Allylamine Cardiotoxicity: II. Histopathology and Histochemistry

The progression of cardiac lesions induced in the rat by allylamine administration (0.1% in drinking water) was studied histopathologically and histochemically. Early changes (4-8 days) consisted of piecemeal acute apical and subendocardial myocardial necrosis with morphologic features of coagulation necrosis and myocytolysis. These early lesions progressed and coalesced; resolution of the subendocardial necrosis was associated with remarkably proliferative fibroblastic tissus. Late lesions (21 days to 3 months) consisted of extensive dense fibrous tissue with adjacent continuing focal necrosis and organization. Although vascular alterations were not present during the early course of injury, after 21 days an exuberant proliferation of cells, predominantly within the intima of intramyocardial smaller arteries and not associated with total occlusion or thrombosis, became evident. Other late lesions included rare intraventricular mural thrombi and cartilagenous metaplasia of trabeculae carnae. Early histochemical alterations (3 days) included focal myocardial cell “calcification,” demonstrated by the alizarin red S stain, and increased monoamine oxidase (MAO) staining in apical subendocardium and periarterial myocytes. As necrosis continued and fibrosis developed (7-21 days) MAO dramatically increased in pericicatricial and periarterial cells. Biochemical measurement of myocardial MAO showed an initial drop in activity, followed by a steady rise to high activity (21 days), especially toward a Type “B” MAO substrate. Although there are many similarities between allylamine-induced myocardial necrosis and ischemic or catecholamine-induced myocardial damage, other unusual findings—especially the early histochemical and chemical MAO alterations and the proliferative late vascular and cicatricial lesions—suggest that the primary pathophysiologic effect of allylamine, mediated through the MAO system, is on the medial smooth muscle of intramyocardial arteries.     

Granulomatous arteritis with massive eosinophilic leukocyte infiltration and transient peripheral eosinophilia subsequent to transarterial embolization therapy with a gelatin sponge.

A 38-year-old man presented with a cavernous hemangioma in the liver. Transarterial embolization (TAE) using a gelatin sponge was carried out 14 days prior to surgical resection of the tumor. Granulomatous arteritis with massive infiltration by eosinophilic leukocytes and histiocytes was present at the periphery of the hemangioma, and transient eosinophilia in the peripheral blood occurred six days after resection. Granulomatous arteritis was evident in medium-sized arteries and there was narrowing or occlusion of the vascular lumen. In the granulomatous cellular infiltrates in the arteries, giant cells of the foreign body type were numerous. An eosinophilic substance differing from fibrin was present in some of the vascular lumina. As this showed staining for collagen, it was considered likely to be fragments of the gelatin sponge. The patient had no symptoms of fever, chills or general fatigue. The clinical course and pathologic findings suggest a causative role of the gelatin sponge in this case of granulomatous arteritis. Vascular change, a rare complication of TAE therapy, may be induced by a hypersensitivity reaction against the intra-arterial gelatin sponge.     

Granulomatous Arteritis with Massive Eosinophilic Leukocyte Infiltration and Transient Peripheral Eosinophilia Subsequent to Transarterial Embolization Therapy with a Gelatin Sponge

A 38-year old man presented with a cavernous hemangioma in the liver. Transarterial embolization (TAE) using a gelatin sponge was carried out 14 days prior to surgical resection of the tumor. Granulomatous arteritis with massive infiltration by eosinophilic leukocytes and histiocytes was present at the periphery of the hemangioma, and transient eosinophilia in the peripheral blood occurred six days after resection. Granulomatous arteritis was evident in medium-sized arteries and there was narrowing or occlusion of the vascular lumen. In the granulomatous cellular infiltrates in the arteries, giant cells of the foreign body type were numerous. An eosinophilic substance differing from fibrin was present in some of the vascular lumina. As this showed staining for collagen, it was considered likely to be fragments of the gelatin sponge. The patient had no symptoms of fever, chills or general fatigue. The clinical course and pathologic findings suggest a causative role of the gelatin sponge in this case of granulomatous arteritis. Vascular change, a rare complication of TAE therapy, may be induced by a hypersensitivity reaction against the intraarterial gelatin sponge. Acta Pathol Jpn 41: 618-622, 1991.     

Subendocardial ischemic myocardial lesions associated with severe coronary atherosclerosis.

Morphologic changes in the subendocardial myocardium that appeared to be caused by severe, chronic subendocardial ischemia were studied in patients with fatal ischemic heart disease admitted to the Specialized Center of Research for Ischemic Heart Disease at the University of Alabama in Birmingham in the period 1970--1977. Thirteen patients were selected for this report on the basis that they had the lesions in the subendocardial myocardium we believe to have been caused by subendocardial ischemia and had no evidence of acute or remote myocardial infarction or other conditions that may have contributed to their terminal illness or death. Clinical findings were unstable angina, congestive heart failure, usually no increase in plasma enzymes indicative of myocardial damage, and electrocardiographic changes consistent with subendocardial ischemia. All 13 patients had 75% or greater stenosis of the three major coronary arteries; none had acute thrombotic or embolic coronary artery occlusion. The left ventricle in all cases was hypertrophied. The subendocardial myocardium showed circumferential pallor, hyperemia, or focal fibrosis without perceptible loss of volume in papillary muscles or trabeculae carneae. Microscopically, acute lesions showed one to two layers of preserved myofibers adjacent to the endocardium, vacuolar change in the deeper fibers, and focal areas of coagulation necrosis of variable size in the myocardium external to the fibers with vacuolar change. Coagulation necrosis was extensive in some cases and usually was not associated with infiltration of neutrophils. The repair reaction involved removal of necrotic sarcoplasm by mononuclear phagocytes, resulting in a reticular-appearing tissue without evidence of stromal collapse. Granulation tissue was not seen. Collagen fibers appeared to be deposited within the area of previous sarcolemmal sheaths. The distribution and morphology of subendocardial myocardial lesions associated with severe coronary atherosclerosis are distinctive and can be distinguished from myocardial necrosis or fibrosis associated with acute total occlusion of a coronary artery.     

Long-term pathological follow-up of cerebral arteriovenous malformations treated by embolization with bucrylate

We examined 17 intracranial arteriovenous malformations that were resected after treatment by embolization using bucrylate (isobutyl-2-cyanoacrylate). In nine specimens removed 5 days to 16 months after embolization therapy, a series of pathologic changes was seen, including patchy mural angionecrosis (adjacent to bucrylate fragments) up to six weeks after embolization, the presence of bucrylate in vessel walls and fibromuscular intimal cushions, and the occurrence (after several months) of entirely extravascular bucrylate. Occasional parts of recanalized vascular malformations were identified. Bucrylate was present within arteriovenous malformations as late as 16 months after embolization, although the amount appeared to be diminished. These findings suggest a specific sequence of events in the interaction between bucrylate and mural components within the malformations and may explain some important complications of embolization therapy (e.g., delayed hemorrhage after embolization).     

Biphasic survival response to amlodipine after myocardial infarction in rats: Association with cardiac vascular remodeling.

In clinical studies, calcium channel blockers have been found to cause adverse cardiovascular reactions after myocardial infarction; however, such effects appear limited to short-acting agents. Thus, our aim was to evaluate the response to a long-acting calcium channel blocker, amlodipine, in terms of both survival and, cardiac and vascular remodeling after infarction. One week after permanent coronary occlusion, rats were randomized to no treatment or daily amlodipine (5 mg/kg) continued for up to 9 months. Amlodipine resulted in improved survival at 200 days (65% versus 26%; p < 0.05), but no difference at 9 months. However, rats with large infarcts died earlier than untreated animals, while those with smaller infarcts died later or survived for nine months. Amlodipine produced no difference in collagen content in non-infarcted tissue or myocyte cross-sectional area versus untreated hearts; however, scar length was increased. In addition, amlodipine was associated with vascular remodeling; muscle:lumen ratio increased in non-infarcted myocardium as did perivascular fibrosis. Vessels within the scar had reduced lumen area because of smooth muscle proliferation. We also examined infarcted hearts subjected to one week of intravenous amlodipine (1 mg/kg) initiated before occlusion and examined three weeks later. In this study, amlodipine exacerbated muscle proliferation in infarct vessels and was associated with less scar collagen. The vascular remodeling associated with amlodipine treatment is considered unfavorable and so the adverse survival for rats with large infarcts was no surprise. However, the prolonged survival associated with smaller infarcts raises the possibility that these vascular changes, under certain circumstances, are beneficial.     

Response to bronchial provocation and exercise in children with cystic fibrosis

Ten of fifteen cystic fibrosis children with positive skin prick tests to common antigens gave an immediate bronchial reaction to the antigen inhaled, five of them also gave a late reaction; however only one gave a history of asthma. The antigen most commonly eliciting a positive skin reaction in cystic fibrosis patients is Aspergillus fumigatus. In six children tested to this antigen the bronchial response varied, two were negative, one gave an immediate reaction and three gave a dual (immediate and late) reaction. None of the children showed the characteristic pattern of response to exercise seen in asthmatic patients, an initial rise in Peak Expiratory Flow Rate followed by a fall of greater than 14% below the resting level. Two patients showed an abnormal rise in Peak Expiratory Flow Rate during exercise, a pattern described previously in cystic fibrosis. The results suggest that bronchial allergy, immediate or late does not completely explain susceptibility to asthma, and that other factors including perhaps the type of bronchial reactivity shown by bronchoconstriction after exercise may be required. However the majority of the children tested had bronchial allergy and anti-allergy therapy such as inhaled sodium cromoglycate may have a place in the management of selected patients with cystic fibrosis.     

Rat pulmonary artery wall injury by chronic intermittent infusions of Escherichia coli endotoxin. Obliterative vasculitis and vascular occlusion

To examine the effect of intermittent endotoxemia on rat pulmonary artery structure and hemodynamic function we infused purified Escherichia coli endotoxin on four occasions over 3 weeks (at 7-day intervals), through an indwelling catheter placed in the external jugular vein. The fourth infusion of endotoxin was associated with widespread but focal alveolar consolidation, reduced perfusion of small pulmonary arteries by lumen occlusion and obliteration, pulmonary vascular wall injury, and a peripheral leukocytosis (mean +/- SEM total leukocytes, endotoxin 133.5 +/- 23 X 10 mm3, control 12.2 +/- 1.2 X 10 mm3, p less than 0.001) in which polymorphonuclear (PMN) leukocytes predominated at the expense of lymphocytes (p2x less than 0.01). The alveolar wall was thickened and the alveolar space was consolidated by degenerating polymorphonuclear leukocytes, mononuclear cells, lipid laden alveolar macrophages, erythrocytes, fibrin, and cell debris. In regions of alveolar consolidation vessel lumens were either narrowed by subendothelial cell collections that consisted either of mononuclear cells or degenerating mural and inflammatory cells, or they were occluded by degenerating inflammatory cells and cell debris. The walls of occluded vessels were evident only by their residual elastic laminae: remnants of lysed endothelial cells lined the intima and the media consisted of degenerating mural and inflammatory cells. Capillary endothelial cells showed extensive hydropic degeneration and lysis of cell contents. Intimal precursor smooth muscle cells were hypertrophied but were not associated with the appearance of mature smooth muscle cells in the walls of small pulmonary arteries. In regions of less severe alveolar consolidation by inflammatory cells, vessel wall injury was still evident but less marked; precursor smooth muscle cells were hypertrophied; subepithelial and subendothelial collections of fluid and fibrin were present; and plasma membranes of endothelial cells were disrupted. Despite extensive pulmonary vascular injury, chronic intermittent endotoxemia did not produce the structural changes associated with pulmonary hypertension (medial thickening and appearance of medial muscle in previously nonmuscular arteries) nor a significant change in pulmonary artery pressure.     

Recurrent perivascular inflammation induced by lipopolysaccharide (endotoxin) results in the formation of atheromatous lesions in vivo

Bacteria and viruses are suspected to induce arteriosclerosis; however, most investigators have focused on coincidences rather than causal relationships. The aim of this work was to establish a rabbit model in which the vessel reaction to local perivascular injection of defined bacterial products can be analyzed. A total of 23 rabbits were randomized to four groups. Groups A and B were fed a normal diet, groups C and D were fed a cholesterol-enriched diet. Groups A and C were treated with a single perivascular injection of bacterial lipopolysaccharide (LPS, endotoxin) placed next to auricular, carotid and femoral arteries, and sodium chloride placed next to the contralateral arteries (control). Group B and D animals were treated with repeated perivascular injections over 90 days. Vascular tissues (n=116 treated segments of 23 rabbits) were analyzed using morphometry at histology, and using immunohistochemistry to detect macrophages, lymphocytes and vascular smooth muscle cells. LPS treatment resulted in transient focal intima thickening. After single LPS application, no increase in atheromatous lesion formation was observed in comparison with controls (group C, lesion area index 0.031+/-0.012 vs 0.015+/-0.006, P=1.0). Repeated LPS application resulted in significant atheromatous lesion formation compared with saline control (group D, lesion area index 0.148+/-0.049 vs 0.008+/-0.006, P=0.003) in hypercholesterolemic rabbits. Repeated LPS inflammation in normocholesterolemic did not lead to atheromatous lesion formation (intima media ratio 0.04+/-0.01 vs 0.04+/-0.007, P=1.0). Single perivascular administration of low-dose bacterial LPS resulted in transient focal intimal thickening, while significant increase in lesion formation occurred after repeated LPS application in cholesterol-fed animals. In conclusion, this animal model will allow the assessment of the impact of defined dosages of different bacterial pathogens onto the vascular wall in the context of atherogenesis. The atheromatous lesion-promoting effect of repeated perivascular administration of LPS supports the hypothesis that bacterial pathogens may be involved in atherogenesis.     

Effect of Renal Embolization with Trisacryl and PAVc

OBJECTIVES

Evaluate the degree of vascular occlusion, vascular recanalization, and necrosis of the vascular wall caused by polyvinyl alcohol-covered polyvinyl acetate (PVAc) particles compared to trisacryl particles after renal embolization.

METHODS

Seventy-nine female albino New Zealand rabbits underwent arterial catheterization of the right kidney. Thirty-three animals were embolized with trisacryl particles, thirty-one with PVAc particles, and fifteen were kept as controls. Four animals were excluded (three trisacryl and one PVAc) due to early death. Five subgroups of six animals were created. The animals in the different groups were sacrificed either 48 hours, 5 days, 10 days, 30 days, or 90 days after embolization. The control group was divided into subgroups of three animals each and kept for the same periods of time. The kidneys were dyed with hematoxylin-eosin and Masson’s trichrome and then examined using optical microscopy.

RESULTS

There were significant differences in the degree of vascular occlusion caused by the trisacryl and the PVAc particles between the five-day and the ten-day groups. Additional differences were noted between the five-day and 48-hour groups in regard to the amount of necrosis. For both findings, the PVAc group members showed adequate tissue reaction (ischemia and volumetric reduction) and less recanalization than those treated with trisacryl.

CONCLUSION

The use of PVAc as an embolization material exhibited an adequate tissue reaction (ischemia and volumetric reduction), more expressive vascular occlusion and necrosis, and less recanalization than the trisacryl material.     

Electron-immunocytochemical studies of perivascular nerves of mesenteric and renal arteries of golden hamsters during and after arousal from hibernation

Electron immunocytochemistry was used to examine perivascular nerves of hamster mesenteric and renal arteries during hibernation and 2 h after arousal from hibernation. Vessels from cold-exposed but nonhibernating, and normothermic control hamsters were also examined. During hibernation the percentage of axon profiles in mesenteric and renal arteries that were immunopositive for markers of sympathetic nerves, tyrosine hydroxylase (TH) and neuropeptide Y (NPY), were increased 2–3 fold compared with normothermic and cold control animals. This increase was reduced markedly only 2 h after arousal from hibernation. The small percentage of nitric oxide synthase-1-positive axon profiles found in mesenteric (but not renal) arteries was also increased during hibernation and returned towards control values after arousal. In contrast, the percentage of perivascular axons immunostaining for vasoactive intestinal polypeptide (VIP), a marker for parasympathetic nerves, was reduced in mesenteric arteries during hibernation. There was no labelling of perivascular nerves for substance P in either mesenteric or renal arteries. It is suggested that the increase in percentage of TH- and NPY-immunostained perivascular nerves may account for the increased vasoconstriction associated with high vascular resistance that is known to occur during hibernation. The reduction in the percentage of axons positive for VIP in hibernating animals would contribute to this mechanism since this neuropeptide is a vasodilator.     

IDIOPATHIC ARTERIAL CALCIFICATION IN A 3-MONTH-OLD CHILD, ASSOCIATED WITH MYOCARDIAL INFARCTION

Idiopathic arterial calcification, which is characterized by intimal fibroblastic proliferation in arteries with mural calcification, may be a cause of sudden death in children. We presented here a three-month-old male infant terminating in sudden death, whose postmortem examination revealed characteristic occlusive disorder of the coronary arteries, associated with secondary myocardial infarction. Histologic study of the coronary arteries demonstrated fibrous intimal proliferation and numerous calcified foci in the internal elastic lamina or in the intima, causing luminal occlusion of the arteries. Similar morphologic changes were found in medium-sized elastic or muscular arteries of other organs. These light microscopic features are consistent with that of so-called idiopathic arterial calcification. Electron microscopic examination of the coronary arteries revealed foamy degeneration of the internal elastic lamina, with focal aggregates of granular high density material. It is suggested that these light and electron microscopic changes of the internal elastic lamina may disclose the fundamental process resulting in mineralization of the lamina, with secondary fibroblastic hyperplasia in the intima.     

Autopsy study of small cardiac scars in Japanese men who lived in Hiroshima, Japan and Honolulu, Hawaii

Japanese men long resident in Honolulu, Hawaii have significantly more ischemic heart disease but significantly fewer small cardiac scars than men in Hiroshima, Japan. These scars occur in three forms:(1)small scars in the mural myocardium which account for the difference in frequency of small lesions in the two cities and are of uncertain etiology; (2)areas of diffuse fibrosis in the papillary muscles. These are equally frequent in the two cities and are associated with advancing age and sclerosis of papillary muscle arteries; and(3)focal scars in the papillary muscles. These are more frequent in Honolulu than Hiroshima. They are healed infarcts due to ischemic heart disease and are associated with a severe degree of extramural coronary artery atherosclerosis. Small mural myocardial scars, when present, are usually found in multiple sites. Their increased frequency in Hiroshima is not explained by differences in age or heart weight. They are more common in the presence of sclerosis of intramural small arteries, but this association also fails to explain the intercity difference. It is supected that the excess of these small cardiac scars in Hiroshima males reflects past privation. There is no evidence that is is related to A-bomb radiation exposure.     

Neoformation of blood vessels in association with rat lung fibrosis induced by bleomycin

We have used intratracheal instillation of bleomycin in rats to study the microanatomical changes of blood vessels associated with lung fibrosis. Bleomycin is a toxic cytostatic drug employed in classical models of lung fibrosis. Wistar rats were submitted to intratracheal injection of 1.5 units of bleomycin and sacrificed 2.5 months later, a timing when marked fibrosis of the lung is observed. We casted the vascular tree of the rat lungs by perfusion with a methacrylate resin. These caste were studied by scanning electron microscopy. Lung tissue was also studied by light microscopy and thin section electron microscopy. The major vascular modifications observed in the bleomycin-treated rats were: (1) neoformation of an elaborate network of vessels located in the peribronchial domains of the lung, and (2) distortion of the architecture of alveolar capillaries. By light microscopy, it was clear that the newly formed vascular network was located in regions of fibrosis (which in the resin casts were digested away). These neoformed vessels appeared to originate from bronchial arteries. Thin section electron microscopy revealed that endothelial cells of the neoformed vessels were plump, presented large nuclei, and showed numerous pinocytotic vesicles that were also observed in subendothelial pericytes. The alveoli of the bleomycin-treated rats were heterogeneous in size and shape in contrast with the homogeneity of alveoli of control animals. The alveolar capillaries of fibrotic lungs appeared to occupy a larger volume of the alveolar wall than alveolar capillaries of control rats. Our findings indicate that lung fibrosis encompasses marked changes of the vascular system, namely, the neoformation of vessels and the rearrangement of alveolar capillaries. These structural changes suggest that fibrotic transformation of the lung is associated with the local generation of angiogenic stimuli. © 1994 Wiley-Liss, Inc.     

Vascular dysfunction by myofibroblast activation in patients with idiopathic pulmonary fibrosis and prognostic significance

In this study, we demonstrated the importance of telomerase protein expression and determined the relationships among telomerase, endothelin-1 (ET-1) and myofibroblasts during early and late remodeling of parenchymal and vascular areas in usual interstitial pneumonia (UIP) using 27 surgical lung biopsies from patients with idiopathic pulmonary fibrosis (IPF). Telomerase+, myofibroblasts α-SMA+, smooth muscle cells caldesmon+, endothelium ET-1+ cellularity, and fibrosis severity were evaluated in 30 fields covering normal lung parenchyma, minimal fibrosis (fibroblastic foci), severe (mural) fibrosis, and vascular areas of UIP by the point-counting technique and a semiquantitative score. The impact of these markers was determined in pulmonary functional tests and follow-up until death from IPF. Telomerase and ET-1 expression was significantly increased in normal and vascular areas compared to areas of fibroblast foci. Telomerase and ET-1 expression was inversely correlated with minimal fibrosis in areas of fibroblast foci and directly associated with severe fibrosis in vascular areas. Telomerase activity in minimal fibrosis areas was directly associated with diffusing capacity of the lung for oxygen/alveolar volume and ET-1 expression and indirectly associated with diffusing capacity of the lungs for carbon monoxide and severe fibrosis in vascular areas. Cox proportional hazards regression revealed a low risk of death for females with minimal fibrosis displaying high telomerase and ET-1 expression in normal areas. Vascular dysfunction by telomerase/ET-1 expression was found earlier than vascular remodeling by myofibroblast activation in UIP with impact on IPF evolution, suggesting that strategies aimed at preventing the effect of these mediators may have a greater impact on patient outcome.     

多层螺旋CT对小儿不典型气管、支气管非金属异物的诊断价值

目的评价多层螺旋CT在小儿不典型气管、支气管非金属异物诊断中的价值。方法回顾性分析30例（男性19例，女性11例，年龄1～5岁，平均年龄3．5岁）经纤维支气管镜检查证实的小儿不典型气管、支气管非金属异物患儿资料,每一患儿均进行多层螺旋CT扫描（层厚2mm，间隔1～2mm，螺距1～2，电压120kV，电流200mA），重建处理包括多平面重建（MPR）、最小密度投影（Min P）和CT仿真内窥镜（CTVE）技术（重建层厚1mm，间隔0．5mm）。使气管、支气管清晰显示，观察非金属异物的有无、位置及其并发症。结果气管异物3例；右侧支气管异物23例，其中右主支气管异物10例．右中间段支气管异物9例，右下叶支气管异物3例，右中叶支气管异物1例；左主支气管异物3例，左下叶支气管异物1例。4种显示方法对小儿不典型气管、支气管非金属异物诊断的敏感性分别为86．7％（26／30）、83.3％（25／30）、70．0％（21／30）、53．3％（16／30）。结论多层螺旋CT是一种非侵入性、无痛苦、安全、易为小儿所接受的检查方法，对小儿不典型气管、支气管非金属异物的诊断、术前筛选、定位、了解手术路径及术后复查等有很大的价值。     

Unusual intravascular material in the brain. Autopsy findings in a patient treated with antihemophilic factor concentrates.

Widespread vascular occlusion caused by unusual particulate material in the brain of a patient who was intensively treated with antihemophilic factor (AHF) concentrates prior to death is described. The intravascular particles were seen partially or completely occluding both veins and arteries of small caliber in the brain and also to a much lesser extent in other organs. The resultant small focal infarcts were predominantly distributed in the cerebral white matter. The pathogenesis of this apparently unique vascular occlusive phenomenon and its relationship, if any, to the massive AHF concentrate infusion in this patient remain unknown.     

明胶海绵在肺结核咯血动脉栓塞中的应用

背景：目前国内用于支气管动脉栓塞的栓塞剂材料主要有明胶海绵、PVA颗粒、藻酸钠微球、弹簧圈等。 目的：分析总结明胶海绵应用于动脉栓塞治疗肺咯血治疗效果。 方法：以“肺咯血、栓塞、肺结核、明胶海绵”为中文关键词,以：“Hemoptysis 、Embolization 、Tuberculosis、 Gelfoam” 为英文关键词,采用计算机检索中国期刊全文数据库、维普数据库(1995-01/2011-05)相关文章。纳入明胶海绵栓塞法治疗肺结核咯血等相关的文章,排除重复研究或Meta分析类文章。 结果与结论：共入选17篇文章进入结果分析。综述了明胶海绵在肺结核咯血动脉栓塞中的应用。包括明胶海绵栓塞剂的介绍,动脉栓塞术止血技术以及用明胶海绵动脉栓塞治疗肺咯血治疗效果及不足等方面的研究内容。高压高温处理后的明胶海绵作为栓塞剂治疗肺咯血,不仅临床疗效满意而且非常经济,适合目前中国的国情。     

Pulmonary histopathology of rats following parenteral injections of nickel chloride

To elucidate the subacute toxic reactions to parenteral administration of Ni2+, male F-344 rats were given daily injections of NiCl2 (62.5 or 125 mumol/kg, sc) for 3 to 6 weeks. Nickel accumulation was greater in lung than in the other major organs, based upon tissue analyses by electrothermal atomic absorption spectrometry. After 5 or 6 weeks of NiCl2 treatment, severe pathological changes developed in the lungs, including a) prominent hydropic and degenerative changes of the endothelium of pulmonary arteries and veins; b) marked proliferation of alveolar lining cells, affecting Type II (granular)pneumocytes; c) thickening of alveolar walls, with proteinaceous alveolar exudate; d) hyperplasia of bronchial epithelium, with cellular atypia and mitoses; and e) focal bronchial pneumonia with intrabronchial exudates. These pulmonary responses to repeated daily injections of NiCl2 were substantially different from the pathological lesions seen 24 to 72 hours after a single sc injection of NiCl2 (500 or 750 mumol/kg), which included perivascular edema, karyorrhexis and pyknosis of mononuclear cells in focal perivascular infiltrates, and mild pulmonary congestion. This study shows that the lung is a primary site of toxicity in rats following parenteral administration of NiCl2; vascular endothelial cells, Type II pneumocytes, bronchial epithelial cells, and mononuclear cells constitute the principal cellular targets for pulmonary toxicity of Ni2+.