小鼠股骨骨折合并坐骨神经损伤的标准化动物模型构建与评价

目的 建立并评价小鼠股骨骨折合并坐骨神经损伤的标准化动物模型。方法 将96只C57BL/6J小鼠随机分为2组,分别为A组：股骨骨折合并坐骨神经损伤组(48只)、B组：股骨骨折组(48只)。A组通过止血钳钳夹致小鼠左侧坐骨神经损伤,于同侧进行股骨开放性骨折联合髓内钢针固定,建立了小鼠股骨骨折合并坐骨神经损伤的模型;B组行左侧股骨开放性骨折联合髓内钢针固定,仅游离坐骨神经,不做钳夹处理。术后仔细观察小鼠行为学变化。于术后第3、5、7、10、14、18天6个时间点,取A组(36只)与B组(36只)左侧坐骨神经,其中每个时间点每组6只,分别通过免疫组化染色来分析坐骨神经损伤修复过程。同时,于第7、14、21和28天4个时间点取小鼠左侧股骨,分别通过股骨X线、Micro-CT、组织学染色来分析并评估在周围神经损伤条件下骨折愈合情况。结果 本实验建立的小鼠股骨骨折合并坐骨神经损伤模型,于建模后第14天小鼠步态基本恢复正常;于第14天坐骨神经纤维结构连续性基本恢复;第7天骨折断端几乎不存在骨痂;至第14天出现少量软骨痂,主要为未分化的间充质干细胞构成;第21天软骨痂开始钙化,骨痂中存在部分肥大的软骨细胞;第28天骨折断端新生骨形成,含有大量肥大的软骨细胞、成骨细胞与骨细胞。结论 通过本研究方法建立的小鼠股骨骨折合并坐骨神经损伤模型愈合过程良好,并较单纯股骨骨折的愈合过程有所迟缓,可很大程度上模拟临床骨折合并周围神经损伤后修复及愈合过程,为合并周围神经损伤的骨折愈合相关研究提供实验基础。     

海水淹溺性肺损伤机制的研究进展

溺水是重要的公共安全问题,是全球意外死亡三大原因之一。肺损伤是溺水患者最常见的并发症之一,其主要表现为严重的呼吸困难和低氧血症,近1/3的患者最终进展为急性肺损伤或急性呼吸窘迫综合症。肺泡上皮细胞是肺泡-毛细血管屏障重要组成部分,淹溺导致其结构和功能的完整性直接破坏促进了肺水肿的发生,同时肺毛细血管通透性增加,中性粒细胞和单核细胞等大量渗出聚集加剧肺内炎症反应。此外,机体氧化应激、细胞间连接和通讯等肺外机制也可导致肺损伤。本文就海水淹溺性肺损伤的相关机制研究进展进行了综述。     

Head injuries coexistent with pelvic or lower extremity fractures-early or delayed osteosynthesis

Summary The authors compared the results of a retrospective analysis of two groups of head-injured patients who had coexistent pelvic or lower extremit fractures. One group was treated with early osteosynthesis within the first 12 hours after trauma, simultaneously with neurosurgical treatment, while the second group was treated neurosurgically and osteosynthesis was postponed for 4 to 10 days. The second group revealed a higher mortality, which was due to fat embolism. We conclude that early osteosynthesis is the treatment of choice in patients with coexistent head injury and lower extremity fractures.     

Parametric assessment of myocardial perfusion during interventional cardiac catheterization by means of X-ray densitometry-short-and long-term results

Summary X-ray densitometric evaluation of digital subtraction angiocardiograms allows an assessment of myocardial perfusion by means of the parameter MEAN RISE TIME (MRT), defined as the time from the onset of local myocardial contrast medium opacification to the point of maximum opacification. Best results are obtained when the response of that parameter is compared before and after stimulation of coronary flow by papaverine. A prolongation of this parameter, especially after papaverine, was indicative of an impairment of myocardial perfusion, when compared to the results obtained by TL-201 scintigraphy.In 50 patients with single vessel coronary artery disease the results of MRT pre and post papaverine before and after coronary angioplasty, as well as after 6 months were evaluated for 204 post-stenotic regions-of-interest. Before angioplasty papaverine induced a significant prolongation of post-stenotic MRT (2.3s ± 0.9s vs. 3.1s ± 0.8s; p<0.01), while after successful angioplasty post-stenotic MRT was measured significantly shorter after stimulation of coronary flow (2.6s ± 1.0s vs. 1.9s ± 0.9s; p<0.01). This indicated an improvement in myocardial perfusion. Nevertheless, 16/50 patients still presented pathological results of post-stenotic MRT after papaverine, although angioplasty was regarded successful. These patients presented a markedly higher rate of restenosis (14/16 patients after 6 months), a higher rate of dissections at the dilatation site and a higher rate of dilated vessels, supplying myocardial areas after a Q-wave myocardial infarction.Thus, these results demonstrate the additional information about the short-and long-term outcome of an angioplasty procedure by densitometric myocardial perfusion analysis.     

Detection of traumatic myocardial injury by means of simultaneous T1-201/Tc-99m pyrophosphate tomography--report of three cases

Trauma to the chest can result in cardiac damage, which maybe missed by clinical examination because of associated injuries.Routinely performed non-invasive tests may also be non-diagnostic.Tc-99m pyrophos-phate (PPi) tomography, in this study combinedwith T1-201, is a promising addition to non-invasive evaluation.In three patients with cardiac injury, this technique successfullydetected and localized myocardial necrosis.     

Prevention of postischemic reperfusion injury: The improvement of myocardial tissue blood flow after ischemia by terminal Nicorandil-Mg cardioplegia

We evaluated the preventive effect of postischemic reperfusion injury by Nicorandil-Mg cardioplegia given just prior to reperfusion as terminal cardioplegia. Twenty seven dogs were placed on cardiopulmonary bypass and the aorta was cross-clamped for 90 min under hypothermic (17–19°C) cardioplegic arrest. The canine hearts were divided into three groups: in group A (n=10) the hearts were reperfused without any treatment; in group B (n=9) the hearts received coronary perfusion with Nicorandil-Mg solution (Nic, 8 mg/l; Mg, 20 mEq/l; glucose, 50 g/l) for 2 min just prior to reperfusion; and in group C (n=8) the hearts received coronary perfusion with Nicorandil-Mg free solution (glucose, 50g/l). During and after ischemia, the myocardial tissue PCO₂ (t-PCO₂) was continuously monitored by an ion-sensitive field effective transistor (ISFET) sensor. In addition, the myocardial tissue blood flow (TBF), oxygen consumption, and lactate flux were then calculated at 5, 10, 20, and 40 min of reperfusion. In the initial reperfusion period, Group B showed an improved TBF compared to group A and C (at 5 min, group B was 42.7±11.9; group A was 29.4±11.2, P<0.025; and group C was 33.9±9.2% of the preischemic control level, P<0.05). T-PCO₂ in group B was significantly decreased at 5 min of reperfusion (group B, 127.5±22.5 42.5±9.7; group A, 117.5±23.0 85.2±17.4, P<0.001; group C, 122.3 mmHg 68.2±18.7 mmHg, P<0.01), and group B had a better metabolic recovery. These results suggest that terminal Nicorandil-Mg cardioplegia might reduce the rate of postischemic reperfusion injury.     

低血流心肌缺血诱导GLUT4基因表达

目的：探讨低血流心肌缺血促进葡萄糖摄取增加的机制。方法：采用Northrn印迹法观察缺血心肌葡萄转运子4（GLUT4）mRNA的表达,并利用蛋白质印迹法分析心肌GLUT4多肽的表达,结果：局部心肌低血流缺血后,心肌GLUT4mRNA和GLUT4多肽表达明显增加;同时伴随缺血心肌葡萄糖摄取明显增多。结论：心肌缺血能刺激GLUT4 mRNA和GLUT4多肽表达,使GLUT4数增加,进而促进心肌葡萄糖摄取增多,使缺血心肌能量需求得以平衡,有助于缺血心肌功能的恢复,提示低血流缺 刺激心肌GLUT4表达是一个重要的代偿性保护机制。