Change of alveolar epithelial type Ⅱ cells and pulmonary surfactant protein A in young rats with acute lung injury

Objective To study the temporal changes of alveolar epithelial type Ⅱ cells and surfactant pro-tein A in young rats with acute lung injury induced by lipopolysaecharide. Method Totally 110 SD young rats (male:53, female : 57) were randomly divided into ALI and normal control groups (six subgroups in each group).LPS(4 mg/kg) was given intraperitoneally in ALI group. The same amount of normal saline was given in the con-trol groups. Eight rats in each subgroup were sacrificed at 6, 12, 24, 36, 48 and 72 hours after the injection.Lung samples were taken for transmission electron microscope examination. RT-PCR was epmloyed for the mea-surement of SP-A mRNA. Western blot was used for the detection of SP-A in the lung tissue. ANOVA and homo-geneity of variance test were performed by SPSS 12.0. Results The microvilli disappeared at 24 hours after the injection of LPS. The number of lamellar body (LBs) was provisionality increased at 24 hours and 48 hours. The ring-like an'angement of LBs around nucleus and the giant LB with vacuole-like deformity were found as the main characteristics of AEC- Ⅱ in ALI at 48 hours. The number of LBs reduced and broken and residual LB remained at 72 hours. SP-A elevated greatly from 24 to 48 hours (P < 0.01), reached peak at 36 hours (6.94 ± 0.80, P <0.01),reached the lowest level(3.87 ±0.50, P <0.01)at 72 hours. Conclusions The pathological changes of AEC-Ⅱ and SP-A in lung tissue wiht ALI are time-dependent. The typical alterations of AEC- Ⅱ occurs at 48 hours accompanied by the compensatory increase of SP-A. AEC- Ⅱ is seriously injuried with the typical changes of LBs and the diminishing of SP-A in lung tissue.     

Change of alveolar epithelial type Ⅱ cells and pulmonary surfactant protein A in young rats with acute lung injury

Objective To study the temporal changes of alveolar epithelial type Ⅱ cells and surfactant pro-tein A in young rats with acute lung injury induced by lipopolysaecharide. Method Totally 110 SD young rats (male:53, female : 57) were randomly divided into ALI and normal control groups (six subgroups in each group).LPS(4 mg/kg) was given intraperitoneally in ALI group. The same amount of normal saline was given in the con-trol groups. Eight rats in each subgroup were sacrificed at 6, 12, 24, 36, 48 and 72 hours after the injection.Lung samples were taken for transmission electron microscope examination. RT-PCR was epmloyed for the mea-surement of SP-A mRNA. Western blot was used for the detection of SP-A in the lung tissue. ANOVA and homo-geneity of variance test were performed by SPSS 12.0. Results The microvilli disappeared at 24 hours after the injection of LPS. The number of lamellar body (LBs) was provisionality increased at 24 hours and 48 hours. The ring-like an'angement of LBs around nucleus and the giant LB with vacuole-like deformity were found as the main characteristics of AEC- Ⅱ in ALI at 48 hours. The number of LBs reduced and broken and residual LB remained at 72 hours. SP-A elevated greatly from 24 to 48 hours (P < 0.01), reached peak at 36 hours (6.94 ± 0.80, P <0.01),reached the lowest level(3.87 ±0.50, P <0.01)at 72 hours. Conclusions The pathological changes of AEC-Ⅱ and SP-A in lung tissue wiht ALI are time-dependent. The typical alterations of AEC- Ⅱ occurs at 48 hours accompanied by the compensatory increase of SP-A. AEC- Ⅱ is seriously injuried with the typical changes of LBs and the diminishing of SP-A in lung tissue.     

Change of alveolar epithelial type Ⅱ cells and pulmonary surfactant protein A in young rats with acute lung injury

Objective To study the temporal changes of alveolar epithelial type Ⅱ cells and surfactant pro-tein A in young rats with acute lung injury induced by lipopolysaecharide. Method Totally 110 SD young rats (male:53, female : 57) were randomly divided into ALI and normal control groups (six subgroups in each group).LPS(4 mg/kg) was given intraperitoneally in ALI group. The same amount of normal saline was given in the con-trol groups. Eight rats in each subgroup were sacrificed at 6, 12, 24, 36, 48 and 72 hours after the injection.Lung samples were taken for transmission electron microscope examination. RT-PCR was epmloyed for the mea-surement of SP-A mRNA. Western blot was used for the detection of SP-A in the lung tissue. ANOVA and homo-geneity of variance test were performed by SPSS 12.0. Results The microvilli disappeared at 24 hours after the injection of LPS. The number of lamellar body (LBs) was provisionality increased at 24 hours and 48 hours. The ring-like an'angement of LBs around nucleus and the giant LB with vacuole-like deformity were found as the main characteristics of AEC- Ⅱ in ALI at 48 hours. The number of LBs reduced and broken and residual LB remained at 72 hours. SP-A elevated greatly from 24 to 48 hours (P < 0.01), reached peak at 36 hours (6.94 ± 0.80, P <0.01),reached the lowest level(3.87 ±0.50, P <0.01)at 72 hours. Conclusions The pathological changes of AEC-Ⅱ and SP-A in lung tissue wiht ALI are time-dependent. The typical alterations of AEC- Ⅱ occurs at 48 hours accompanied by the compensatory increase of SP-A. AEC- Ⅱ is seriously injuried with the typical changes of LBs and the diminishing of SP-A in lung tissue.     

Change of alveolar epithelial type Ⅱ cells and pulmonary surfactant protein A in young rats with acute lung injury

Objective To study the temporal changes of alveolar epithelial type Ⅱ cells and surfactant pro-tein A in young rats with acute lung injury induced by lipopolysaecharide. Method Totally 110 SD young rats (male:53, female : 57) were randomly divided into ALI and normal control groups (six subgroups in each group).LPS(4 mg/kg) was given intraperitoneally in ALI group. The same amount of normal saline was given in the con-trol groups. Eight rats in each subgroup were sacrificed at 6, 12, 24, 36, 48 and 72 hours after the injection.Lung samples were taken for transmission electron microscope examination. RT-PCR was epmloyed for the mea-surement of SP-A mRNA. Western blot was used for the detection of SP-A in the lung tissue. ANOVA and homo-geneity of variance test were performed by SPSS 12.0. Results The microvilli disappeared at 24 hours after the injection of LPS. The number of lamellar body (LBs) was provisionality increased at 24 hours and 48 hours. The ring-like an'angement of LBs around nucleus and the giant LB with vacuole-like deformity were found as the main characteristics of AEC- Ⅱ in ALI at 48 hours. The number of LBs reduced and broken and residual LB remained at 72 hours. SP-A elevated greatly from 24 to 48 hours (P < 0.01), reached peak at 36 hours (6.94 ± 0.80, P <0.01),reached the lowest level(3.87 ±0.50, P <0.01)at 72 hours. Conclusions The pathological changes of AEC-Ⅱ and SP-A in lung tissue wiht ALI are time-dependent. The typical alterations of AEC- Ⅱ occurs at 48 hours accompanied by the compensatory increase of SP-A. AEC- Ⅱ is seriously injuried with the typical changes of LBs and the diminishing of SP-A in lung tissue.     

Change of alveolar epithelial type Ⅱ cells and pulmonary surfactant protein A in young rats with acute lung injury

Objective To study the temporal changes of alveolar epithelial type Ⅱ cells and surfactant pro-tein A in young rats with acute lung injury induced by lipopolysaecharide. Method Totally 110 SD young rats (male:53, female : 57) were randomly divided into ALI and normal control groups (six subgroups in each group).LPS(4 mg/kg) was given intraperitoneally in ALI group. The same amount of normal saline was given in the con-trol groups. Eight rats in each subgroup were sacrificed at 6, 12, 24, 36, 48 and 72 hours after the injection.Lung samples were taken for transmission electron microscope examination. RT-PCR was epmloyed for the mea-surement of SP-A mRNA. Western blot was used for the detection of SP-A in the lung tissue. ANOVA and homo-geneity of variance test were performed by SPSS 12.0. Results The microvilli disappeared at 24 hours after the injection of LPS. The number of lamellar body (LBs) was provisionality increased at 24 hours and 48 hours. The ring-like an'angement of LBs around nucleus and the giant LB with vacuole-like deformity were found as the main characteristics of AEC- Ⅱ in ALI at 48 hours. The number of LBs reduced and broken and residual LB remained at 72 hours. SP-A elevated greatly from 24 to 48 hours (P < 0.01), reached peak at 36 hours (6.94 ± 0.80, P <0.01),reached the lowest level(3.87 ±0.50, P <0.01)at 72 hours. Conclusions The pathological changes of AEC-Ⅱ and SP-A in lung tissue wiht ALI are time-dependent. The typical alterations of AEC- Ⅱ occurs at 48 hours accompanied by the compensatory increase of SP-A. AEC- Ⅱ is seriously injuried with the typical changes of LBs and the diminishing of SP-A in lung tissue.     

Change of alveolar epithelial type Ⅱ cells and pulmonary surfactant protein A in young rats with acute lung injury

Objective To study the temporal changes of alveolar epithelial type Ⅱ cells and surfactant pro-tein A in young rats with acute lung injury induced by lipopolysaecharide. Method Totally 110 SD young rats (male:53, female : 57) were randomly divided into ALI and normal control groups (six subgroups in each group).LPS(4 mg/kg) was given intraperitoneally in ALI group. The same amount of normal saline was given in the con-trol groups. Eight rats in each subgroup were sacrificed at 6, 12, 24, 36, 48 and 72 hours after the injection.Lung samples were taken for transmission electron microscope examination. RT-PCR was epmloyed for the mea-surement of SP-A mRNA. Western blot was used for the detection of SP-A in the lung tissue. ANOVA and homo-geneity of variance test were performed by SPSS 12.0. Results The microvilli disappeared at 24 hours after the injection of LPS. The number of lamellar body (LBs) was provisionality increased at 24 hours and 48 hours. The ring-like an'angement of LBs around nucleus and the giant LB with vacuole-like deformity were found as the main characteristics of AEC- Ⅱ in ALI at 48 hours. The number of LBs reduced and broken and residual LB remained at 72 hours. SP-A elevated greatly from 24 to 48 hours (P < 0.01), reached peak at 36 hours (6.94 ± 0.80, P <0.01),reached the lowest level(3.87 ±0.50, P <0.01)at 72 hours. Conclusions The pathological changes of AEC-Ⅱ and SP-A in lung tissue wiht ALI are time-dependent. The typical alterations of AEC- Ⅱ occurs at 48 hours accompanied by the compensatory increase of SP-A. AEC- Ⅱ is seriously injuried with the typical changes of LBs and the diminishing of SP-A in lung tissue.     

Change of alveolar epithelial type Ⅱ cells and pulmonary surfactant protein A in young rats with acute lung injury

Objective To study the temporal changes of alveolar epithelial type Ⅱ cells and surfactant pro-tein A in young rats with acute lung injury induced by lipopolysaecharide. Method Totally 110 SD young rats (male:53, female : 57) were randomly divided into ALI and normal control groups (six subgroups in each group).LPS(4 mg/kg) was given intraperitoneally in ALI group. The same amount of normal saline was given in the con-trol groups. Eight rats in each subgroup were sacrificed at 6, 12, 24, 36, 48 and 72 hours after the injection.Lung samples were taken for transmission electron microscope examination. RT-PCR was epmloyed for the mea-surement of SP-A mRNA. Western blot was used for the detection of SP-A in the lung tissue. ANOVA and homo-geneity of variance test were performed by SPSS 12.0. Results The microvilli disappeared at 24 hours after the injection of LPS. The number of lamellar body (LBs) was provisionality increased at 24 hours and 48 hours. The ring-like an'angement of LBs around nucleus and the giant LB with vacuole-like deformity were found as the main characteristics of AEC- Ⅱ in ALI at 48 hours. The number of LBs reduced and broken and residual LB remained at 72 hours. SP-A elevated greatly from 24 to 48 hours (P < 0.01), reached peak at 36 hours (6.94 ± 0.80, P <0.01),reached the lowest level(3.87 ±0.50, P <0.01)at 72 hours. Conclusions The pathological changes of AEC-Ⅱ and SP-A in lung tissue wiht ALI are time-dependent. The typical alterations of AEC- Ⅱ occurs at 48 hours accompanied by the compensatory increase of SP-A. AEC- Ⅱ is seriously injuried with the typical changes of LBs and the diminishing of SP-A in lung tissue.     

Change of alveolar epithelial type Ⅱ cells and pulmonary surfactant protein A in young rats with acute lung injury

Objective To study the temporal changes of alveolar epithelial type Ⅱ cells and surfactant pro-tein A in young rats with acute lung injury induced by lipopolysaecharide. Method Totally 110 SD young rats (male:53, female : 57) were randomly divided into ALI and normal control groups (six subgroups in each group).LPS(4 mg/kg) was given intraperitoneally in ALI group. The same amount of normal saline was given in the con-trol groups. Eight rats in each subgroup were sacrificed at 6, 12, 24, 36, 48 and 72 hours after the injection.Lung samples were taken for transmission electron microscope examination. RT-PCR was epmloyed for the mea-surement of SP-A mRNA. Western blot was used for the detection of SP-A in the lung tissue. ANOVA and homo-geneity of variance test were performed by SPSS 12.0. Results The microvilli disappeared at 24 hours after the injection of LPS. The number of lamellar body (LBs) was provisionality increased at 24 hours and 48 hours. The ring-like an'angement of LBs around nucleus and the giant LB with vacuole-like deformity were found as the main characteristics of AEC- Ⅱ in ALI at 48 hours. The number of LBs reduced and broken and residual LB remained at 72 hours. SP-A elevated greatly from 24 to 48 hours (P < 0.01), reached peak at 36 hours (6.94 ± 0.80, P <0.01),reached the lowest level(3.87 ±0.50, P <0.01)at 72 hours. Conclusions The pathological changes of AEC-Ⅱ and SP-A in lung tissue wiht ALI are time-dependent. The typical alterations of AEC- Ⅱ occurs at 48 hours accompanied by the compensatory increase of SP-A. AEC- Ⅱ is seriously injuried with the typical changes of LBs and the diminishing of SP-A in lung tissue.     

The role of erlotinib in the acute lung injury and the expression of surfactant protein A北大核心CSCD

Objective: To investigate the role of erlotinib in the expression of surfactant protein A (SP-A) in LPS-induced acute lung injury (ALI) of mice model. Methods: C57BL/6 mice were randomly (random number) divided into control group (n=6), ER group (n=6), LPS group (n=6), and ER+LPS group (n=6). In the LPS group, 2 mg/kg LPS was instilled into trachea of mice to induce lung injury. In control group, normal saline was instilled into trachea of mice instead. In the ER+LPS group and ER group, 100 mg/kg of erlotinib was instilled into stomach of mice, and one hour later. 2 mg/kg LPS was instilled into trachea of mice in ER+PLS group to induce lung injury. Twenty-four hours later, bronchoalveolar lavage fluid (BALF) and lung tissue of mice in four groups were collected. HE staining were used for evaluating pathological changes of lung injury. Lung wet/dry weight ratio, protein concentrations and total cell numbers in the BALF were measured to determine the degree of pulmonary edema. Immunohistochemical staining and Western Blot were used for testing the protein expression of SP-A, Data of multiple groups were analyzed by one way variance (ANOVA) and inter-group comparisons were made by the least significant difference (LSD) tests. Results: There was no significant difference in lung injury score (LIS) between control group (0.056±0.008) and ER (0.064±0.037) group, The LIS in LPS group (0.846±0.047) was higher than that in control group, however the LIS in ER+LPS group (0.279±0.020) was significant lower than that in LPS group (P < 0.05). Lung wet/dry weight, SP-A concentration and total cell numbers in the bronchoalveolar lavage fluid revealed that the degree of pulmonary edema in LPS group was higher than that in control group, and this pulmonary edema was reversed by erlotinib treatment. Immunohistochemical staining and Western blot showed that the expression of SP-A in LPS group was decreased compared with control group, but it was recovered after erlotinib treatment (P < 0.05). Conclusions: Erlotinib could protect the LPS-induced ALI, and it may be related to the regulation of SP-A. © 2018 Chinese Medical Association. All rights reserved.     

Change of alveolar epithelial type Ⅱ cells and pulmonary surfactant protein A in young rats with acute lung injury

Objective To study the temporal changes of alveolar epithelial type Ⅱ cells and surfactant pro-tein A in young rats with acute lung injury induced by lipopolysaecharide. Method Totally 110 SD young rats (male:53, female : 57) were randomly divided into ALI and normal control groups (six subgroups in each group).LPS(4 mg/kg) was given intraperitoneally in ALI group. The same amount of normal saline was given in the con-trol groups. Eight rats in each subgroup were sacrificed at 6, 12, 24, 36, 48 and 72 hours after the injection.Lung samples were taken for transmission electron microscope examination. RT-PCR was epmloyed for the mea-surement of SP-A mRNA. Western blot was used for the detection of SP-A in the lung tissue. ANOVA and homo-geneity of variance test were performed by SPSS 12.0. Results The microvilli disappeared at 24 hours after the injection of LPS. The number of lamellar body (LBs) was provisionality increased at 24 hours and 48 hours. The ring-like an'angement of LBs around nucleus and the giant LB with vacuole-like deformity were found as the main characteristics of AEC- Ⅱ in ALI at 48 hours. The number of LBs reduced and broken and residual LB remained at 72 hours. SP-A elevated greatly from 24 to 48 hours (P < 0.01), reached peak at 36 hours (6.94 ± 0.80, P <0.01),reached the lowest level(3.87 ±0.50, P <0.01)at 72 hours. Conclusions The pathological changes of AEC-Ⅱ and SP-A in lung tissue wiht ALI are time-dependent. The typical alterations of AEC- Ⅱ occurs at 48 hours accompanied by the compensatory increase of SP-A. AEC- Ⅱ is seriously injuried with the typical changes of LBs and the diminishing of SP-A in lung tissue.     

Anesthesia (9)

Lumbar plexus clock reduces pain and blood loss associated with total hip arthroplasty. (Hôpitaux Universitaires de Genéve, Geneva, Switzerland) Anesthesiology 2000;93:115–121. In this study, 60 patients undergoing total hip arthroplasty were randomized to receive general anesthesia with (plexus group, n = 30) or without (control group, n = 30) a posterior lumbar plexus block. The block was performed after induction using a nerve stimulator, and 0.4 mL/kg bupivacaine, 0.5%, with epinephrine was injected. General anesthesia was standardized, and supplemental fentanyl was administered per hemodynamic guidelines. Postoperative pain and patient‐controlled intravenous morphine use were serially assessed for 48 h. The proportion of patients receiving supplemental fentanyl intraoperatively was more than 3 times greater in the control group (20 of 30 vs. 6 of 29, P = 0.001). In the postanesthesia care unit, a greater than fourfold reduction in pain scores was observed in the plexus group and “rescue” morphine boluses were administered 10 times less frequently. Pain scores and morphine consumption remained significantly lower in the plexus group until 6 h after randomization. Operative and postoperative (48 h) blood loss was decreased modestly in the treated group. Epidural‐like distribution of anesthesia occurred in 3 of 28 plexus group patients, but no other side effects were noted. Conclude that posterior lumbar plexus block provides effective analgesia for total hip arthroplasty, reducing intraoperative and postoperative opioid requirements. Blood loss during and after the procedure is diminished. Epidural anesthetic distribution should be anticipated in a minority of cases. Comment by Alan David Kaye, MD, PhD. The benefits of regional anesthetic techniques are well established for patients undergoing total hip arthroplasty. For example, it is common knowledge to the clinical anesthesiologist that regional anesthesia results in reduced blood loss as well as a reduction in thromboembolic events postoperatively. This interesting study considered a posterior lumbar plexus block since a significant portion of the hip is innervated via branches of the lumbar plexus. A randomized, double‐blinded trial of 60 consecutive patients undergoing total hip arthroplasty under general anesthesia was performed. Thirty patients had general anesthesia alone and 30 patients had general anesthesia with the lumbar plexus block. Pain scores and morphine consumption postoperatively were evaluated over a 48‐h period. Patients in the control group required supplemental narcotic (20/30) versus those in the lumbar plexus block group (6/30). No BIS monitor was employed simply with the end point of additional analgesic being an increase in blood pressure or heart rate greater than 130% of the baseline. Epidural‐like distribution of anesthesia occurred in 3 of 28 patients receiving the block. Incidence of nausea and vomiting was similar in both groups and pain scores were significantly lower until the 6‐h period postoperatively. There was a block‐associated reduction in hemorrhage. These results are not surprising; however, it would be unlikely that this block would be done in a repeated series and the authors describe a continuous catheter‐based technique, which they have presented in abstract form for longer‐term postoperative pain relief. The associated complications with this block must be weighed with these positive and predictable findings. The complexity of proper placement of this block compared with other regional techniques and its potential side effects would make this block difficult to implement in the operating room. The authors should be complemented for this study and great consideration for its potential benefits in clinical practice should be considered.     

Antiherpes effects and pharmacokinetic properties of 9-(4-hydroxybutyl) guanine and the (R) and (S) enantiomers of 9-(3,4-dihydroxybutyl)guanine.

Three acyclic guanosine analogs with similar structures, the (R) and (S) forms of 9-(3,4-dihydroxybutyl)guanine and 9-(4-hydroxybutyl)guanine, were compared for antiherpes activity in vivo and in vitro. The three guanosine analogs were viral thymidine kinase-dependent inhibitors of virus multiplication. In cell cultures, (S)-9-(3,4-dihydroxybutyl)guanine was the least active of these three drugs against a variety of herpes simplex virus type 1 (HSV-1) and type 2 (HSV-2) strains. This was also the case for a certain HSV-1 or HSV-2 strain in different cell lines. In cell cultures, (R)-9-(3,4-dihydroxybutyl)guanine and 9-(4-hydroxybutyl)guanine had similar antiherpes activities. However, in vivo in cutaneous HSV-1 infections in guinea pigs treated topically and in systemic HSV-2 infections in mice treated orally or intraperitoneally, only (R)-9-(3,4-dihydroxybutyl)guanine had a therapeutic effect. The extremely short half-life in plasma and the high clearance of 9-(4-hydroxybutyl)guanine as compared with those of (R)-9-(3,4-dihydroxybutyl)guanine probably made 9-(4-hydroxybutyl)guanine inefficacious when given intraperitoneally or orally to mice infected with herpesvirus. On the other hand, no kinetic differences between (R)-9-(3,4-dihydroxybutyl)guanine and 9-(4-hydroxybutyl)guanine were observed in penetration through guinea pig skin ex vivo, and no preferential metabolism of 9-(4-hydroxybutyl)guanine in skin was noted. We deduced that high thymidine levels in guinea pig skin preferentially antagonize the antiviral effect of 9-(4-hydroxybutyl) guanine in cutaneous HSV-1 infections.     

Open study of 2-amino-9-(hydroxyethoxymethyl)-9H-purine (desciclovir) in the treatment of herpes zoster

An oral pro-drug of acyclovir, 2-amino-9-(2-hydroxyethoxymethyl)-9H-purine (desciclovir) was evaluated in an open study comprising of 20 patients with herpes zoster. The clinical effects were comparable to those obtained with oral and intravenous acyclovir, even with a dosage of only 125 mg thrice daily. There was adequate absorption though considerable individual variation occurred. No effects of concomitant food intake were demonstrated. The finding of possible impaired conversion of desciclovir to acyclovir in one patient was unexplained and deserves attention in future studies. Likewise, more studies are needed to understand the occurrence of transient high peak plasma concentrations of acyclovir. Side-effects other than those already known with the use of acyclovir, namely reversible tubular damage, were not observed.     

假性甲状旁腺功能减退症9例临床分析

目的:提高临床医生对假性甲状旁腺功能减退症的认识。方法:对9例假性甲状旁腺功能减退症进行回顾性分析。结果:男3例,女6例。临床特征:(1)病程1月~13年;(2)起病年龄6~14岁;(3)所有患者均为散发,无家族史;(4)5例以癫痫起病,3例以低钙抽搐起病,1例以生长发育迟缓就诊;(5)患者均有明显低血钙(1.22~1.59mmol/L)、高血磷(1.53~3.35mmol/L)和甲状旁腺激素水平升高(12.52~159.0pmol/L);(6)首次发病后有6例曾被误诊。5例被误诊为癫痫,1例误诊为脑囊虫病;(7)1例合并甲状腺功能低下,5例有Albright骨营养不良(AHO);(8)9例患者均有颅内钙化,其中8例有双侧基底节区钙化,2例小脑齿状核钙化。结论:该病常于儿童起病,患者易被误诊为癫痫。为降低误诊率,临床医生需提高对该病的认识,对于儿童期发病,有或无家族史伴低血钙和先天性发育畸形者尤应注意。应进一步作血钙、血磷、血甲状旁腺和甲状腺激素水平及头颅CT检查。     

前入路腹腔镜肾上腺肿瘤切除术9例报告

目的　探讨前入路腹腔镜技术在肾上腺手术中的应用。方法　 2 0 0 1年 10月～ 2 0 0 2年 8月共行前入路腹腔镜肾上腺切除术 9例。其中原发性醛固酮增多症 5例 ,嗜铬细胞瘤 3例 ,皮质醇增多症 1例。结果　 9例手术均获得成功。手术时间 80～ 2 3 0min ,平均 (12 8± 5 8 6)min。 5 0～ 2 10ml,平均出血 (96± 43 )ml。所有患者术中及术后均未输血 ,无明显并发症。术后病理证实为良性病变。结论　腹腔镜肾上腺切除术具有损伤小、术后恢复快和住院时间短等优点 ,而前入路腹腔镜肾上腺手术具有视野清晰、解剖关系明显操作空间大的优点 ,可用于大多数肾上腺良性肿瘤的治疗 ,具有良好的临床应用前景。