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)

Since pyelocalicectasis alone is common in fetuses, we reviewed reports of fetal hydronephrosis that resolved spontaneously or at birth. Severe fetal hydronephrosis with calicectasis or parenchymal thinning rarely resolves spontaneously before or after birth. We also reviewed the clinical and experimental literature on renal hypertrophy. After unilateral nephrectomy in neonatal animals or after birth with congenital absence of one kidney in humans, the remaining kidney hypertrophies very quickly. In infants and young animals, the eventual size of the remaining kidney is inversely proportional to the age at which one kidney is lost. This improvement in residual renal function seen after renal loss in infancy, compared with older children, itself constitutes a strong argument for early relief of obstruction. If contralateral renal hypertrophy has occurred, the treated damaged kidney may resume growth in parallel with its hypertrophied mate but does not become as large or recover normal potential for growth. In other words, if correction of a unilateral obstruction is deferred until contralateral hypertrophy occurs, the obstructed kidney then has less potential for recovery of function.
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PMID:Natural history of fetal and neonatal hydronephrosis. 218 53

Recent studies suggest that neutrophil accumulation and activation in postischemic myocardium may be responsible for myocardial no reflow, which is characterized by an incomplete restoration of blood flow after reperfusion. To examine this further, 11 open chest, anesthetized dogs received bolus injections of a bovine neutrophil antiserum that produced an average 81 +/- 5% depletion of circulating neutrophils, and 10 control dogs received nonimmune serum. Each animal underwent 2 h of left circumflex artery occlusion followed by 4 h of reperfusion. Simultaneous two-dimensional echocardiography and radioactive microsphere blood flow studies were performed at baseline, 2 h of occlusion and early (approximately 5 min) and 4 h of reperfusion. During occlusion, both groups developed similar reductions in myocardial blood flow and levels of ischemic zone myocardial wall thinning. At early reperfusion, similar levels of hyperemia and regional hypokinesia were observed for both groups. By late reperfusion, both groups experienced significant no reflow in the subendocardium (p less than 0.05) and reduced reflow in the mid-myocardium. Regional depression in ischemic zone function persisted throughout the reperfusion period in both groups. However, infarct size expressed as a percent of left ventricular weight, assessed by triphenyltetrazolium chloride staining, was smaller for the neutrophil depletion group compared with the control group (8.7 +/- 1.3% versus 13.1 +/- 1.8%, p less than 0.05). It is concluded that an 81% neutrophil depletion fails to modify the no reflow phenomenon or improve functional recovery after 2 h of coronary artery occlusion and 4 h of coronary reperfusion despite modification of the ultimate size of necrosis.
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PMID:Neutrophil depletion fails to modify myocardial no reflow and functional recovery after coronary reperfusion. 258 73

With the use of an epicardial Doppler probe, systolic wall thickening was selectively measured in the inner, mid, and outer layers of the left ventricular (LV) wall in 16 conscious dogs undergoing a 15-min left anterior descending artery (LAD) occlusion followed by 7 days of reperfusion (REP). Under control conditions, percent thickening fraction (ThF) was significantly greater (P less than 0.01) in the inner layer [36.0 +/- 2.3% (mean +/- SE)] than in the mid (28.6 +/- 2.1%) or outer (21.3 +/- 2.2%) layers. During LAD occlusion, 11 dogs exhibited transmural dyskinesis (group 1), whereas 5 had transmural hypokinesis (group 2). In group 1, all layers exhibited comparable degrees of paradoxical systolic thinning during LAD occlusion. After REP, however, recovery was delayed in the inner compared with the mid and outer layers. At 2 h, ThF averaged 34.2 +/- 11.9% of base line in the endocardium vs. 61.7 +/- 16.2% in the midmyocardium and 51.0 +/- 12.3% in the epicardium (F = 4.29, P less than 0.002); similar differences were noted at 3 and 4 h. In the mid and outer layers, ThF returned to base-line values by 24 h, whereas in the inner layer it was still significantly depressed (P less than 0.05) at 24 h (77.3 +/- 5.1% of base line) and recovered by 48 h. The inner-to-outer ThF ratio was decreased (P less than 0.01) for 24 h after REP, indicating maldistribution of thickening in the "stunned" myocardium. In group 2, all layers exhibited hypokinesis during LAD occlusion. Again, recovery of function after REP was delayed in the endocardium compared with the other layers. This study demonstrates that after both severe ischemia resulting in dyskinesis and mild ischemia resulting in hypokinesis, REP is associated with slower recovery of function in the inner than in the outer layers. Thus myocardial "stunning" is a nonuniform phenomenon with maximal severity in the subendocardium.
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PMID:Nonuniform transmural recovery of contractile function in stunned myocardium. 276 26

Immediate percutaneous transluminal coronary angioplasty has been advocated for patients with a residual stenosis after coronary thrombolysis because of the possibility that the residual stenosis may restrict reflow and thereby increase infarct size. Because there are few experimental data bearing on this issue, we measured left ventricular function, myocardial blood flow, and infarct size in 20 anesthetized open-chest dogs during 2 hr of left circumflex occlusion and 4 hr of reperfusion. Ten animals were reperfused through a critical stenosis of the left circumflex artery (critical stenosis group) and the remaining 10 animals underwent full reperfusion without stenosis (control group). In both groups, a comparable degree of echocardiographic systolic wall thinning was present during occlusion and partial recovery of global and regional left ventricular function in the two groups. Subendocardial blood flow was decreased in the critical stenosis group relative to the control group at 5 min after reperfusion (0.52 +/- 0.16 ml/min/g in the critical stenosis group vs 1.55 +/- 0.32 ml/min/g in the control group, p less than .05) but not at 4 hr after reperfusion, when a reduced reflow response was seen in both groups. No differences in subepicardial blood flow were seen in the two groups of animals. Infarct size was slightly greater in the critical stenosis group than the control group, but this difference was not statistically significant (infarct/risk area ratio: 55.5 +/- 7.8% in the critical stenosis group vs 39.4 +/- 9.7% in the control group, p = .21). A close inverse exponential relationship was seen between infarct size/risk area ratio and subendocardial blood flow during occlusion (r = .89, p = .001). Two control animals had high levels of subendocardial collateral flow (greater than 0.2 ml/min/g); when these animals were excluded from analysis, differences in the infarct size/risk area ratio in the control and critical stenosis groups were less striking: (55.5 +/- 7.8% in the critical stenosis group vs 48.4 +/- 9.6% in the control group). Thus, the presence of a critical stenosis results in restriction of hyperemic blood flow to the subendocardium after reperfusion but does not influence infarct size or early left ventricular functional recovery.
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PMID:The effects of a critical stenosis on myocardial blood flow, ventricular function, and infarct size after coronary reperfusion. 334 86

Regional diastolic wall motion was studied with sonomicrometry in 30 open chest anaesthetised dogs after left anterior descending stenosis or occlusion. Post-systolic shortening and thickening, defined as the magnitude of segment shortening or wall thickening that occurred after end systole, was measured in peripheral and central ischaemic segments. These post-systolic events developed concurrently with impaired systolic shortening or thickening, either immediately after acute coronary occlusion or during progressive stenosis, and persisted with the development of dyskinesis and during reperfusion. The magnitude of these events in dyskinetic segments of 24 dogs was considerable, reaching 50(2)% (mean(SEM)) and 33(3)% of shortening or thickening that was present before coronary occlusion. Post-systolic shortening and thickening were maximum at 100(2) ms after peak negative dP/dt. Significant correlations were found between systolic shortening or thickening before coronary occlusion and post-systolic shortening (r = 0.74, 56 segments) or thickening (r = 0.84, 19 segments) after occlusion, but there was no correlation between post-systolic shortening or thickening and dyskinetic lengthening or thinning. In seven dogs followed for 4 h after coronary occlusion post-systolic shortening fell by 15% in peripheral segments and by 70% in central segments (p less than 0.002). In 17 dogs reperfused after 60 (n = 9) or 90 (n = 8) min of coronary occlusion the maximal recovery of systolic shortening early after reperfusion was significantly related to the magnitude of post-systolic shortening immediately before reperfusion (60 min occlusion r = 0.84, 90 min occlusion r = 0.88). These data show that post-systolic shortening is a marker of potential for early recovery of function of acutely ischaemic myocardium and suggest that it is due, at least in part, to an active process.
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PMID:Post-systolic shortening: a marker of potential for early recovery of acutely ischaemic myocardium in the dog. 344 Feb 62

This study examined the relationships between the left ventricular (LV) regional function, regional myocardial blood flow (RMBF), and myocellular necrosis after sudden proximal occlusion of the left anterior descending coronary artery (LAD) in 36 awake, unsedated dogs. Net wall thickening during systole (NET) was used to assess regional LV function, was expressed as percent control, and was measured with chronically implanted ultrasonic crystals. RMBF was measured with 8- to 10-micrometer radioactive microspheres. In regions with a moderate degree of functional loss, NET fell to 35.3 +/- 2.2% of control at 5 minutes when RMBF fell from 1.9 +/- 0.08 to .086 +/- 0.09 ml/g per min (P less than 0.05). No significant change occurred in midwall or epicardial RMBF. The relationship between endocardial flow and NET was non-linear (r = 0.69, P less than 0.0001). In these segments, subsequent changes in RMBF were unrelated to corresponding functional alterations through 24 hours. In segments with paradoxic systolic wall thinning RMBF fell in endocardial, midwall, and epicardial layers; endocardial ischemia was most severe (0.30 +/- 0.05 ml/g per min). Segmental myocellular necrosis was most severe in the endocardial layer and correlated significantly with both RMBF and segmental function. Myocellular necrosis increased in severity as flow was reduced below 70-75% of normal. Thus, in this model of LV ischemia, (1) regional LV functional loss is most sensitive to reductions in endocardial RMBF; (2) subsequent increases in RMBF are largely unassociated with functional recovery; (3) transmural ischemia results in paradoxical systolic wall thinning.
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PMID:Interrelationships between regional left ventricular function, coronary blood flow, and myocellular necrosis during the initial 24 hours and 1 week after experimental coronary occlusion in awake, unsedated dogs. 723 98

Following prolonged ischemia, if not adequately reperfused, myocardium undergoes necrosis, scarring and thinning. The myocardium tends to dilate in the noninfarcted ventricular area, giving rise to ventricular remodelling. If the ischemic myocardium is adequately reperfused it can be saved and its temporarily depressed functions eventually be recuperated (viable myocardium). The extent of recovery of the postinfarction viable myocardium seems to affect ventricular remodelling. The integrity of the microcirculation of the non-contractile myocardium following prolonged ischemia is fundamental in maintaining a contractile reserve adequate enough for a functional recovery (myocardial viability). Protection of the microcirculation during ischemia-reperfusion is therefore of great importance for the role that the microcirculation plays in ensuring myocardial viability. Experimental studies and initial clinical observations showed that calcium-antagonists exert a beneficial effect in this respect. VAMI is a multicentre, randomized double-blind, placebo-controlled study whose aim is to ascertain the potentiality of verapamil in limiting regional functional damage in patients with acute myocardial infarction and undergoing early thrombolysis.
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PMID:[Myocardial viability in acute myocardial infarction and verapamil]. 763 65

100 cases of RMVD underwent MVP successfully among 104 RMVD patients (utilization of MVP: 96%). The lesions included: MS in 31 cases, MI in 9, both in 60. preoperative cardiac function status was class III to IV in 94 cases. There were 6 early deaths and 6 late deaths (follow-up: 0.5-3.5 years). Postoperative cardiac function in 82 cases (93.2%) improved to class I to II. The authors focus their discussion on specific surgical technique and consider full functional recovery of mitral apparatus is the key for the success in MVP. The refined technique of removal of calcium deposits and thinning out of the proliferative fibrosis of the diseased valve have greatly increased the utilization of MVP. Eight standards in judgement to produce satisfactory mitral function under direct vision are described.
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PMID:[Report on 100 cases of rheumatic mitral valve disease treated with the valvuloplasty technique]. 804 11

Reperfusion alone during acute myocardial infarction (AMI) preserves left ventricular (LV) topography but causes 'stunning', with delayed or no recovery of function. To determine whether adjunctive intravenous nitroglycerin (NTG) accelerates functional recovery, we prospectively measured function and topography by repeated two-dimensional echocardiography between 1 day and 6 months in 5 groups of patients (n = 73) with a first AMI: placebo (group 1), NTG alone (group 2), NTG combined with successful reperfusion after 4 h (group 3) or failed reperfusion (group 4), and successful reperfusion alone (group 5). Asynergy decreased promptly (p < 0.001) and ejection fraction improved (p < 0.001) between day 1 and 6 months in groups 2 and 3 compared to baseline and groups 1, 4 and 5. Infarct expansion and thinning found in group 1 were prevented in groups 2, 3, 4 and 5. Diastolic volume increased in the anterior subgroup 1 but not 2, 3, 4 and 5. This is the first demonstration that reperfusion combined with adjunctive NTG produces earlier, greater and persistent recovery of LV function in addition to attenuation of remodeling in patients after AMI.
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PMID:Prompt improvement of left ventricular function and preservation of topography with combined reperfusion and intravenous nitroglycerin in acute myocardial infarction. 909 19

The use of adult stem cells for myocardial tissue repair might be limited in elderly and sick people because their cells are depleted and exhausted. The present study was conducted to explore the potential of human umbilical cord blood (UCB) CD133+ progenitor cells for myocardial tissue repair in a model of extensive myocardial infarction (MI). CD133+ progenitor cells were isolated from newborn UCB. Cells (1.2-2 x 10(6)) or saline (control) was infused intravenously 7 days after permanent coronary artery ligation in athymic nude rats. Left ventricular (LV) function was assessed before and 1 month after infusion by echocardiography. Tracking of human cells was performed by fluorescent in situ hybridization for human X and Y chromosomes or by immunostaining for HLA-DR or HLA-ABC. One month after delivery, LV fractional shortening improved by 42 +/- 17% in cell-treated hearts and decreased by 39 +/- 10% in controls (p = .001). Anterior wall thickness decreased significantly in controls but not in treated hearts. Microscopic examination revealed that the UCB cells were able to migrate, colonize, and survive in the infarcted myocardium. Human cells were identified near vessel walls and LV cavity and were occasionally incorporated into endothelial cells in six of nine cell-treated animals but not in controls. Scar tissue from cell-treated animals was significantly populated with autologous myofibroblasts as indicated by colocalization of HLA-DR and alpha-smooth muscle actin staining. In conclusion, the present work suggests that, after MI, intravenous delivery of human UCB-derived CD133+ cells can produce functional recovery by preventing scar thinning and LV systolic dilatation.
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PMID:Human umbilical cord blood-derived CD133+ cells enhance function and repair of the infarcted myocardium. 1619 18


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