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T J Nevalainen

Publications and source records attributed to T J Nevalainen.

At least 145 records · Page 8Linked to original sources
PubMed1980

Experimental pancreatitis in the rat. Sodium taurocholate-induced acute haemorrhagic pancreatitis.

Sodium taurocholate injected into the pancreatic duct system of the rat caused acute haemorrhagic pancreatitis. The pancreatic lesions were immediate and characterized by interstitial oedema, extensive necrotic changes of the acinar cells, and haemorrhages during the first 24 h after the injection. In animals surviving 72 h there were marked acinar atrophy and pancreatic fibrosis. The mortality increased according to the amount of sodium taurocholate injected. Except for necrosis of occasional liver cells, other organs examined were histologically normal. This investigation created an experimental model for studying the pathogenesis of acute pancreatitis. The results support the hypothesis that bile can initiate acute haemorrhagic pancreatitis.

Acute Disease↗
PubMed1980

Experimental pancreatitis in the rat. Ultrastructure of sodium taurocholate-induced pancreatic lesions.

Necrotic lesions caused by the intraductal injection of sodium taurocholate in rat pancreas were studied by electron microscopy. The early (1 and 15 min after the injection) ductal cells were often necrotic. The acinar cell damage was characterized by mitochondrial swelling, vesiculation of the granular endoplasmic reticulum, and dissolution of cellular membranes. At later time intervals (1, 3, and 6 h) there were necrotic acinar cells with heterogeneous cytoplasmic inclusions representing degenerative cell organelles and their remnants. At 6, 12, and 24 h there were autophagic vacuoles in sublethally damaged acinar cells. The zymogen granules seemed relatively well preserved throughout the experiment. The vascular lesions consisted of endothelial detachment, extravasation of erythrocytes, thrombosis, and poikilocytosis. It was concluded that the initial cell injury was caused by the detergent action of the injected bile salt.

Animals↗
PubMed1980

Experimental pancreatitis in the rat. The role of phospholipase A in sodium taurocholate-induced acute haemorrhagic pancreatitis.

Acute haemorrhagic pancreatitis was induced in rats by injecting 0.2 ml of 5% (92.9 mmol/l) aqueous solution of sodium taurocholate into the common biliopancreatic duct. Lysolecithin was separated from the pancreatic homogenate by thin-layer chromatography and quantified by phosphorus determination. The lysolecithin content increased rapidly, remained elevated for 12 h, and returned to the control level 24 h after the injection. Treatment with a trypsin inhibitor, aprotinin (Trasylol), given intraperitoneally and intravenously during 2 h postoperatively (800,000 units/kg of body weight) had no beneficial effects compared with physiological saline treatment. When the animals were treated similarly with a phospholipase A inhibitor, procaine hydrochloride (40 mg/kg of body weight), 45% of them survived 72 h (p less than 0.01). It was concluded that phospholipase A, which converts lecithin into lysolecithin, plays a significant role in the pathogenesis of acute pancreatitis.

Acute Disease↗
PubMed1978

Ultrastructure of gastric leiomyosarcoma.

Samples of gastric leiomyosarcomas from two male patients (69 years and 57 years of age) were studied by electron microscopy. The tumour cells contained abundant 50--90 A thick microfilaments and microtubules. Another cell type, regarded as immature leiomyosarcoma cell, contained numerous profiles of granular endoplasmic reticulum, free ribosomes and a well developed Golgi apparatus. There were intercellular junctions of zonula adherens-type between adjacent tumour cells. It was concluded that electron microscopy offers a valuable aid in the diagnosis of gastric neoplasms of smooth muscle origin.

Aged↗
PubMed1978

Ultrastructural and histochemical observations on serous ovarian cystadenomas.

One hundred and twelve serous ovarian cystadenomas (46 benign, 33 tumours of borderline malignancy and 33 malignant tumours) were investigated with histological and mucin histochemical methods. Electron microscopy was applied to 9 benign, 6 borderline and 5 malignant tumours. The epithelium of the benign serous cystadenomas contained ciliated and nonciliated columnar cells, which sometimes were edematous ("pale cells"), and smaller basal cells. The large Golgi apparatus with small secretory vesicles and occasional larger secretory granules was located in the apical cytoplasm. There were numerous pinocytotic vesicles at the basal plasma membrane. The extracellular mucin in the cystic lumen and the mucin on the apical epithelial border consisted of material with vic-glycols (1.2-hydroxyl groups) mixed with sulpho- and carboxymucin. With increasing degree of malignancy the number of ciliated cells diminished and were not found in the malignant epithelium. The number of nucleoli and the amount of carboxymucin with sialic acid residues increased with increasing degree of malignancy. However, there were no single consistent ultrastructural feature which could be considered as a reliable criterion for malignancy of these tumours in the absence of invasive growth. The findings support the view that serous ovarian cystadenomas are of coelomic origin.

Adult↗
PubMed1978

Pathology of mucinous ovarian cystadenomas. 2. Ultrastructural findings.

Fourteen mucinous ovarian cystadenomas of different grades of malignancy (7 benign, 4 borderline and 3 malignant) were investigated by electron microscopy. The main tumour cell type was a columnar mucous epithelial cell with short microvilli. With increasing grade of malignancy the shape and size of these cells became more irregular and the number of mucous granules in them decreased. Most of the mucous granules had a dense core and a less dense reticular component, which stained well with the periodic acid-silver methenamine (PASM) technique. Goblet cells with the usual ultrastructure were found rather frequently. The tumours in a given group of malignancy were relative similar to each other in their light and electron microscopic appearance. However, a number of tumours contained argyrophil and argentaffin cells in addition to the columnar and goblet cells. The findings of the present study support the view that the mucinous ovarian cystadenomas arise from the ovarian surface epithelium via a metaplastic process.

Adult↗
PubMed1978

Quantitation of ultrastructural changes in mouse pancreatic acinar cells caused by foreign serum.

Quantitative changes in the pancreatic acinar cell organelles were studied in BALB/c mice injected with 1.0 ml fresh rabbit serum intraperitoneally. Groups of 5 mice were killed at 0, 1, 3, 6 and 12 h after the serum injection. Pancreatic tissue was processed for electron microscopy by glutaraldehyde and osmium tetroxide fixation and Epon embedding. The proportions of acinar cell cytoplasm (volume fractions) occupied by zymogen granules, granular endoplasmic reticulum, Golgi apparatus, mitochondria and lysosomes (including autophagosomes) were determined by the point counting method from electron micrographs. The volume fraction of lysosomes increased during the first 3 h and remained markedly elevated up to 12 h. The volume fractions of zymogen granules increased from 12 to 28% in 12 h. It was concluded that the secretory mechanism of pancreatic acinar cells was injured by the foreign serum. The injury caused accumulation of zymogen granules and increased autophagic activity in the acinar cells.

Animals↗
PubMed1978

The effect of ischaemia on the function and fine structure of the microvasculature of myocardium.

Seventeen mongrel dogs were subjected to ligation of the circumflex branch of the left coronary artery. At intervals from 10 to 300 minutes after ligation, 10 ml of a sodium fluorescein and colloidal thorium hydroxide solution were injected via an intra-arterial catheter placed distal to the ligature. Up to 20 minutes after ligation this tracer solution evenly perfused the left ventricular wall including the posterior papillary muscle (PPM). During 25 to 50 minutes there was a progressive patchy loss of perfusion into the PPM although the sub-epicardial region was evenly perfused. After 60 or more minutes of ischaemia it was not possible to inject this tracer solution into the subendocardial region. Electron microscopic examination indicated that this loss of vascular competence was possibly due to vasospasm of some vessels in the marginal zone between the perfused and non-perfused areas and was unlikely to be due to intravascular thrombosis, endothelial cell swelling, or to compression of vessels due to cell or tissue oedema.

Animals↗
PubMed1978

An association between the onset of rigor and loss of vascular competence in early myocardial infarcts.

Experimental myocardial ischaemia was induced in 12 anaesthetized mongrel dogs by ligation of the circumflex branch of the left coronary artery. Twenty minutes after ligation 1% sodium fluorescein injected into the artery distal to the ligature evenly perfused the left ventricular wall in the vicinity of the posterior papillary muscle (PPM) but, when injected 90 minutes after ligation, the PPM and adjacent subendocardial myocardium was not perfused by this tracer. Measurements with a linear variable transducer and standard load demonstrated that after 20 minutes ischaemia, the PPM had a similar percentage compressibility to the corresponding unaffected anterior papillary muscle but, after 90 minutes, the compressibility of the PPM was significantly reduced. Scanning electron microscopy of the marginal zone between the perfused and unperfused parts of the myocardium revealed many collapsed vessels which contained small groups of tightly packed erythrocytes indicating that the loss of vascular competence was probably due to the plugging of small vessels by erythrocytes.

Animals↗
PubMed1978

The effect of rigor mortis on the passage of erythrocytes and fluid through the myocardium of isolated dog hearts.

The effect of normal and artificially induced rigor mortis on the vascular passage of erythrocytes and fluid through isolated dog hearts was studied. Increased rigidity of 6-mm thick transmural sections through the centre of the posterior papillary muscle was used as an indication of rigor. The perfusibility of the myocardium was tested by injecting 10 ml of 1% sodium fluorescein in Hanks solution into the circumflex branch of the left coronary artery. In prerigor hearts (20 minute incubation) fluorescein perfused the myocardium evenly whether or not it was preceded by an injection of 10 ml of heparinized dog blood. Rigor mortis developed in all hearts after 90 minutes incubation or within 20 minutes of perfusing the heart with 50 ml of 5 mM iodoacetate in Hanks solution. Fluorescein injected into hearts in rigor did not enter the posterior papillary muscle and adjacent subendocardium whether or not it was preceded by heparinized blood. Thus the vascular occlusion caused by rigor in the dog heart appears to be so effective that it prevents flow into the subendocardium of small soluble ions such as fluorescein.

Animals↗