THE TISSUE GROWTH AND THE CONTENT OF PGE2 IN CERVICAL CANCER.

The aim of this study was to investigate whether flurbiprofen axetil can inhibit the tissue growth and the content of PGE2 in cervical cancer or not. Fifty female BALB/c nude mice were randomly divided into control group (C), tumor + saline group (T), tumor + flurbiprofen axetil 10 mg/kg (Cfl0) group, tumor + flurbiprofen axetil 25 mg/kg (Cf25) group, tumor + flurbiprofen axetil tumor 50 mg/kg (Cf50), so that each group had 10 animals. Then, the animal model of human cervical carcinoma was established, and the relative tumor volume (RTV), relative tumor proliferation rate (T/C) and tumor inhibition rate were measured. The content of PGE2 in tumor tissue was determined by using enzyme-linked immunosorbent assay. There was no tumor formation in group C, and the time of tumor growth in other groups was non-statistically different. The RVT in Cf50 group was lower than in other groups. It was evident from the curve of tumor growth that the tumor weight in T group was evidently higher than that of administration groups (p < 0.01). The tumor inhibition rates of Cf10, Cf25 and Cf50 groups were 16.8, 19.6 and 36%, respectively, and the relative tumor proliferation rate were 85, 91 and 72%, respectively. The PGE, level of Cf50 was statistically (p < 0.01) lower than that of Cfl0 and Cf25 groups. Flurbiprofen axetil can inhibit the growth of cervical cancer transplanted tumor in nude mice and this inhibitory effect was maximal in Cf50 group. Flurbiprofen axetil can inhibit the production of PGE2 in tumor tissue of cervical carcinoma in nude mice.

Effect of preemptive analgesia with parecoxib sodium in patients undergoing radical resection of lung cancer.

OBJECTIVE: To discuss the effect of preemptive analgesia with parecoxib sodium in patients undergoing radical resection of lung cancer. METHODS: 115 cases of lung cancer patients with American society of anesthesiologists class (ASA) grade I~II who received selective operation were randomly divided into the research group and the control group. The research group patients were given preoperative parecoxib sodium 40 mg plus postoperative normal saline 2 ml, while the control group patients were treated with preoperative normal saline 2 ml plus postoperative parecoxib sodium 40 mg. The pain condition at postoperative 1, 2, 4, 8, 12, 24 and 48 h were evaluated by visual analogue scale (VAS), and emergence agitation was tested by agitation score. RESULTS: Finally there were 56 cases and 57 cases can be used for evaluation in the research group and control group. The VAS scores after 1, 2, 4, 8, 12, 24 and 48 h in the research group and control group were [2.23±0.45, 2.35±0.48, 2.51±0.51, 2.41±0.45, 2.28±0.42, 2.16±0.39, 2.11±0.40] and [3.80±0.62, 4.01±0.64, 4.31±0.67, 4.10±0.64, 3.65±0.70, 3.12±0.66, 2.46±0.53], respectively. The research group were obviously lower than the control group, the difference were statistically significant (P<0.05). The rate of agitation was 24.44% (11/56) in the research group, significantly lower than the control group of 59.65% (34/57) (P<0.05). CONCLUSION: Preemptive analgesia with parecoxib sodium can obviously relieve acute pain using in patients undergoing radical resection of lung cancer, and is helpful to reduce the incidence of emergence agitation.

The impact of anesthetic techniques on survival for patients with colorectal cancer: evidence based on six studies.

BACKGROUND/AIMS: Epidural-supplemented general anesthesia is perceived as a more beneficial method over general anesthesia since it reduces incidence of side effects, provides better postoperative pain relief and lowers the possibility to use immunosuppressive anesthetics. However, previous prospective and retrospective studies reported conflicting results in the effects of epidural anesthesia on post-operative outcomes of colorectal cancer surgery. Therefore, this study aims to pool available evidence to assess the association between epidural anesthesia and the post- operative outcomes in this group of patients. METHODOLOGY: Relevant studies were searched in databases and a meta-analysis was performed to estimate the association between epidural anesthesia and overall survival and recurrence free survival. RESULTS: Compared with the anesthetic choice without epidural anesthesia, epidural-supplemented anesthesia is associated with significantly longer overall survival (HR: 0.72, 95% CI: 0.55-0.94, p = 0.01) but not with prolonged recurrence free survival (HR: 1.06, 95% CI: 0.96-1.16, p = 0.23). These results showed a highlevel of robustness in sensitive test. CONCLUSION: Although epidural anesthesia might not lead to improved recurrence free survival, it had significant benefit in improving overall survival and reducing all-cause of death. It might be a useful anesthetic technique for colorectal cancer patients undergoing surgery. However, prospective studies are required to confirm whether this benefit is causative with epidural anesthesia.

Impact of epidural analgesia on quality of life and pain in advanced cancer patients.

Patients with advanced cancer often experience chronic postoperative pain and poor quality of life. The objective of this study was to determine if epidural self-controlled analgesia reduced the incidence of chronic pain and improved the quality of life when compared with intravenous self-controlled analgesia. A total of 50 patients diagnosed with advanced cancer who received analgesia treatment were randomly divided into two groups, epidural self-controlled analgesia group (EA group, n = 26) and intravenous self-controlled analgesia group (IA group, n = 24). Visual analog scale (VAS) and Karnofsky score were used to assess the pain and the quality of life, respectively. A multifunction monitor was used to continuously record the physical signs of patients after treatment. The physical signs, such as heart failure, respiration, pulse, blood pressure, and oxygen saturation, in the two groups were better after analgesia treatment. Meanwhile, the respiration and oxygen saturation in the EA group were significantly improved compared with that of the IA group (p < .05). The VAS in the EA group was significantly lower than that in the IA group (p < .05), and the Karnofsky score in the EA group was significantly higher than that in the IA group (p < .05). Moreover, patients treated with EA felt more satisfied and experienced fewer complications than those with IA (p < .05). The epidural self-controlled analgesia may greatly improve the quality of life and relieve the pain in patients with advanced cancer.

Biophysical study on the interaction of an anesthetic, vecuronium bromide with human serum albumin using spectroscopic and calorimetric methods.

The interactions between an anesthetic, vecuronium bromide (VB) and human serum albumin (HSA) have been investigated systematically by steady-state/time-resolved fluorescence, circular dichroism (CD), UV-vis absorption, Fourier transform infrared spectroscopy (FTIR), mass spectroscopy and differential scanning calorimetry (DSC) methods under physiological conditions. The fluorescence quenching observed is attributed to the formation of a complex between HSA and VB, and the reverse temperature effect of the fluorescence quenching has been found and discussed. Fluorescence analysis has proved that there is one classical binding site on HSA for VB with a relative weak binding constant of 1.07 × 10(4)M(-1) at 298 K. The primary binding pattern is determined by hydrogen bonding or van der Waals forces occurring in site I of HSA with ΔG°=-2.30 × 10(4)J mol(-1), ΔS°=-233 J mol(-1)K(-1) and ΔH°=-9.23 × 10(4)J mol(-1) at 298 K. VB could slightly change the secondary structure and induce unfolding of the polypeptides of protein. The DSC results provide quantitative information on the effect of VB on the stability of serum albumin. It is shown that VB can efficiently bind with HSA and be transported to the focuses needed.

Small interfering RNA-mediated knockdown of NF-κBp65 attenuates neuropathic pain following peripheral nerve injury in rats.

Recent reports show that the nuclear factor-κB (NF-κB) can control numerous genes encoding inflammatory and nociceptive mediators and play an important role in the development of central pain sensitization. The aim of the present study is to assess the role of NF-κB signal pathway and its downstream pro-inflammatory cytokines in the modulation of neuropathic pain, by using small interfering RNAs (siRNAs) technique, which has been shown to result in potent, long-lasting post-transcriptional silencing of specific genes. We developed a highly efficient method of lentivirus-mediated delivery of short-hairpin RNA (shRNA) targeting NF-κBp65 for gene silencing. This method successfully transduced LV-shNF-κBp65 into cultured spinal cord neurons in vitro and spinal cord cells in vivo, inhibited the expression of NF-κBp65 and pro-inflammatory factors (TNF-α, IL-1ß and IL-6) and alleviated mechanical allodynia and thermal hyperalgesia for more than 4weeks in chronic constriction injury (CCI) model of rats. Taken together, our results suggest that siRNA against NF-κBp65 is a potential strategy for analgesia. Furthermore, the lentiviral vector derived shRNA approach shows a great promise for the management of neuropathic pain and the study of functional NF-κBp65 gene expression.

Effect of inhalational anesthetics on cytotoxicity and intracellular calcium differently in rat pheochromocytoma cells (PC12).

Isoflurane, a commonly used inhaled anesthetic, induces apoptosis in rat pheochromocytoma cells (PC12) in a concentration-and time-dependent manner with unknown mechanism. We hypothesized that isoflurane induced apoptosis by causing abnormal calcium release from the endoplasmic reticulum (ER) via activation of inositol 1,4,5-trisphosphate (IP3) receptors. Alzheimer's presenilin-1 (PS1) mutation increased activity of IP3 receptors and therefore rendered cells vulnerable to isoflurane-induced cytotoxicity. Sevoflurane and desflurane had less ability to disrupt intracellular calcium homeostasis and thus being less potent to cause cytotoxicity. This study examined and compared the cytotoxic effects of various inhaled anesthetics on PC12 cells transfected with the Alzheimer's mutated PS1 (L286V) and the disruption of intracellular calcium homeostasis. PC12 cells transfected with wild type (WT) and mutated PS1 (L286V) were treated with equivalent of 1 MAC of isoflurane, sevoflurane and desflurane for 12 h. MTT reduction and LDH release assays were performed to evaluate cell viability. Changes of calcium concentration in cytosolic space ([Ca2+]c) were determined after exposing different types of cells to various inhalational anesthetics. The effects of IP3 receptor antagonist xestospongin C on isoflurane-induced cytotoxicity and calcium release from the ER in L286V PC12 cells were also determined. The results showed that isoflurane at 1 MAC for 12 h induced cytoxicity in L286V but not WT PC12 cells, which was also associated with greater and faster elevation of peak [Ca2+]c in L286V than in the WT cells. Xestospongin C significantly ameliorated isoflurane cytotoxicity in L286V cells, as well as inhibited the calcium release from the ER in L286V cells. Sevoflurane and desflurane at equivalent exposure to isoflurane did not induce similar cytotoxicity or elevation of peak [Ca2+]c in L286V PC12 cells. These results suggested that isoflurane induced cytoxicity by partially causing abnormal calcium release from the ER via activation of IP3 receptors in L286V PC12 cells. Sevoflurane and desflurane at equivalent exposure to isoflurane did not induce similar elevation of [Ca2+]c or neurotoxicity in PC12 cells transfected with the Alzheimer's PS1 mutation.

[Influence of various ventilation manier on rat's lung and the expression of lung endotoxin receptor CD14 mRNA].

OBJECTIVE: To observe the influence of mechanical ventilation (MV) on rat's lung and the expression changes of lung endotoxin receptor CD14 mRNA. METHODS: Forty-eight male SD rats weighing 330-360 g were randomly divided into 4 groups (n = 12 each): group R received no mechanical ventilation, group P received small MV (VT = 6 ml/kg, PEEP = 8 mm Hg), group M received conventional MV (VT = 12 ml/kg, PEEP = 0 mm Hg), and group N received large tidal volume mechanical ventilation (VT = 40 ml/kg, PEEP = 0 mm Hg). The animals were anesthetized with intraperitoneal pentobarbital 100 mg x kg(-1), tracheotomized and mechanically ventilated (I:E = 1:1, FiO2 = 21%). The respiratory rate (RR) of MV was adjusted to maintain the end-tidal carbon dioxide in the rang of 35-45 mm Hg throughout the procedure. Right carotid artery and left femoral vein were cannulated for BP monitoring and fluid and drug administration. 6 rats in each group were injected 50 mg/kg Evans Blue (EB). The experiment was culminated in 3 hours, then the rats were killed by exsanguination via arteria carotis interna. Morphologic change scores of the rats' lungs, wet/dry weight ratio of lung tissue (W/D), bronchial lavage fluid (BALF) inflammatory cell population, and permeability of vessel wall were evaluated. The concentration of TNF-alpha and MIP-2 in the plasma were determined by enzyme immunoassay method (ELISA). The expressions of lung tissue endotoxin receptor CD14 were detected by RT-PCR, macrophage CD14 in BALF was also detected by immunohistochemistry. RESULTS: pulmonary pathomorphology scores: there were no alteration in R group and P group, but it were slightly increased in M group, there was significantly elevated in N group as compare to M group (F = 8.0, P = 0.000). Pulmonary tissue wet/dry weight ratio (W/D): Compare with R group, There was no statistically significant difference in P group and M group; the elevation in N group (t = 4.103, P = 0.02), EB: Compare with R group, There was no statistically significant difference in P group and M group; the obviously elevation in N group (t = 36.634, P = 0.000). WBC in BALF: Compare with R group, there was no change in P group, the elevation in M group (t = 4.272, P = 0.02), there was significantly elevated in N group (F = 26.68, P = 0.000). TNF-alpha had no manifest variation in 4 groups. MIP-2: compare with R group (31.5 +/- 2.4), There was no statistically significant difference in P group (35.4 +/- 5.3), the elevation in M group (44.7 +/- 6.9, t = 7.85, P = 0.04), there was significantly elevated in N group (167.7 +/- 11.8, t = 27.779, P = 0.000). The expressions of macrophage CD14 protein in BALF and lung tissue CD14 mRNA were fundamentally coincident in R group and P group; the expressions of CD14 mRNA were elevated, but the expressions of CD14 protein were no change in M group; the expressions of CD14 in N group manifestly elevated (P = 0.000). CONCLUSIONS: Conventional MV induces minor injury in rat's lung and can up regulate the expression of CD14 mRNA in the lung, but not up regulate the expression of CD14 protein; large tidal volume MV induces injury of rat's lung and evidently up regulates CD14 expression in the lung. Protective MV can avoid the above mentioned variations in rat's lung.