18F-FDG micro-PET代谢显像评估大鼠放射性认知功能障碍的实验研究

目的 研究大鼠放射性脑损伤模型中葡萄糖代谢与神经元活性的相关性,探讨2-¹⁸F-2-脱氧-D-葡萄糖（¹⁸F-FDG）micro-PET用于放射性认知功能障碍评估的潜在价值。方法 将3周龄雄性SD大鼠按照随机数表法分成对照组以及全脑照射组,每组10只,脑照射组利用小动物精确放疗仪给予10 Gy X射线照射,对照组不予照射。通过Morris水迷宫（MWM）实验评估大鼠认知功能,对两组大鼠脑部micro-PET图像数据进行对比分析,免疫组织化学染色检测神经元活性标记物c-Fos蛋白在脑内的表达变化,免疫荧光染色检测幼稚神经元标志物DCX及新生成熟神经元标志物BrdU/NeuN阳性细胞数的变化。结果 照射3个月后,与对照组相比,全脑照射的大鼠在MWM定向航行实验中第2至4天的潜伏期均显著延长（t=2.179、3.393、3.219,P<0.05）,MWM空间探索实验中的目标象限的探索时间百分比减少（t=3.857,P<0.01）,提示全脑照射可引起海马依赖性认知能力下降;SPM分析micro-PET图像显示全脑照射组海马区域葡萄糖代谢显著降低（t=5.12,P<0.05）;此外,全脑照射组海马区域神经元活性标记蛋白c-Fos的表达显著减少（t=14.22,P<0.01）,幼稚神经元标志物DCX及新生成熟神经元标志物BrdU/NeuN阳性细胞数均较对照组减少（t=18.77、9.304,P<0.01）。结论 全脑放疗后海马区域的葡萄糖代谢减低,与海马神经元活性下降及神经发生减少相一致,表明¹⁸F-FDG micro-PET可以作为评估放射性认知功能障碍的有效方法。     

Lesion evolution after gamma knife irradiation observed by magnetic resonance imaging

PURPOSE: Our study is focused on the magnetic resonance imaging (MRI) observation of lesion development and hippocampus related functional impairments in rats after irradiation with a Leksell Gamma knife (LGK). MATERIALS AND METHODS: We exposed 32 three-month-old Long-Evans rats to various radiation doses (25 Gy, 50 Gy or 75 Gy). The rats were scanned by a 4.7 T magnetic resonance (MR) spectrometer at several timepoints (1 - 18 months) after irradiation. The lesion size was evaluated by manual segmentation; the animals were behaviorally tested in a Morris water maze and examined histologically. RESULTS: We found that a dose of 25 Gy induced no edema, necrosis or behavioral change. The response of the rats to higher doses was not uniform; the first occurrence of lesions in the rat brains irradiated with 50 and 75 Gy was detected six months post-irradiation. Functional impairment correlated well with the lesion size and histology. CONCLUSIONS: Rat brains showed the development of expanding delayed lesions after 50 or 75 Gy doses from the LGK during the first year after irradiation.     

Lesion evolution after gamma knife irradiation observed by magnetic resonance imaging

Purpose: Our study is focused on the magnetic resonance imaging (MRI) observation of lesion development and hippocampus related functional impairments in rats after irradiation with a Leksell Gamma knife (LGK).

Materials and methods: We exposed 32 three-month-old Long-Evans rats to various radiation doses (25 Gy, 50 Gy or 75 Gy). The rats were scanned by a 4.7 T magnetic resonance (MR) spectrometer at several timepoints (1 – 18 months) after irradiation. The lesion size was evaluated by manual segmentation; the animals were behaviorally tested in a Morris water maze and examined histologically.

Results: We found that a dose of 25 Gy induced no edema, necrosis or behavioral change. The response of the rats to higher doses was not uniform; the first occurrence of lesions in the rat brains irradiated with 50 and 75 Gy was detected six months post-irradiation. Functional impairment correlated well with the lesion size and histology.

Conclusions: Rat brains showed the development of expanding delayed lesions after 50 or 75 Gy doses from the LGK during the first year after irradiation.     

灯盏花素对创伤性脑损伤大鼠学习记忆功能的影响

目的 观察灯盏花素对创伤性脑损伤大鼠学习记忆功能和脑氧自由基的影响.方法 通过液压损伤法建立大鼠创伤性脑损伤模型,水迷宫实验和避暗实验测定大鼠学习记忆功能,并于测试后取脑测定总超氧化物歧化酶（T-SOD）、丙二醛（MDA）含量.结果 在Morris水迷宫实验中,灯盏花素能明显缩短脑创伤大鼠逃避潜伏期;在避暗实验中,灯盏花素能显著延长脑创伤大鼠学习记忆潜伏期,减少错误次数.灯盏花素可以显著降低脑创伤大鼠脑组织MDA含量和显著增加T-SOD含量.结论 灯盏花素可改善脑创伤大鼠学习记忆功能,其作用与抑制氧自由基反应有关.     

大剂量低分割照射大鼠局部肝脏的早期实验研究

目的探讨大剂量低分割照射局部肝脏的耐受剂量和早期病理变化特征。方法 70只W istar大鼠随机分为高剂量（48 Gy）组、中剂量（24 Gy）组、低剂量（8 Gy）组、对照组,设定右肝为照射靶区,8 Gy次/,3次/w,隔日1次。照射后第7、14、28、42 d和2个月时分批处死,取肝组织行常规HE染色和超微结构电镜扫描。结果各剂量组肝脏受照射的体积分数差异无统计学意义（P〉0.05）。高剂量组出现肝小静脉内皮细胞损伤及肝小叶中央静脉和肝窦小静脉阻塞性病变等改变,照射后2个月肝星状细胞激活并有胶原纤维合成。中剂量组4 w内呈现与高剂量组类似改变,6 w后无明显病变。低剂量组和对照组未观察到病理改变。结论当大鼠2/3肝脏受到高剂量照射,早期出现典型的肝小静脉损伤病变,其基础是肝小静脉内皮细胞特别是肝窦内皮细胞持续广泛损伤;2个月后肝脏启动纤维化进程,形成放射性肝损伤。     

TBI大鼠海马糖皮质激素受体表达变化对认知功能的影响

目的 研究创伤性脑损伤(traumatic brain injury,TBI)后大鼠海马区糖皮质激素受体(ghcocorticoid receptor,GR)表达的变化对认知功能的影响.方法 建立大鼠脑损伤模型,应用免疫组化、Western blot和Morris水迷宫检测伤后大鼠海马区GR表达与学习记忆功能的关系.结果伤后4～10 d大鼠海马区GR持续低表达;Morris水迷宫检测伤后大鼠出现认知功能障碍.结论 TBI大鼠海马区GR表达变化与认知功能的障碍改变具有相关性.

Abstract：

Objective To explore the effect of glucocorticoid receptor(GR)expression in rat hippocampus on cognitive function after traumatic brain injury(TBI). Methods The TBI model wag established in rats.Then,immunohistochemistry and Western blot were used to detect the GR expression and evaluate its relation with cognitire dysfunction by Morris water maze. Results Expression of hippocampal GR was down-regulated 4-10 days after TBI.Morris water maze test showed significant impairment of the cognitive function in rats. Conclusion There is correlation between expression change of hippocampal GR and cognitive dysfunction.     

Quantitative in vivo proton MR spectroscopic evaluation of the irradiated rat brain

PURPOSE: To investigate if in vivo localized proton magnetic resonance spectroscopy (MRS) can detect putative metabolic changes in the irradiated rat brain and quantitatively measure brain metabolite changes in this model. MATERIALS AND METHODS: A total of 20 adult male Fischer 344 rats were exposed to a fractionated regimen of whole brain irradiation (WBI) (total 45 Gy, given as five Gy fractions, twice per week for 4.5 weeks); 10 control rats received sham irradiation. A total of 52 weeks after WBI, all animals were subjected to high-resolution MRI and in vivo proton MRS to determine structural and brain metabolite changes. Brain metabolites were measured by using single-voxel MRS. Quantitative analysis of detectable metabolites was performed by using the spectral analysis method, LCModel. RESULTS: Significant differences in brain metabolite concentrations were detected in rat brains irradiated with a clinically relevant fractionated radiotherapy regimen in 52 weeks, in comparison to age-matched sham-irradiated rats. CONCLUSION: These findings indicate that quantitative in vivo MRS may serve as a sensitive imaging tool to noninvasively detect neurochemical changes in the irradiated brain.     

MgSO4对大鼠急性放射性脑损伤后NSE和S-100蛋白表达的影响

目的探讨MgSO4对电离辐射诱发的脑组织损伤的保护作用。方法将成熟的SD大鼠36只随机分为空白对照组、实验对照组和MgSO4实验用药组，用6MeV电子线对实验大鼠行20Gv全脑单次垂直照射，吸收剂量率为200cGy／min；实验用药组大鼠于照射前1d、照射后即刻、照后连续3d分别给予10％的MgSO4腹腔注射，分别于照射后1、7、14和30d处死大鼠，取其脑组织，用免疫组织化学法测定神经元特异性稀醇化酶（NSE）、S-100蛋白的相对含量，并与对照组进行比较。结果在上述时间点，脑内海马区S-100和NSE表达有时间规律，照射后1周S-100蛋白的表达和照射后24hNSE的表达组间存在一定差别。与空白对照组相比，实验对照组大鼠脑组织中NSE表达显著下降（P〈0．05），S-100表达显著升高（P〈0．05）；与实验对照组相比，在照射后7d，MgSO4可明显抑制S-100的表达（P〈0．05），诱导NSE的表达（P〈0．05）。结论 脑组织中S-100和NSE表达水平的变化是辐射诱导的急性脑损伤的敏感指标，MgSO4可降低S-100的表达水平并升高NSE在神经元中的含量，早期使用对急性放射性脑损伤有保护作用。     

大鼠放射性口腔黏膜炎模型的建立

目的 建立放射性口腔黏膜炎动物模型。方法 70只SD大鼠左侧颊黏膜接受X射线照射,共8次,总吸收剂量为80Gy。照射20、40、60和80 Gy后,以及80 Gy照射结束后2、4、6、8、14和21 d随机处死6只,取左侧颊黏膜进行病理组织学检查,右侧颊黏膜作为自身对照。结果 当总吸收剂量达到60 Gy时左侧颊黏膜开始出现肉眼可见的红斑,照射80 Gy后开始出现单个或多个溃疡,80 Gy照射结束后4 d左右出现大面积溃疡,80 Gy照射结束后2周左右溃疡基本愈合.结论 该模型制作方法能较好地模拟大鼠放射性口腔黏膜炎的发病过程,可用于放射性口腔黏膜炎的实验研究。     

Structure-function analysis of angiotensin-converting enzyme inhibitors as modifiers of radiation-induced pulmonary endothelial dysfunction in rats

We have previously demonstrated that thiol-containing collagen antagonists (penicillamine) and angiotensin-converting enzyme (ACE) inhibitors (Captopril and CL242817) ameliorate endothelial dysfunction in irradiated rat lung. The purpose of the present study was to determine whether the non-thiol ACE inhibitor CGS13945 also modifies radiation-induced pulmonary endothelial dysfunction in rats sacrificed 2 months after a single dose (0-30 Gy) of 60 Co gamma rays to the right hemithorax. The CGS13945 was administered in the feed continuously after irradiation at a regimen of 30 mg (kg body weight)-1 day-1. Four markers of lung endothelial function were monitored: ACE activity, plasminogen activator (PLA) activity, and prostacyclin (PGI2) and thromboxane (TXA2) production. Right lung ACE and PLA activities decreased with increasing radiation dose, and CGS13945 significantly ameliorated both responses. Dose-reduction factors (DRF) for the inhibitor were 1.80 for ACE activity and 1.41 for PLA activity (p less than 0.05). In contrast, lung PGI2 and TXA2 production increased with increasing radiation dose, and CGS13945 did not influence either response significantly. Thus the ACE inhibitor CGS13945 modifies radiation-induced pulmonary endothelial dysfunction in rats, indicating that the presence of a thiol group is not essential for therapeutic efficacy in this class of compounds. On the other hand, CGS13945 exhibits a differential sparing of radiation-induced pulmonary endothelial dysfunction, as does penicillamine. A structure-function analysis of the present and previous data indicates that all of the ACE inhibitors tested (Captopril, CL242817 and CGS13945) spare the radiation-induced suppression in lung ACE and PLA activity; all of the thiol compounds tested (penicillamine, Captopril and CL242817) spare the radiation-induced elevation in lung PGI2 and TXA2 production; and the thiol ACE inhibitors (Captopril and CL242817) spare all four endothelial responses. These data confirm a novel and potentially important application for ACE inhibitors as modifiers of radiation-induced lung injury, and suggest that there are at least two components to their mechanism of therapeutic action in this model.     

αB-晶体蛋白在放射性白内障大鼠眼晶状体中的表达

目的 检测受不同剂量X射线照射的大鼠晶状体中可溶性αB-晶体蛋白的表达水平,探讨αB-晶体蛋白与放射性白内障形成之间的关系。方法 用直线加速器X射线一次性照射SD雄性大鼠双眼,建立放射性白内障模型。将大鼠分为健康对照组、实验对照组和5、15及25 Gy照射组。于照射后3个月将大鼠处死,取晶状体作匀浆,取其上清液(可溶性晶状体蛋白质)采用免疫印迹法(Western blot) 检测αB-晶体蛋白的表达。结果 健康对照组、实验对照组和5 Gy组未出现晶状体混浊,15和25 Gy的照射组逐渐形成典型放射性白内障。蛋白免疫印迹结果显示随着照射剂量的增加,SD大鼠眼晶状体内可溶性αB-晶体蛋白逐渐减少,差异有统计学意义(F=40.764,P<0.05) 。结论 在放射性白内障中晶状体内可溶性αB-晶体蛋白表达减少,在白内障形成中起重要作用。     

IL-1beta, TNFalpha and IL-6 induction in the rat brain after partial-body irradiation: role of vagal afferents

PURPOSE: To evaluate the central nervous system neuroimmune and inflammatory responses during the prodromal phase of the acute irradiation syndrome in rat brains after partial-body exposure (head-protected) and to investigate the potential neural signalling pathways from the irradiated periphery to the non-irradiated brain. MATERIAL AND METHODS: The study included four groups of rats: one irradiated group and one sham irradiated group, each containing non-vagotomized and vagotomized rats. In vagotomized rat groups, the subdiaphragmatic vagal section surgery was carried out 45 days before the irradiation exposure. The rats were partial-body irradiated with the head shielded with (60)Co gamma-rays to a dose of 15 Gy. They were sacrificed 6 h after the end of exposure. The hypothalamus, hippocampus, thalamus and cortex were then collected, and the concentrations of IL-1beta, TNFalpha and IL-6 in each were measured by ELISA assays. RESULTS: Six hours after irradiation, IL-1beta levels had increased in the hypothalamus, thalamus and hippocampus, and TNFalpha and IL-6 levels had increased significantly in the hypothalamus. Vagotomy before irradiation prevented these responses. CONCLUSIONS: It was concluded that the hypothalamus, hippocampus, thalamus and cortex react rapidly to peripheral irradiation by releasing pro-inflammatory mediators. The results also show that the vagus nerve is one of the major ascending pathways for rapid signalling to the brain with respect to partial body irradiation.     

Long-term cognitive effects of human stem cell transplantation in the irradiated brain

Abstract

Purpose: Radiotherapy remains a primary treatment modality for the majority of central nervous system tumors, but frequently leads to debilitating cognitive dysfunction. Given the absence of satisfactory solutions to this serious problem, we have used human stem cell therapies to ameliorate radiation-induced cognitive impairment. Here, past studies have been extended to determine whether engrafted cells provide even longer-term benefits to cognition.

Materials and methods: Athymic nude rats were cranially irradiated (10 Gy) and subjected to intrahippocampal transplantation surgery 2 days later. Human embryonic stem cells (hESC) or human neural stem cells (hNSC) were transplanted, and animals were subjected to cognitive testing on a novel place recognition task 8 months later.

Results: Grafting of hNSC was found to provide long lasting cognitive benefits over an 8-month post-irradiation interval. At this protracted time, hNSC grafting improved behavioral performance on a novel place recognition task compared to irradiated animals not receiving stem cells. Engrafted hESC previously shown to be beneficial following a similar task, 1 and 4 months after irradiation, were not found to provide cognitive benefits at 8 months.

Conclusions: Our findings suggest that hNSC transplantation promotes the long-term recovery of the irradiated brain, where intrahippocampal stem cell grafting helps to preserve cognitive function.     

大鼠全脑照射后早期海马区磁共振波谱研究

目的 探讨放射性脑损伤模型大鼠海马区代谢变化与认知功能障碍及早期病理演变的关系。方法雌性SD大鼠65只,随机分为对照组5只和10、20、30 Gy单次照射组各20只,于照射后2及4周、2及6个月(各5只)Y迷宫法测定大鼠的学习、记忆能力,定量分析照射后2及4周海马区N-乙酰天门冬氨酸/肌酸(NAA/ Cr)、胆碱复合物/肌酸(Cho/ Cr)的参数变化,电子显微镜观察海马区的超微结构改变。结果照射后2及4周、2及6个月大鼠学习、记忆能力较对照组下降,照射剂量越大,学习记忆力下降越明显。10 Gy照射组2及4周NAA/Cr与Cho/Cr比值低于对照组(t＝2.345、 2.578与2.503、3.025, P<0.05),20 Gy照射组(t=5.755、4.700与4.606、4.658, P<0.01),30 Gy照射组(t=10.956、6.766与9.571、6.377, P<0.01)显著低于对照组。电镜观察显示:照射后4周海马区神经元有不同程度的线粒体肿胀、毛细血管内皮水肿及髓鞘板层解离。结论 ¹H-MRS能无创性动态监测放射性脑损伤海马区生化代谢改变,对早期海马异常的检测比MRI更敏感,¹H-MRS变化可在一定程度上反映脑损伤严重程度。     

每周重复照射建立大鼠放射性肺损伤模型的评价

目的评价每周小剂量重复照射大鼠放射性肺损伤模型的可行性、科学性及实用性。方法36只Wistar种雌性大鼠,按5:1比例随机分为照射组(A组)30只、对照组(B组)6只。6-MV直线加速器对A组大鼠右肺进行分次照射(5Gy/次,1次/周,累积剂量最高为30Gy),于照射后第4、6、8、12、26周处死,每时相点处死6只,B组于第4周末处死。观察动物活体外观、肺的大体标本、行HE染色观察大鼠肺组织学变化、ELISA法检测血清和SP法检测肺组织中的TGF-β1蛋白表达。结果A组受照肺组织表现出放射性肺炎及肺纤维化,大鼠血清和肺组织TGF-β1表达第4周表达升高,到第12周达到高峰,26周下降。结论每周小剂量重复照射所制作的大鼠放射性肺损伤模型稳定可靠,动物死亡率低,符合临床放疗实际。     

硫酸镁对大鼠急性放射性脑损伤后脂质过氧化的抑制作用

目的探讨硫酸镁对电离辐射诱发的脑组织损伤的保护作用。方法将成熟的SD大鼠60只随机分为空白对照组、实验对照组和硫酸镁实验用药组，用6MeV电子线对实验大鼠进行20Gy全脑单次垂直照射，分别于1d、7d、14d和30d处死，取其脑组织，用考马斯亮蓝法测定总蛋白相对浓度，黄嘌呤氧化法测定超氧化物歧化酶（SOD）活性，硫代巴比妥酸法测定丙二醛（MDA）浓度，并与空白对照组进行比较。结果与空白对照组相比，实验对照组大鼠脑组织中SOD活性显著下降（P〈0．05），MDA浓度显著升高（P〈0．05）；与实验对照组相比，硫酸镁实验用药组大鼠脑组织中SOD活力在照射后7d呈逐渐上升趋势，MDA浓度明显降低（P〈0．05）。结论早期使用硫酸镁可抑制辐射引起的脑组织中脂质过氧化的程度，减轻自由基对脑组织的损伤程度。     

Control of radiation-induced pneumopathy and lung fibrosis by angiotensin-converting enzyme inhibitors and an angiotensin II type 1 receptor blocker

Purpose : This report summarizes our experiences on the protective effect of angiotensin-converting enzyme (ACE) inhibitors, especially captopril and an angiotensin II type 1 receptor blocker on radiation-induced pulmonary injury. Method : In the first series of experiments, adult male Sprague Dawley rats were given a single dose of either 20 or 30 Gy of gamma rays to a 35 cm 2 right hemithorax port, whilst shielding the left, contralateral, lung. Perfusion scans and autopsies were performed at intervals up to 12 months post-radiation. Three different ACE inhibitors, penicillamine and pentoxifylline were given as radiation protectors and their activity compared. A model of irradiation for total bone marrow transplant (BMT) was used for the second group of experiments. Male WAC/Rij/MCW rats received total-body irradiation and a regimen of cyclophosphamide (CTX) in preparation for bone marrow transplant. The modifiers were two ACE inhibitors, captopril and enalapril, and L-158,809, an angiotensin II (A II) type 1 receptor blocker. All drugs were administered in the rats? drinking water and all were well-tolerated. Results : In the irradiated rats, pulmonary damage progressed from the presence of blebs and detachment from basement membranes of endothelial cells a few days after injury, to severe arteritis and interstitial collagen deposition at 3 months, and then on to severe pneumonitis and extensive pulmonary fibrosis at 6 months. Marked increase of hydroxyproline was also found in the lungs at 6 months. These morphological changes were associated with significant decrease of ACE and plasminogen activator activity (PLA) and a marked increase of prostaglandins (PG12) and thromboxane (Txa2), substances considered as indicators of endothelial pulmonary damage. ACE inhibitors captopril, CL 24817, enalapril and CGS 13945 prevented the markers of endothelial dysfunction. Captopril and CL 24817, which contain a sulphydryl (-SH) radical in their moiety and the AII type 1 receptor blocker, L-158,809, were the most efficient in protecting the lung parenchyma from the inflammatory response and subsequent fibrosis. Penicillamine, an SH-containing compound with weak ACE inhibitory activity was also a strong antifibrotic agent but showed only modest anti-inflammatory properties. Additionally, in the irradiated rats, captopril also reduced the incidence of squamous cell skin carcinomas and subcutaneous sarcomas consequent to the highest doses of radiation. Conclusion : ACE inhibitors and one AII type 1 receptor blocker were effective in protecting lungs from radiation-induced pneumonitis and the development of lung fibrosis in two models of rat radiation injury. In the first series of experiments (unilateral irradiation), those ACE inhibitors containing a sulphydryl radical were more effective than those without it. This observation led to the question of whether this protective effect is related to inhibition of AII synthesis or rather to some of the collateral pharmacologic properties of these drugs, such as anti-oxidation or protease inhibition. The AII receptor blocker, however, was shown to be equally effective, if not better, in its antifibrotic capacity than any ACE inhibitor with or without an SH radical, reaffirming the role of AII in modulation of collagen synthesis.     

Absence of protective role of afferent nerves in early intestinal mucosal alterations induced by abdominal irradiation in rats

Purpose : To assess the early effects of primary afferent nerve suppression by systemic treatment with the neurotoxin capsaicin in an acute model of abdominal irradiation in rats (10 Gy, gamma). Materials and methods : Changes in myeloperoxidase (MPO) activity, calcitonin gene-related peptide (CGRP) tissue content, number of mast cells and apoptotic cells were determined in jejunum and ileum in four groups of rat male Wistar (vehicle sham-irradiated, vehicle irradiated, capsaicin sham-irradiated and capsaicin irradiated) at 1 and 3 days post-irradiation. Results : In vehicle irradiated rats, CGRP was significantly increased from the first day after irradiation in jejunal mucosa; MPO activity increased in both segments at day 3 but not at day 1 after irradiation; the number of detectable mucosal mast cells dropped to nearly zero on days 1 and 3, while the apoptotic cells in the intestinal mucosa were significantly increased at day 1. Similar results were obtained for mast cells and apoptosis in capsaicin irradiated rats as compared to capsaicin sham-irradiated rats, while MPO activity was significantly increased and CGRP concentration in jejunal mucosa significantly decreased from the first day in these rats in comparison with capsaicin sham-irradiated rats. Conclusions : Intestinal sensory innervation seems not to have a major protective role against a radiation-induced intestinal inflammatory reaction.     

Absence of protective role of afferent nerves in early intestinal mucosal alterations induced by abdominal irradiation in rats

PURPOSE: To assess the early effects of primary afferent nerve suppression by systemic treatment with the neurotoxin capsaicin in an acute model of abdominal irradiation in rats (10Gy, gamma). MATERIALS AND METHODS: Changes in myeloperoxidase (MPO) activity, calcitonin gene-related peptide (CGRP) tissue content, number of mast cells and apoptotic cells were determined in jejunum and ileum in four groups of rat male Wistar (vehicle sham-irradiated, vehicle irradiated, capsaicin sham-irradiated and capsaicin irradiated) at 1 and 3 days post-irradiation. RESULTS: In vehicle irradiated rats, CGRP was significantly increased from the first day after irradiation in jejunal mucosa; MPO activity increased in both segments at day 3 but not at day 1 after irradiation; the number of detectable mucosal mast cells dropped to nearly zero on days 1 and 3, while the apoptotic cells in the intestinal mucosa were significantly increased at day 1. Similar results were obtained for mast cells and apoptosis in capsaicin irradiated rats as compared to capsaicin sham-irradiated rats, while MPO activity was significantly increased and CGRP concentration in jejunal mucosa significantly decreased from the first day in these rats in comparison with capsaicin sham-irradiated rats. CONCLUSIONS: Intestinal sensory innervation seems not to have a major protective role against a radiation-induced intestinal inflammatory reaction.