Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0851184 (thinning)
 11,252 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An abnormal elevation in collagen concentration or myocardial fibrosis occurs in the hypertrophied left ventricle of the rat with renovascular hypertension (RHT). The structural nature and functional consequences of this fibrosis and the mechanisms involved in its appearance were reviewed for various phases of hypertrophy. Within days after the onset of renal ischemia, type I collagen messenger ribonucleic acid is expressed. An interstitial fibrosis follows, characterized by an increased dimension of existing perimysial fibers and the appearance of fibrillar collagen in spaces previously devoid of collagen, together with a perivascular fibrosis of intramyocardial coronary arteries. These expressions of myocardial fibrosis are associated with an increase in diastolic and systolic myocardial stiffness. Endomyocardial fibrosis serves to further increase diastolic stiffness while myocytes encircled by fibrillar collagen become atrophic. Each of these consequences of myocardial fibrosis reduce myocyte length-dependent force generation. At 32 weeks of RHT there is an obvious diastolic and systolic dysfunction of the ventricle together with heart failure that includes ventricular dilatation, wall thinning and reduced ejection fraction. The mechanisms involved in mediating fibrosis in RHT appear to be multiple. Myocyte necrosis and fibroblast proliferation have been associated with elevated circulating angiotensin II. Necrosis in RHT was not seen with captopril pretreatment or in the hypertension and hypertrophy that accompanied infrarenal aorta banding. An alteration in coronary artery permeability may be responsible for the perivascular fibrosis that is not seen with captopril pretreatment. Thus in RHT, the hemodynamic status of the ventricle determines myocyte hypertrophy while the elevation in circulating angiotensin II is responsible for the remodeling of nonmyocyte compartments, including the appearance of myocardial fibrosis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Myocardial fibrosis and pathologic hypertrophy in the rat with renovascular hypertension. 213 51

Resetting of arterial and arteriolar wall structural components have been studied in the white rat kidney glomeruli after experimental ischemia (30 min, 1-3 h) without blood flow recovery and with the following recirculation for 3-30 days. The experiments have established that acute renal ischemia caused by the vascular leg ligation for 30-60 min without the following blood flow recovery results in slight microstructural alterations of arterial and arteriolar wall elements. With increased ischemia duration (2-3 h) pathological changes become more prominent and separation of vascular endothelial cells and defibering of the internal elastic membrane take place. In transitory (30-60 min) ischemia of the remaining kidney (one kidney is removed) three days later desquamation of endothelial cells occurs in some arteries. Thinning of arterial walls and overstrain of internal elastic membrane are observed. However, later on (in 30 days) short-term ischemia (30 min) is followed by complete recovery of structural components of arterial and arteriolar walls. In more durable ischemia (2-3 h) of the remaining kidney the recovered blood flow causes marked destructive life-threatening changes in vascular walls.
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PMID:[Morphological evaluation of the state of the structural elements of arterial and arteriolar walls in experimental kidney ischemia]. 394 24

ATP-depletion in renal cultured cells has been used as a model for studying various cytoskeletal and functional alterations induced by renal ischemia. This communication explores the reversibility of these effects utilizing a novel method [1] that depleted ATP (ATP-D) to 2% of control within 30 minutes and caused complete recovery (REC) of ATP in one hour. Under confocal microscopy, ATP-D (30 min) caused thinning of F-actin from the microvilli, cortical region, and basal stress fibers, with the concurrent appearance of intracellular F-actin patches. These changes were more pronounced after 60 minutes of ATP-D. One hour of REC following 30 minutes of ATP-D produced complete recovery of F-actin in each region of the cell. However, after 60 minutes of ATP-D, a heterogeneous F-actin recovery pattern was observed: almost complete recovery of the apical ring and microvilli, thinned cortical actin with occasional breaks along the basolateral membrane, and a dramatic reduction in basal stress fiber density. The time course of cortical actin and actin ring disruption and recovery coincided with a drop recovery in the transepithelial resistance and the cytoskeletal dissociation and reassociation of the Na,K-ATPase. Additionally, the microvilli retracted into the cells during ATP-D, a process that was reversed during REC. Triton extraction and confocal microscopy demonstrated that villin remained closely associated with microvillar actin during both ATP-D and REC. These distinctive regional differences in the responses of F-actin to ATP depletion and repletion in cultured renal epithelial cells may help to clarify some of the differential tubular responses to ischemia and reperfusion in the kidney.
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PMID:Actin and villin compartmentation during ATP depletion and recovery in renal cultured cells. 858 43

Structural alterations of the kidneys and their vascular system were studied in condition of arterial circulation deficiency induced by narrowing of the isthmus of the aorta in 30 pups. The animals were followed up from 6 to 24 months. The model of chronic renal ischemia was achieved in which there was a fall in blood flow in the descending aorta and in pressure of blood coming to the kidneys. The capacity of the arterial part of the renal circulation with reactive thinning of the walls of renal arteries of different caliber was diminished. Adaptation of a part of these vessels caused closure rearrangement and decreased blood filling of glomerular capillaries with collaboration of some of them. The capacity of renal venous collectors increased due to blood deposit. Sclerotic changes of renal arteries, veins and glomeruli, atrophy of renal parenchyma, stromal overgrowth developed with time.
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PMID:[The kidneys and their vascular system in deficient inflow of arterial blood (an experimental study)]. 1688 90

Optical coherence tomography (OCT) is a rapidly emerging imaging modality that can provide non-invasive, cross-sectional, high-resolution images of tissue morphology in situ and in real-time. In the present series of studies, we used a high-speed OCT imaging system equipped with a frequency-swept laser light source (1.3 mum wavelength) to study living kidneys in situ. Adult, male Munich-Wistar rats were anesthetized, a laparotomy was performed and the living kidneys were exposed for in situ observation. We observed the kidneys prior to, during and following exposure to renal ischemia induced by clamping the renal artery. The effects of intravenous mannitol infusion (1.0 ml of 25%) prior to and during renal ischemia were also studied. Finally, living kidneys were flushed with a renal preservation solution, excised and observed while being stored at 0-4 degrees C. Three-dimensional OCT data sets enabled visualization of the morphology of the uriniferous tubules and the renal corpuscles. When renal ischemia was induced, OCT revealed dramatic shrinkage of tubular lumens due to swelling of the lining epithelium. Three-dimensional visualization and volumetric rendering software provided an accurate evaluation of volumetric changes in tubular lumens in response to renal ischemia. Observations of kidneys flushed with a renal preservation solution and stored at 0-4 degrees C also revealed progressive and significant loss of tubular integrity over time. Intravenous infusion of mannitol solution resulted in thinning of the tubular walls and an increase in the tubular lumen diameters. Mannitol infusion also prevented the cell swelling that otherwise resulted in shrinkage of proximal tubule lumens during ischemia. We conclude that OCT represents an exciting new approach to visualize, in real-time, pathological changes in the living kidney in a non-invasive fashion. Possible clinical applications are discussed.
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PMID:High-resolution optical coherence tomography imaging of the living kidney. 1826 76

The paper provides a retrospective study of long-term results of ureterocalicostomy (UC) performed in one specialized center. The study included 37 patients who underwent UC as a primary (43.2%) or secondary (56.8%) operation for intrarenal hydronephrosis or urolithiasis. All surgical interventions were classified into two groups according to the type of kidney resection: Type I - if the kidney parenchyma was more than 10 mm, the entire lower pole of the kidney was removed (72.9%); Type II - if the parenchyma was less than 10 mm, a part of the lower pole (1.5-2.0 cm) was removed in the zone of maximal parenchymal thinning (24.3%). All resections, depending on the angle of their plane, were also divided into transverse (48.6%) and oblique (51.4%). Early postoperative complications were observed in 14 (37.8%) patients. All complications were not severe and were classified as Grade I-II according to the Clavien-Dindo system. The univariate analysis showed that the predictors of UC complications are the long duration of the operation, warm renal ischemia for more than 20 minutes, the secondary nature of the operation, as well as the presence of acute pyelonephritis and urinary extravasation before the operation. The rate of good long-term results was 81.1% (n=30), satisfactory - 13.5% (n=5), poor - 5.4% (n=2). The reliable prognostic value in terms of negative surgery results had: the thickness of the renal parenchyma below 10 mm, as well as the use of Type II resection of the renal parenchyma. Conclusion. A high level of good UC results was demonstrated. The most important predictor was the renal parenchyma thickness less than 10 mm.
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PMID:URETEROCALICOSTOMY FOR RECONSTRUCTION OF THE UPPER URINARY TRACT. 3284 Nov 77