【摘要】：第一部分神經(jīng)源性肺水腫家兔模型的制備 背景 神經(jīng)源性肺水腫(Neurogenic pulmonary edema, NPE)是中樞神經(jīng)系統(tǒng)(Central nervous system, CNS)損傷后急性的威脅生命的并發(fā)癥,通常在嚴(yán)重CNS損傷后數(shù)分鐘至數(shù)小時(shí)內(nèi)發(fā)生。NPE缺乏流行病學(xué)數(shù)據(jù)資料,小兒患者NPE少見,但臨床上容易漏診。近年來,腸道病毒71型(Enterovirus71, EV71)感染所致手足口病成為重要的公眾健康問題,重癥感染患兒常合并中樞神經(jīng)系統(tǒng)受累,并發(fā)NPE和心肺衰竭者預(yù)后不良,病死率、致殘率高。 NPE確切的發(fā)病機(jī)制至今仍未十分明確,主要有沖擊傷理論-血流動(dòng)力性學(xué)說和滲透缺陷理論-肺毛細(xì)血管通透性學(xué)說,目前普遍認(rèn)為是這兩種機(jī)制共同作用的結(jié)果,交感神經(jīng)過度興奮在NPE發(fā)生中起重要作用。多年來,國內(nèi)外研究學(xué)者在深入研究其發(fā)病機(jī)制及治療的過程中,建立了多種動(dòng)物模型制備方法。目前,通過EV71感染的方式,可成功復(fù)制出中樞神經(jīng)系統(tǒng)受累模型,但未復(fù)制出NPE。因此,本部分研究的目的是選擇除EV71感染以外的其他方法,制備神經(jīng)源性肺水腫模型,同時(shí)觀察NPE發(fā)生過程中交感神經(jīng)興奮和血流動(dòng)力學(xué)變化,為后續(xù)進(jìn)行神經(jīng)源性肺水腫的研究打下基礎(chǔ)。 目的 1.復(fù)制神經(jīng)源性肺水腫家兔模型。 2.觀察神經(jīng)源性肺水腫發(fā)生過程中交感神經(jīng)興奮和血流動(dòng)力學(xué)變化。 方法 1.18只健康成年新西蘭兔隨機(jī)分為3組：正常組6只,NPE組6只,生理鹽水組(NS組)6只。 2.NPE模型通過小腦延髓池注射纖維蛋白原和凝血酶誘發(fā)形成。 3.家兔麻醉后按分組給予不同處理：①正常組：麻醉后不予其他處理,作為空白對(duì)照；②NPE組：麻醉后,進(jìn)行手術(shù)操作(氣管插管、PiCCO動(dòng)靜脈導(dǎo)管置管),小腦延髓池穿刺并注射纖維蛋白原和凝血酶；③NS組：麻醉后,進(jìn)行手術(shù)操作(氣管插管、PiCCO動(dòng)靜脈導(dǎo)管置管),小腦延髓池穿刺并注射等量生理鹽水。 4.實(shí)驗(yàn)過程中,正常組觀察麻醉后0h、1h、2h、3h、4h、5h、6h呼吸、心率變化；NPE組、NS組,1)觀察小腦延髓池穿刺注射藥物前后,呼吸(RR)、心率(HR)、平均動(dòng)脈血壓(MABP)的變化及其幅度變化；2)觀察不同時(shí)點(diǎn)(基礎(chǔ)狀態(tài)B0,小腦延髓池穿刺注射后1min、5min、10min、15min、30min、1h、2h、3h、4h、5h、6h) MABP動(dòng)態(tài)變化；3)分別于基礎(chǔ)水平(B0)、注射后15min (P15min)、實(shí)驗(yàn)結(jié)束時(shí)(或P6h)留取血標(biāo)本,檢測血漿腎上腺素(EPI)、去甲腎上腺素(NE)濃度。 5.實(shí)驗(yàn)結(jié)束后處死動(dòng)物,立即開胸,觀察氣管導(dǎo)管有無水腫液自行溢出及肺胸膜下出血程度,評(píng)估肺水腫程度,并行組織病理形態(tài)學(xué)檢查。 結(jié)果 小腦延髓池注射纖維蛋白原和凝血酶誘導(dǎo)了家兔神經(jīng)源性肺水腫。各項(xiàng)觀察指標(biāo)變化如下： 1)呼吸指標(biāo)：各組的基礎(chǔ)RR無統(tǒng)計(jì)學(xué)差異(P0.05)。正常組在觀察時(shí)間點(diǎn)內(nèi),呼吸無明顯變化(P0.05)。NPE組、NS組小腦延髓池穿刺注射后即刻(P1min),與基礎(chǔ)水平(B0)相比,RR明顯增快(P0.01)；兩組間RR增快的幅度(△RR)差異無統(tǒng)計(jì)學(xué)意義。 2)平均動(dòng)脈血壓、心率變化：各組的基礎(chǔ)HR無統(tǒng)計(jì)學(xué)差異(P0.05)。正常組在觀察時(shí)間點(diǎn)內(nèi),心率無明顯變化(P0.05)。NPE組、NS組小腦延髓池穿刺注射后即刻(P1min),與B0時(shí)比較,MABP升高(P0.01),HR增快(P0.05)；兩組間MABP升高的幅度(ΔMABP)差異有統(tǒng)計(jì)學(xué)意義(P0.01),HR增快的幅度(△HR)差異無統(tǒng)計(jì)學(xué)意義(P0.05)。NPE組,MABP隨時(shí)間有下降趨勢,短時(shí)間內(nèi)降至基礎(chǔ)水平,甚至較低值；NS組,MABP隨時(shí)間逐漸降至并維持于基礎(chǔ)水平。 3)血漿腎上腺素(EPI)、去甲腎上腺素(NE)水平：NPE組和NS組的EPI、 NE基礎(chǔ)水平(B0)均無差異(P0.05)。與B0相比,NS組EPI、NE水平在P15min、P6h均無明顯變化(P0.05)。與B0相比,NPE組EPI水平在P15min、 P6h均明顯升高(P0.01)；NE水平在P15min (P0.01)、P6h升高(P0.05)。NPE組與NS組相比,EPI水平在P15min、P6h均明顯升高(P0.01)；NE水平在P15min (P0.01)、P6h升高(P0.05)。 4)氣管導(dǎo)管水腫液：實(shí)驗(yàn)結(jié)束,開胸后不擠壓肺,NPE組可見粉紅色泡沫狀液體自行從氣管導(dǎo)管溢出；NS組、正常組均未見氣管導(dǎo)管水腫液。 5)肺組織肉眼觀：NPE組肺組織明顯腫脹,體積增大,邊緣變鈍,外觀暗紅,大片淤血,肺切面可見粉紅色泡沫狀液體。NS組、正常組肺組織無明顯腫脹,邊緣銳利,外觀呈粉紅色,無淤血,肺切面未見泡沫狀液體。 6)肺胸膜下出血程度：NPE組均有嚴(yán)重的肺水腫,各肺可見Ⅱ-Ⅲ級(jí)肺胸膜下出血,其中2/12為Ⅱ級(jí),10/12為Ⅲ級(jí)；NS組和正常組均未見肺胸膜下出血,即肺胸膜下出血程度均為0級(jí)。 7)肺組織病理形態(tài)學(xué)：NPE組家兔肺組織肺泡隔明顯變寬,部分肺泡可見肺泡隔斷裂,肺泡腔融合,紅細(xì)胞浸潤至肺間質(zhì)或肺泡腔,有的肺泡腔內(nèi)可見均質(zhì)淡染的粉紅色滲出物。NS組和正常組家兔肺組織肺泡隔正常,肺泡腔完整,未見紅細(xì)胞浸潤,肺泡腔干燥無滲出。 結(jié)論 1.小腦延髓池注射纖維蛋白原和凝血酶后,家兔發(fā)生交感神經(jīng)興奮改變。 2.小腦延髓池注射纖維蛋白原和凝血酶后,家兔出現(xiàn)氣管導(dǎo)管水腫液和肺組織病理學(xué)肺水腫改變。 3.小腦延髓池注射纖維蛋白原和凝血酶的方法,可用于制備家兔神經(jīng)源性肺水腫模型。 第二部分AngⅡ系統(tǒng)在家兔神經(jīng)源性肺水腫中作用的實(shí)驗(yàn)研究 背景 近年來研究發(fā)現(xiàn),除了存在一個(gè)全身的腎素-血管緊張素系統(tǒng)(Renin-angiotensin system, RAS),機(jī)體多個(gè)器官和組織也存在獨(dú)立的局部RAS。研究發(fā)現(xiàn),急性肺損傷時(shí),肺組織局部RAS激活,如急性呼吸窘迫綜合征、胎糞吸入綜合征、哮喘、嚴(yán)重急性呼吸綜合征。因而我們探討神經(jīng)源性肺水腫(Neurogenic pulmonary edema, NPE)發(fā)生的肺損傷中,局部RAS是否激活,并觀察血管緊張素轉(zhuǎn)換酶抑制劑對(duì)于NPE的影響,從而為臨床防治NPE提供新的突破口。 目的 1.在纖維蛋白誘導(dǎo)的NPE家兔模型中,探討NPE發(fā)生時(shí)局部RAS是否激活。 2.給予血管緊張素轉(zhuǎn)換酶抑制劑干預(yù)NPE,觀察其對(duì)NPE的影響。 方法 1.在NPE模型確認(rèn)的基礎(chǔ)上,添加NPE干預(yù)組,即依那普利拉組(Ena組),6只健康成年新西蘭兔,造模15min后,靜脈注射依那普利拉(0.5mg/kg)。實(shí)驗(yàn)中納入的組別為正常組、NPE組、Ena組。 2.實(shí)驗(yàn)過程中,觀察Ena組不同時(shí)點(diǎn)(基礎(chǔ)狀態(tài)B0,小腦延髓池穿刺注射后1min、5min、10min、15min、30min、1h、2h、3h、4h、5h、6h)的呼吸(RR)、平均動(dòng)脈壓(MABP)、心率(HR)的動(dòng)態(tài)變化。 3.實(shí)驗(yàn)結(jié)束后處死動(dòng)物,1)立即打開胸腔,觀察氣管導(dǎo)管有無水腫液自行溢出及肺胸膜下出血情況,評(píng)估肺水腫程度；2)留取左肺下葉,常規(guī)HE染色行病理組織形態(tài)學(xué)檢查；3)留取右肺組織,測定肺組織Ang Ⅱ濃度及肺組織ACE、ACE2、AT1R mRNA表達(dá)水平。 結(jié)果 1.肺組織Ang Ⅱ水平NPE組較正常組(539.7±146.6vs253.4±37.2pg/ml)和Ena組(539.7±146.6vs308.7±35.4pg/ml)均增高(P0.05); Ena組與正常組相比,差異無統(tǒng)計(jì)學(xué)意義(P0.05)。 2.肺組織ACE、ACE2、AT1R mRNA表達(dá)水平RT-PCR結(jié)果顯示： ①ACE mRNA表達(dá)水平三組間比較,差異無統(tǒng)計(jì)學(xué)意義(P0.05),表達(dá)水平趨勢為NPE組正常組Ena組。 ②ACE2mRNA表達(dá)水平與正常組相比,NPE組與Ena組ACE2mRNA表達(dá)水平均有下調(diào)(P0.05); NPE組與Ena組比較,ACE2mRNA表達(dá)水平無差異(P0.05)。 ③AT1R mRNA表達(dá)水平三組間比較,差異無統(tǒng)計(jì)學(xué)意義(P0.05)。 ④ACE/ACE2mRNA表達(dá)水平三組間比較,差異無統(tǒng)計(jì)學(xué)意義(P0.05),趨勢為NPE組Ena組正常組。 3.肺水腫評(píng)估 1)氣管導(dǎo)管水腫液：正常組、Ena組氣管導(dǎo)管內(nèi)均未見粉紅色泡沫水腫液自行溢出,NPE組氣管導(dǎo)管內(nèi)可見水腫液。 2)肺胸膜下出血程度：正常組12/12為0級(jí)；NPE組2/12為Ⅱ級(jí),10/12為Ⅲ級(jí)；Ena組2/12為Ⅰ級(jí),8/12為Ⅱ級(jí),2/12為Ⅲ級(jí)。 4.組織病理學(xué)肺損傷評(píng)分 肺泡過度擴(kuò)張,Ena組vs NPE組,1.2±0.1vs2.8±0.4分,差異有統(tǒng)計(jì)學(xué)意義(P0.01)；肺間質(zhì)水腫,Ena組vs NPE組,1.3±0.2vs2.3±0.5分,差異有統(tǒng)計(jì)學(xué)意義(P0.01)；肺泡滲出,Ena組vs NPE組,1.5±0.2vs1.8±0.3分,差異無統(tǒng)計(jì)學(xué)意義(P0.05)。肺損傷總計(jì)得分,Ena組vs NPE組,1.3±0.1vs2.3±0.4分,差異有統(tǒng)計(jì)學(xué)意義(P0.01)。正常組未見肺泡過度擴(kuò)張、肺間質(zhì)水腫、肺泡滲出,肺損傷評(píng)分為0。 結(jié)論 1.NPE發(fā)生時(shí),家兔肺組織Ang Ⅱ濃度升高,ACE2mRNA表達(dá)下調(diào),肺組織局部RAS激活。 2.依那普利拉干預(yù)NPE,家兔肺組織Ang Ⅱ濃度、病理學(xué)肺損傷評(píng)分降低,提示血管緊張素轉(zhuǎn)換酶抑制劑可能有減輕家兔NPE時(shí)肺損傷的作用。
[Abstract]:Part one preparation of rabbit model of neurogenic pulmonary edema
background
Neurogenic pulmonary edema (NPE) is an acute life-threatening complication after the injury of the central nervous system (Central nervous system, CNS)..NPE lacks epidemiological data for several minutes to several hours after severe CNS injury. Children are rarely seen in NPE, but they are easily missed clinically. In recent years, intestines have been found. Hand foot and mouth disease (HMD) caused by Enterovirus71 (Enterovirus71, EV71) infection is an important public health problem. Patients with severe infection often merge with the central nervous system, and the patients with NPE and cardiopulmonary failure have poor prognosis, high mortality and high disability rate.
The exact pathogenesis of NPE is still not very clear, mainly including the theory of impact injury, the theory of hemodynamic and the theory of permeability defect, the theory of pulmonary capillary permeability, which is generally believed to be the result of the joint action of these two mechanisms. The sympathetic excitability plays an important role in the occurrence of NPE. In the process of studying its pathogenesis and treatment, a variety of animal model preparation methods have been established. At present, the central nervous system involvement model can be successfully replicated by EV71 infection, but NPE. has not been replicated. The purpose of this part is to select other methods except EV71 infection to prepare the neurogenic pulmonary edema model. The changes of sympathetic nerve excitation and hemodynamics during the development of NPE were observed to lay a foundation for the follow-up study of neurogenic pulmonary edema.
objective
1. the rabbit model of neurogenic pulmonary edema was replicated.
2. to observe sympathetic excitation and hemodynamic changes in the course of neurogenic pulmonary edema.
Method
1.18 healthy adult New Zealand rabbits were randomly divided into 3 groups: 6 in normal group, 6 in group NPE, and 6 in saline group (group NS).
The 2.NPE model was induced by injection of fibrinogen and thrombin through the cerebellopontine cisterna.
3. rabbits were given different treatments after anesthesia: (1) normal group: after anesthesia, no other treatment, as blank control; group NPE: after anesthesia, operation (tracheal intubation, PiCCO arteriovenous catheterization), cerebellar medullary pool puncture and injection of fibrinogen and thrombin; group NS: after anesthesia, operation (trachea) Intubation, PiCCO arteriovenous catheterization, puncture of cerebellar medullary cistern and injection of equivalent saline.
4. during the experiment, the normal group observed 0h, 1H, 2h, 3h, 4h, 5h, 6h respiration, heart rate change, NPE, NS, 1) before and after the cerebellar medullary cistern puncture injection, respiration (RR), heart rate (HR), mean arterial pressure (MABP) changes and amplitude changes; 2) observation of different points (after cerebellar medullary cistern puncture injection, 10 Min, 15min, 30min, 1H, 2h, 3h, 4h, 5h, 6h) MABP dynamic changes; 3) respectively at the base level (B0), after the injection, at the end of the experiment, to leave the blood samples, to detect the plasma adrenaline, the concentration of norepinephrine.
5. after the end of the experiment, the animals were killed and the chest was opened immediately to observe the self overflow of the tracheal tube and the degree of the hemorrhage of the pulmonary pleura. The degree of pulmonary edema was evaluated and the histopathological examination was performed.
Result
Neurogenic pulmonary edema was induced by injection of fibrinogen and thrombin in cerebellopontine cisterna.
1) respiratory index: there was no statistical difference in the base RR of each group (P0.05). In the normal group, there was no significant change in the respiration (P0.05).NPE group in the observation time point, and the cerebellum medullary pool in NS group was immediately after injection (P1min), and the RR increased significantly (P0.01) compared with the basic level (B0), and there was no significant difference in the amplitude (delta RR) of the RR in the two groups.
2) mean arterial blood pressure and heart rate change: there was no statistical difference in the base HR of each group (P0.05). In the normal group, there was no significant change in heart rate (P0.05).NPE in the observation time point. In group NS, the cerebellar medullary pool was injected immediately after injection (P1min). Compared with B0, MABP increased (P0.01) and HR increased (P0.05); there was a statistical difference between the amplitude of MABP increase (delta) among the two groups. Learning significance (P0.01), the amplitude of HR faster (delta HR) had no statistical significance (P0.05).NPE group, MABP decreased with time, decreased to the base level and even lower in a short time, and MABP in NS group gradually declined and maintained at the base level with time.
3) plasma adrenaline (EPI) and norepinephrine (NE) level: EPI in group NPE and NS group, and NE base level (P0.05). Compared with B0, NS group EPI, NE level is no obvious change. Compared with group NS, EPI levels were significantly higher in P15min and P6h (P0.01); NE levels were higher in P15min (P0.01) and P6h (P0.05).
4) edema fluid of tracheal catheter: the end of the experiment, no squeezing of the lungs after the opening of the chest, and the NPE group can see that the pink foam liquid spilt from the tracheal catheter; in group NS, no tracheal ductus edema fluid is found in the normal group.
5) the naked eye view of lung tissue: the lung tissue of group NPE was obviously swollen, the volume increased, the edge became dull, the appearance was dark red, the blood was red, the pink foam liquid was found in group.NS, the lung tissue of the normal group had no obvious swelling, the edge was sharp, the appearance was pink, no blood, no foam like liquid in the cut face of the lung.
6) the degree of pulmonary and pleural hemorrhage: there were severe pulmonary edema in group NPE, and sub pleural hemorrhage of class II - III in each lung, of which 2/12 was grade II and 10/12 was grade III; no sub pleura hemorrhage was found in group NS and normal group, that is, the degree of sub pleural hemorrhage was grade 0.
7) pathomorphology of lung tissue: pulmonary alveolar septum in NPE group was broadened obviously, alveolar septum was seen in some alveoli, alveolar cavities were fused, red cells infiltrated into pulmonary interstitial or alveolar cavity. In some alveoli, there were homogeneous and light stained pink exudate in.NS group and normal group of pulmonary alveolus in normal group, intact alveolar cavity and no red cells. Infiltration of the alveolar cavity without exudation.
conclusion
1. after injection of fibrinogen and thrombin in the cerebellopontine cisterna, the sympathetic excitation in rabbits changed.
2. After injection of fibrinogen and thrombin into cerebellomedullary cistern, edema of tracheal tube and pulmonary histopathological changes of pulmonary edema occurred in rabbits.
3. the method of injecting fibrinogen and thrombin into cerebellar medullary cistern can be used to prepare rabbit model of neurogenic pulmonary edema.
The second part is the experimental study of the role of Ang II system in rabbit neurogenic pulmonary edema.
background
In recent years, in addition to the existence of a systemic renin angiotensin system (Renin-angiotensin system, RAS), multiple organs and tissues of the body also have independent local RAS. studies. In acute lung injury, the local RAS activation of the lung tissue, such as acute respiratory distress syndrome, meconium aspiration syndrome, asthma, and severe acute respiration, is found. Therefore, we explored the activation of local RAS in the lung injury of Neurogenic pulmonary edema (NPE) and the effect of angiotensin converting enzyme inhibitor on NPE, thus providing a new breakthrough for the clinical prevention and treatment of NPE.
objective
1. in the fibrinogen induced NPE rabbit model, we explored whether local RAS activation occurred in NPE.
2. angiotensin-converting enzyme inhibitor was used to interfere with NPE and observe its effect on NPE.
Method
1. on the basis of NPE model confirmation, the NPE intervention group was added, that is, 6 healthy adult New Zealand rabbits in the enalapril group (group Ena), and after the modeling of 15min, the intravenous injection of enalpli (0.5mg/kg). The group included in the experiment was the normal group, the NPE group, and the Ena group.
2. during the experiment, the dynamic changes of Ena group (basal state B0, 1min, 5min, 10min, 15min, 30min, 1H, 2h, 3h, 4h, 5h, heart rate) were observed.
3. after the end of the experiment, animals were killed, 1) immediately open the thoracic cavity, observe the endotracheal tube with self-propelled fluid overflow and pulmonary pleura hemorrhage, evaluate the degree of pulmonary edema; 2) leave the left lower lobe, routine HE staining, pathological histomorphology examination; 3) leave the right lung tissue, determine the lung tissue Ang II concentration and ACE, ACE2, AT1R mRNA table of lung tissue Up to the level.
Result
1. the level of Ang II in the lung tissue was higher than that of the normal group (539.7 + 146.6vs253.4 + 37.2pg/ml) and Ena group (539.7 + 146.6vs308.7 + 35.4pg/ml) (P0.05), and there was no significant difference between the group Ena and the normal group (P0.05).
2. the expression level of ACE, ACE2 and AT1R mRNA in lung tissue RT-PCR results showed that:
(1) there was no significant difference in the expression level of ACE mRNA between the three groups (P0.05), and the trend of expression was NPE group normal group Ena group.
2. Compared with the normal group, the expression level of ACE2mRNA in group NPE and Ena group was down (P0.05), and there was no difference in the level of ACE2mRNA expression between group NPE and Ena group (P0.05).
(3) there was no significant difference in the expression level of AT1R mRNA between the three groups (P0.05).
(4) there was no significant difference in the level of ACE/ACE2mRNA expression between the three groups (P0.05), and the trend was NPE group Ena group normal group.
3. assessment of pulmonary edema
1) Tracheal catheter edema fluid: Normal group, Ena group tracheal catheter no pink foam edema fluid spontaneous overflow, NPE group tracheal catheter edema fluid can be seen.
2) Degree of pulmonary subpleural hemorrhage: normal group 12/12 was grade 0; NPE group 2/12 was grade II, 10/12 was grade III; Ena group 2/12 was grade I, 8/12 was grade II, 2/12 was grade III.
4. histopathological lung injury score
Pulmonary alveolus overexpansion, group Ena vs NPE group, 1.2 + 0.1vs2.8 + 0.4 points, the difference was statistically significant (P0.01); pulmonary interstitial edema, Ena group vs NPE group, 1.3 + 0.2vs2.3 + 0.5 points, the difference was statistically significant (P0.01); alveolar exudation, Ena group vs groups, 1.5 + 0.3 points, the difference was not statistically significant. Total score of lung injury There was no alveolar hyperdilatation, interstitial edema, alveolar exudation and lung injury score in the normal group.
conclusion
When 1.NPE occurred, the concentration of Ang II in lung tissue increased, the expression of ACE2mRNA was downregulated, and local RAS activation in lung tissue.
2. in NPE, the concentration of Ang II in rabbit lung tissue and the score of pathological lung injury were reduced, suggesting that angiotensin converting enzyme inhibitor may reduce the effect of NPE on lung injury in rabbits.
【學(xué)位授予單位】：復(fù)旦大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2012
【分類號(hào)】：R725.6

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