26例创伤性膈疝的诊断治疗体会

创伤性膈疝多发生在严重的胸部和腹部的损伤。近年来,创伤性膈疝的发病率呈升高趋势,且往往是复合性损伤,使其临床表现错综复杂,很易造成误诊、漏诊,进而影响疗效。我院自１９８７年７月～１９９９年６月共收治２６例创伤性膈疝,现将其诊断和处理的体会介绍如下。１临床资料 本组男２０例、女６例,年龄６～６３岁。左侧２１例,右侧５例。刀刺伤５例为开放性损伤;余２１例均为闭合性损伤,其中车祸９例、挤压伤４例、坠落伤３例、倒塌伤３例、拳击伤２例。合并其它损伤１９例,包括多发性肋骨骨折、颅骨骨折、骨盆骨折、血气胸,胃…     

11例陈旧性膈疝的诊治

创伤性膈疝尤其是陈旧性创伤性膈疝易被误诊,可造成严重后果。自１９７４年至１９９８年２月,我科共收治创伤性膈疝３７例,其中陈旧性创伤性膈疝１１例。报告探讨如下。临床资料本组１１例全是男性,年龄４～６０岁,平均３３２岁。受伤至确诊时间１５天～２８年,平...     

创伤性膈疝手术治疗16例

创伤性膈疝手术治疗１６例厦门市第一医院李树来郑秀木我院１９７４年３月～１９９４年１０月共收治创伤性膈疝１６例，现报告如下。一、一般资料本组男性１２例，女性４例；年龄６～６６岁，平均３４岁。受伤原因主要为车祸、挤压伤及高空坠落伤，共１３例，刀刺伤２例，...     

创伤性膈疝误诊6例分析

创伤性膈疝误诊６例分析福建省第二人民医院黄泽文陈文南京军区福州总医院肖海创伤性膈疝发病隐袭，术前不易明确诊断。一旦误诊、漏诊，可导致胃肠绞窄坏死等严重并发症，重者危及生命。作者结合１９９１年１月～１９９６年６月间收治的１２例膈疝病人中６例误诊的体会，...     

38例创伤性膈疝治疗体会

目的:探讨创伤性膈疝的诊断治疗经验。方法:对1998年1月—2011年1月收治的创伤性膈疝38例临床资料进行分析总结。结果:38例创伤性膈疝均行手术修补,全部治愈。结论:根据外伤史、CT检查可以确诊,一经确诊,应尽早手术治疗。     

创伤性膈疝32例临床分析

创伤性膈疝发生在胸、腹部闭台或开放性外伤之中。故称创伤性膈疝.病人受伤当时出现的膈疝,称为急性创伤性膈疝.病人受伤后,随着膈肌裂隙逐渐扩大形成的膈疝,称为迟发性创伤性膈疝,创伤性膈疝的发生率,近年有上升的趋势。我们统计了自1971年3月～1990年5月计32例膈疝病例,现分析如下:     

创伤性膈疝32例临床分析

目的总结创伤性膈疝的诊治经验。方法回顾分析1995年1月至2008年8月32例创伤性膈疝临床资料。结果32例均手术治疗，治愈29例，死亡3例，2例死于出血性休克，1例死于多器官功能衰竭。结论创伤性膈疝早期诊断、及时手术，正确处理合并脏器伤是提高治愈率的关键。     

小儿创伤性膈疝手术的麻醉及围术期管理

小儿创伤性膈疝手术的麻醉及围术期管理福建医科大学附属第二医院谢银玉，黄珍治小儿创伤性膈疝在临床工作中较少见，是一种常伴有多部位、多脏器损伤的临床急症。现将我院１９８５年５月～１９９５年１１月收治５例小儿创伤性膈疝手术的麻醉处理报告如下。一、临床资料本...     

创伤性膈疝合并重型颅脑损伤2例诊治体会

目的：对创伤性膈疝合并重型颅脑损伤患者进行临床分析,为临床诊治工作提供指导。方法：对本院2007～2009年收治的2例创伤性膈疝合并重型颅脑损伤患者的资料进行回顾性分析。2例患者均先行开颅血肿清除术,并均行胸部CT检查,1例于1周后确诊为左侧膈疝;1例于1个月后确诊为左侧膈疝,行手术治疗。结果：2例患者均治愈,无手术死亡,术后随访均康复良好。结论：对创伤性膈疝合并重型颅脑损伤患者均应在颅脑病情适当稳定、可耐受手术的前提下,尽早及时采取积极的手术治疗,手术治疗效果好。     

急性创伤性膈疝的诊断与治疗

目的总结急性创伤性膈疝的临床诊断与治疗经验。方法对25例创伤性膈疝的临床资料进行回顾性分析。结果全组术前确诊22例,误诊3例,治愈20例,死亡5例。结论创伤性膈疝一经确诊应尽早手术治疗,提高治愈率,降低病死率。     

经胸、经腹贲门癌根治术的优劣势分析

目的 探讨经胸和经腹贲门癌根治术的优劣势.方法 分析于2003至2010年术前评估后选择经胸和经腹贲门癌根治术53例患者的术后淋巴结转移分析、术后并发症及生存期探讨经胸及经腹贲门癌根治术的优劣.结果 两组手术均无死亡病例、无吻合口瘘.经腹组切缘阳性1例,后经 放射治疗随访3年无复发,经腹组无中转手术改胸腹联合.经胸组术后无并发血气胸.开始后续治疗的时间或出院时间≤14 d,常见并发症差异无统计学意义,全部随访1年、2年、3年生存率差异均无统计学意义.结论 术前准确评估后,选择性采用经胸或经腹贲门癌根治术,患者术后复发转移率和生存率无差异.经腹手术可避免开胸并发症,特别是对不能耐受开胸手术的患者提供了手术机会.     

Release and vascular activity of endothelium-derived relaxing factor in atherosclerotic rabbit aorta.

A diet containing 0.3% cholesterol was given to male New Zealand rabbits for 16 weeks; this produced atherosclerotic lesions (fatty streaks) on 80% of the intimal surface of the thoracic aorta and on 45% of the intimal surface of the abdominal aorta. The endothelium-dependent relaxations induced by acetylcholine, substance P and ionophore A23187 were inhibited in the atherosclerotic aortas. Besides the endothelium-independent relaxations induced by nitroglycerine, the relaxations induced by atrial natriuretic peptide (ANF) were also significantly reduced in the more atherosclerotic thoracic aorta. In bioassay experiments it was found that acetylcholine and substance P caused a smaller release of endothelium-derived relaxing factor (EDRF) from atherosclerotic thoracic aortas than from control thoracic aortas: the EDRF released by the vasodilators evoked less relaxation in atherosclerotic detector abdominal aortas than in control detector abdominal aortas. Nitric oxide evoked significantly less transient relaxation in the atherosclerotic thoracic and abdominal aortas than in the respective control tissues. The data indicate that as experimental atherosclerosis in the rabbit progresses, both vascular activity and EDRF release become affected; this leads to a complete loss of endothelium-dependent relaxation in the more atherosclerotic blood vessels.     

ET-receptor function in relation to blood pressure in spontaneously hypertensive and aortic-banded rats

Endothelin-1 (ET-1), a potent endogenous vasoconstrictor, has been proposed to play a pathophysiologic role in hypertension. The aim of this study was to find out whether changes in ET-receptor function are cause or consequence of blood pressure elevation in hypertension. For this purpose, we assessed ET-receptor function [as ET-1-induced [3H]inositol phosphate (IP) accumulation] in slices of left ventricle and renal cortex and in rings of thoracic and abdominal aorta from spontaneously hypertensive rats (SHR) at the age of 8 weeks (i.e. developing hypertension), 12 and 24 weeks (established hypertension) vs. normotensive age-matched Wistar-Kyoto (WKY) rats, and from supra-renal aortic-banded (AOB) rats at the age of 8, 12 and 24 weeks (i.e. 4, 8 and 20 weeks after AOB) vs. sham-operated (SOP) age-matched WKY rats. In the SHR with established hypertension ET-1-induced IP formation was altered in all tissues investigated: it was significantly increased vs. WKY rats in left ventricle, and significantly decreased in renal and aortic tissues. Similarly, in AOB rats at all ages ET-1-induced IP formation was changed in those tissues that were under pressure load [heart (increase) and thoracic aorta (decrease)] vs. SOP rats, whereas in those tissues not under pressure load (kidney and abdominal aorta) ET-1-induced IP formation was not different between AOB and SOP rats. Moreover, in 8-week-old SHR (where hypertension is not yet established) ET-1-induced IP formation was not significantly different compared to WKY rats (with the exception of thoracic aorta). We conclude that, at least in SHR and AOB rats, changes in ET-1 signalling are secondary to the elevation in blood pressure.     

Sigma-1 receptor stimulation with fluvoxamine activates Akt-eNOS signaling in the thoracic aorta of ovariectomized rats with abdominal aortic banding

In the present study, we investigated the vasculoprotective effect of sigma-1 receptor stimulation with fluvoxamine on pressure overload hypertrophy-induced vascular injury in the thoracic aorta and defined mechanisms underlying that activity. Wistar rats underwent bilateral ovariectomy, and two weeks later were further treated with abdominal aortic stenosis. To confirm the vasculoprotective role of sigma-1 receptor signaling, we treated rats with the agonist fluvoxamine (at 0.5 and 1.0 mg/kg) and with the antagonist NE-100 (at 1.0mg/kg) for 4 weeks orally once a day after the onset of aortic banding. Interestingly, sigma-1 receptor expression in the thoracic aorta decreased significantly 4 weeks after pressure overload-induced hypertrophy in vehicle treated ovariectomized rats. Fluvoxamine administration significantly attenuated pressure overload-induced vascular injury with concomitant increase in receptor expression and subsequent decrease in IP3 receptor expression. Fluvoxamine treatment also significantly restored pressure overload-induced impaired Akt phosphorylation and stimulated eNOS protein expression as well as Akt-mediated eNOS phosphorylation (Ser1177). Fluvoxamine's vasculoprotective effect was nullified by co-administration of a sigma-1 receptor antagonist. No changes in phosphorylation of ERK1/2 or PKCα in the aorta were observed following pressure overload and after fluvoxamine treatment. Our findings confirm, for the first time, a potential role for sigma-1 receptor expression and signaling in the thoracic aorta in attenuating hypertrophy-induced vascular injury in ovariectomized rats. Thus, we demonstrate, for the first time, a potential role in the thoracic aorta for sigma-1 receptor expression and signaling via Akt-eNOS in attenuating hypertrophy-induced vascular injury in ovariectomized rats.     

Inositolphosphate formation in thoracic and abdominal rat aorta following Gq/11-coupled receptor stimulation

Although thoracic and abdominal rat aorta are often used as a classical pharmacological preparation for the assessment of vascular drug effects, little is known on regional differences among these two parts of the aorta with regard to their reaction to Gq/11-coupled receptor activation. Thus, we determined, in rings from thoracic and abdominal aorta from 12-week-old male Wistar rats, the effects of noradrenaline (NA; 10(-8)-10(-4) M), endothelin-1 (ET-1; 10(-10)-10(-6) M) and the thromboxane A2 mimetic U 46619 (10(-8)-10(-5) M) on inositolphoshate (IP) formation (assessed as accumulation of total [3H]IPs in [3H]myoinositol prelabelled rings). NA, ET-1 and U 46619 concentration-dependently increased IP formation; maximum increases were, however, significantly more pronounced in thoracic than in abdominal aorta. Similarly, NA, ET-1 and U 46619 evoked significantly larger maximum contractions in thoracic than in abdominal aorta. NA-induced [3H]IP formation could be inhibited with BMY 7378 (10(-9)-10(-4) M) and with 5-methyl-urapidil (5-MU; 10(-9)-10(-5) M) both exhibiting biphasic concentration-inhibition curves. The pKi-values for BMY 7378 at the high affinity site were in thoracic aorta 8.93+/-0.28 (n=5), and in abdominal aorta 8.76+/-0.35 (n=4) and at the low affinity site 6.45+/-0.2 (thoracic aorta) and 6.55+/-0.27 (abdominal aorta). pKi-Values for 5-MU in thoracic aorta at the high affinity site were 8.25+/-0.34 (n=4), and at the low affinity site 6.61+/-0.39 . In abdominal aorta reliable pKi-values could not be calculated for 5-MU due to a low signal-to-noise ratio. On the other hand, in both preparations the ETA-receptor antagonist BQ-123 (10(-9)-10(-5) M) and the TP-receptor antagonist SQ 29548 (10(-9)-10(-5) M) inhibited ET-1- and U 46619-induced IP formation, respectively, with monophasic concentration-inhibition curves: pKi-values for BQ-123 were: 8.16+/-0.24 (thoracic aorta) and 8.10+/-0.35 (abdominal aorta) and for SQ 29548: 8.2+/-0.3 (thoracic aorta) and 8.5+/-0.3 (abdominal aorta). The amount of immunodetectable Gq/11-protein was similar in both tissues. We conclude that responses to NA, ET-1 and U 46619 (IP formation and contractile force) are larger in thoracic than in abdominal aorta. ET-1 effects on IP formation are mediated by ETA-receptors and U 46619 effects by TP-receptors. NA effects are mediated by alpha1D- and alpha1A-adrenoceptors; alpha1B-adrenoceptors seem to play a minor role.     

Does segmental difference in alpha 1-adrenoceptor subtype explain contractile difference in rat abdominal and thoracic aortae?

The cyclooxygenase inhibitor, indomethacin, depresses adrenergic agonist constriction of endothelium-denuded rat abdominal, but not thoracic, aorta. In order to explain this finding, we explored the possibility of segmental differences in the population of alpha 1-adrenoceptor (AR) subtypes. In endothelium-denuded tissues, phenylephrine elicited concentration-dependent contractions in the thoracic and abdominal aortic rings with potencies and maximal effects that, respectively, did not differ significantly (P > .05). Indomethacin (1 x 10(-5) M) inhibited phenylephrine-induced contractions only in abdominal aorta. The subtype-selective alpha 1D-AR antagonist, BMY 7378, was found to antagonize contractions to phenylephrine competitively in abdominal (pA2 8.44) and thoracic (pA2 8.56) aortic rings. These data are consistent with published alpha 1D-AR functional potency and clonal alpha 1D-AR binding affinity. In addition, cumulative concentration-contraction curves for phenylephrine were competitively antagonized in the rat abdominal and thoracic aortae by prazosin, 5-methylurapidil and WB 4101, with pA2 values of 9.39 and 9.61, 7.64 and 7.85, and 9.43 and 9.58, respectively. These compounds with varying degrees of subtype selectivity inhibited contractions of the thoracic and abdominal aortae with affinities consistent with those determined at the alpha 1D-AR subtype. The results of this study suggest that the contraction to phenylephrine of the rat abdominal and thoracic aorta is mediated via the same alpha 1D-AR subtype.     

多层螺旋CT对急性胸腹部创伤的诊断价值探讨

目的 探讨多层螺旋CT(MSCT)对急性胸腹部创伤的诊断价值.方法 80例急性胸腹部创伤患者,均行X线平片诊断和MSCT诊断.观察比较两种诊断方法的诊断结果和影像质量,分析急性胸腹部创伤的CT表现.结果 MSCT诊断符合率为100.00％(80/80),高于X线平片诊断的75.00％(60/80),差异有统计学意义(P...     

胸段食管癌术后预防照射靶区的最优尺度分析

目的探讨胸段食管癌术后复发、转移的临床特征,了解术后放疗的靶区。方法回顾性分析144例食管癌术后复发转移部位,应用最优尺度分析描述其分布与原发肿瘤部位关系。结果144例术后复发转移病例肿瘤中位进展时间18．43个月（15．68-21．18个月）。共发生复发转移362个部位,其中吻合口复发、远处转移、颈部／锁骨上淋巴结、I～II区、川区、IV区、V区、VI区、VII区、VIII区、X～XI区、腹部淋巴结转移分别是19例（13．2％）、48例（33.3％）、52例（36．1％）、40例（27．8％）、34例（23．6％）、45例（31_3％）、35例（24．3％）、2例（1．4％）、45例（31．3％）、13例（9．0％）、1例（0．7％）、28例（19．4％）。原发灶在胸上段的与颈部-／锁骨上转移,吻合口无复发有联系;原发灶在胸中段的与无远处转移、腹部淋巴结无转移、…区、VII区转移有联系;原发灶在胸下段的与远处转移、腹部淋巴结转移,颈部／锁骨上淋巴结、I～II区、III区、IV区、V区、VII区无转移有联系。其他淋巴结区情况尚无法明确。结论不支持胸段食管癌术后包括颈部／锁骨上、纵隔及腹部淋巴结等部位的大野照射;不同原发灶部位建议区别对待,胸上段食管癌颈部／锁骨上区为必需照射靶区,吻合口可不作为靶区;胸中段食管癌3区、7区为必需照射靶区,腹部淋巴结可不作为靶区,可不加用化疗。胸下段食管癌颈部／锁骨上、I～II区、II区、IV区、V区、VII区可不作为靶区,腹部淋巴结必需作为靶区,因胸下段食管癌因与远处转移有联系,建议加用化疗。胸上段食管癌病例数较少,结果不一定可信。     

Regional variation in norepinephrine-stimulated calcium uptake in rabbit aorta

This study was conducted to determine if there is a difference in the calcium handling mechanism of the thoracic and abdominal aortic regions of the rabbit aorta. Isolated segments of aorta from both regions were studied in HEPES buffer at 37 degrees C and bubbled with 100% oxygen using identical procedures. Intracellular calcium levels were determined after segments had been exposed to 45Ca-labeled buffer during experimental procedures and subsequently washed with a 'quench' solution of zero calcium, 2 mM EGTA, and HEPES buffer, maintained at 0 degree C. The results suggest that the thoracic region is capable of taking up more calcium under resting conditions compared to the abdominal aorta. During stimulation with norepinephrine, both regions show significantly increased calcium influx rates after 10 min of exposure to the agonist, but only in the abdominal region is this effect maintained after 60 min of norepinephrine stimulation. Net (summation of calcium influx and efflux) intracellular calcium levels are significantly increased by norepinephrine in the thoracic but not in the abdominal aorta. Taken together, these data suggest that, compared to the thoracic aorta, the abdominal aorta may possess a more effective calcium efflux mechanism which may be able to fully compensate for the norepinephrine-stimulated increase in calcium influx.     

灌肠在胸外科术前准备中的应用

目的　探讨灌肠在胸外科术前准备中的应用价值。方法　选择 2 0 0 3年 2月至 2 0 0 4年 1月接受肺切除手术患者 96例 ,随机分为试验组和对照组 ,每组各 48例。对照组采用常规胸外科手术术前准备 ;试验组在常规术前准备的基础上 ,术前晚以洁达甘油灌肠剂 110ml灌肠。统计术后 3d内出现腹胀、便秘人数 ,统计学方法采用 χ2 检验。结果　试验组术后出现腹胀 2例 (4 .17% ) ,便秘 3例 (6.2 5 % )。对照组术后腹胀 10例 (2 0 .83 % ) ,便秘 11例 (2 2 .92 % )。两组比较差异有显著性 (P <0 .0 5 )。结论　对于胸部手术病人 ,术前灌肠可有效地减少术后腹胀、便秘 ,有利于患者术后恢复 ,具有一定的应用价值。