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Query: UMLS:C0851184 (thinning)
 11,252 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cell transplantation has been proposed as a future therapy for various myocardial diseases. It is unknown, however, whether the encouraging results obtained in animal models of ischemia and reperfusion, cryoinjury or cardiomyopathy can be reproduced in the setting of permanent coronary artery occlusion and extensive myocardial infarction (MI). Embryonic cardiac cells were isolated and cultured for 3 days to confirm viability, morphology and to label cells with BrdU or the reporter gene LacZ. Seven days after extensive MI, rats were randomized to cell (1.5x10(6)) transplantation (n=11) or culture medium injection (n=16) into the myocardial scar. Echocardiography study was performed before and 53+/-3 days after implantation to assess left ventricular (LV) remodeling and function. During follow-up, there was no mortality among cell-treated rats v 4 of 16 control rats (P=0.12). X-gal staining, BrdU and alpha -SMA immunohistochemistry identified the engrafted cells 1 week, 4 weeks and 8 weeks after transplantation, respectively. Antibodies against alpha -SMA, connexin-43, fast and slow myosin heavy chain revealed grafts in various stages of differentiation in 10 of 11 cell-treated hearts. Many of them, however, kept their embryonic phenotype and were isolated from the host myocardium by scar tissue. Serial echocardiography studies revealed that cell transplantation prevented scar thinning, LV dilatation and dysfunction while control animals developed scar thinning, significant LV dilatation accompanied by progressive deterioration in LV contractility. Transplantation of embryonic cardiomyocytes after extensive MI in a rat model attenuate LV dilatation, infarct thinning, and myocardial dysfunction. Still, many grafts remain isolated and do not differentiate into an adult phenotype, even when studied 2 months after grafting.
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PMID:Influence of embryonic cardiomyocyte transplantation on the progression of heart failure in a rat model of extensive myocardial infarction. 1143 38

The aim of the study was to characterize the impact of short-lived total coronary occlusions in closed-chest pigs on radial wall thickening within the "at-risk" myocardial segment by using gray-scale M-mode echocardiography. Twelve pigs underwent a series of 20-second total circumflex coronary artery occlusions with an angioplasty balloon. Myocardial thickening/thinning indexes were continuously monitored before ischemia, during ischemia, and on reperfusion by high-resolution M-mode recordings of the posterior wall obtained from parasternal views. The timing of regional events was compared with global systolic time intervals derived from the color Doppler myocardial imaging velocity data. Each occlusion induced a rapid decrease in end-systolic thickening (epsilon(ES)), closely paralleled by an increase in postsystolic thickening in the ischemic segment. After 20 seconds of ischemia, epsilon(ES) decreased by -86% and postsystolic thickening increased by +100%, whereas maximal thickening decreased only by -34% in comparison with preocclusion values. All wall thickening parameters returned to baseline after 15 seconds of reperfusion. During acute total ischemia in a closed-chest animal model, the changes in regional myocardial function were best characterized by the combined analysis of systolic and postsystolic thickening abnormalities and by their respective timings relative to global cardiac events markers.
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PMID:Changes in systolic and postsystolic wall thickening during acute coronary occlusion and reperfusion in closed-chest pigs: Implications for the assessment of regional myocardial function. 1144 14

Renal biopsy specimens from patients with systemic lupus erythematosus (SLE) rarely show changes that are pathogenetically and morphologically unrelated to SLE. The morphology and behavior of these nonlupus nephritides are not well known. Two hundred fifty-two renal biopsies performed on 224 patients with SLE collected from 3,036 native kidney biopsies performed between 1975 and 1998 were reviewed, and those that showed nonlupus nephritides (index biopsies) were selected for studies. Thirteen biopsy specimens with nonlupus nephritides were identified in 13 patients, who belonged to 3 clinically distinct groups. Group I included 6 patients in whom SLE was diagnosed at the time of index biopsies. The index biopsies in these patients showed focal segmental glomerusclerosis (FSGS; 3 cases), Immunoglobulin (Ig) M nephropathy (1 case), and thin basement membrane disease (1 case). The diagnostic features for FSGS included segmental sclerosis involving at least 1 glomerulus, absence of lupus nephritis or other conditions that may cause nonspecific segmental sclerosis of glomeruli such as ischemia or nephrosclerosis, and nephrotic-range proteinuria. There was uniform, global, diffuse and marked thinning of the glomerular basement membrane in the case of thin basement membrane disease. Group II included 3 patients in whom SLE was diagnosed 2 to 9 years before the time of index biopsies and SLE was active at the time of biopsy. The index biopsies in these patients showed FSGS (2 cases) and hypertensive nephrosclerosis (1 case). Group III included 4 patients in whom SLE was diagnosed 5 to 36 years before the time of index biopsies and SLE was inactive at the time of biopsy. The index biopsies in these patients showed 1 case each of amyloidosis, FSGS, hypertensive nephrosclerosis, and allergic acute tubulointerstitial nephritis. Previous renal biopsies, performed in 5 patients, showed IgM nephropathy (1 case), diffuse proliferative lupus GN (1 case), focal proliferative lupus GN (1 case), and mesangial proliferative lupus GN (2 cases). Follow-up biopsies, performed in 3 patients, confirmed the diagnosis of FSGS (2 cases) and hypertensive nephrosclerosis (1 case) noted in the index biopsies. Nonlupus nephritides may occasionally be encountered in SLE patients, regardless of clinical or serologic disease activity. These renal lesions display a broad morphologic spectrum in which FSGS seems most frequent. Renal biopsy plays a crucial role in identifying these lesions, which may have prognostic and therapeutic implications distinct from those of lupus nephritis.
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PMID:Nonlupus nephritides in patients with systemic lupus erythematosus: a comprehensive clinicopathologic study and review of the literature. 1167 48

Gravid Nya:NYLAR mice, infected with Toxoplasma gondii on gestation day 7, experienced embryo resorptions, abortions, stillbirths, and a reduction in average litter size by one-third. Postnatally, all congenitally infected pups showed growth retardation, cachexia, and hind limb weakness. Some pups developed necrotic petechiae on the ears and tail, and a blood-tinged nasal discharge. Coronal sections of the cerebellum at age 1 month revealed developmental abnormalities including: persistence of remnants of an external granular layer; fragmented and disoriented Bergmann glial foot processes; numerous ectopic granule cells stranded in the molecular layer; focal disorganization and edema of the Purkinje cell layer; and thinning of the internal granular layer. Our working hypothesis is that the cerebellar anomalies originated with parasite invasion of the fetal vascular endothelium leading to vasculitis and microcirculatory dysfunction, perivascular edema, perfusion impairment, and tissue anoxia. In the cerebellar folia, the cellular migration defects are attributed to edema-induced swelling and fragmentation of the Bergmann glial foot processes that guide migrating neurons, whereas the focal loss of Purkinje and granule cells is ascribed to hypoxia-ischemia. Although Toxoplasma cysts were detected in the cerebellum, morphologic evidence of parasite association with neuropathology was not obtained.
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PMID:Cerebellar anomalies in congenital murine toxoplasmosis. 1210 72

The neuroprotective effect of MCI-9042 (Mitsubishi Pharma Corporation) was investigated on glutamate-induced retinal ganglion cell (RGC) death in vitro and on rat retinal ischemia in vivo. RGCs were purified from retinal cells isolated from 6-day-old Wistar rats and cultured in serum-free media. After application of 25 microM glutamate, the viability of RGCs treated with or without several serotonin 2 (5-HT(2)) receptor antagonists: MCI-9042, M-1 (a major metabolite of MCI-9042), ketanserin, and LY-53857; was evaluated by calcein-acetoxymethyl ester staining. Retinal ischemia was induced by intraocular pressure (IOP) elevation (130 mmHg, 50 min). Rats were intraperitoneally injected with MCI-9042 at a dose of 3, 30 mg/kg or base at 30 min before and just after ischemia-reperfusion. Retinal damages were evaluated by histology, morphometric analysis and electroretinograms (ERGs) recordings at 7 days after ischemia-reperfusion. 25 microM glutamate decreased the number of viable RGCs to about 60 to 65% of untreated RGCs. MCI-9042, M-1, ketanserin, and LY-53857 significantly reduced glutamate-induced RGC death at concentrations of more than 100 nM, 1 nM, 1 microM and 100 nM, respectively. Ischemia-reperfusion caused thinning of the thickness between the inner plexiform layer and the outer plexiform layer and attenuation of a-and b-waves in ERG recordings. The intraperitoneal injection of MCI-9042 significantly reduced morphological and functional damages in retinal ischemia. Our data demonstrate that 5-HT(2) receptor antagonists including MCI-9042 and M-1 have the neuroprotective effects in cultured RGCs and that MCI-9042 protects against ischemic retinal diseases.
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PMID:Effect of MCI-9042, a 5-HT2 receptor antagonist, on retinal ganglion cell death and retinal ischemia. 1263 9

The present study in rats investigated whether basic fibroblast growth factor (bFGF) plays an important role in cardioprotection against myocardial cell death and arrhythmias in acute myocardial infarction (AMI). After ligating the left coronary artery in 62 Wistar rats, 20 Eg of human recombinant bFGF was injected into the infarcted myocardium in 33 rats (group F), while saline was used for 29 control rats (group C). The development of ventricular tachyarrhythmias was assessed during the first 30 min of ischemia. After 24 h occlusion, the hearts of the surviving rats (group F: n=13, group C: n=10) were excised to assess minimum infarct wall thickness and infarct size, determine the number of TUNEL-positive cardiomyocytes and to analyze Bcl-2 and Bax expression by immunohistochemical staining and Western blotting. The incidence of ventricular tachycardia was higher in group C than in group F (p<0.05). The thinning ratio was higher in group F than in group C (p<0.05). There were fewer TUNEL-positive cardiomyocytes in the infarct border area in group F than in group C (p<.0001). Western blot analysis showed greater expression of Bcl-2 in group F than in group C (p<0.05), but similar expression of Bax in the 2 groups. In conclusion, intramyocardial administration of bFGF prevented ischemia-induced myocardial cell death and arrhythmias.
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PMID:Protective effect of basic fibroblast growth factor against myocyte death and arrhythmias in acute myocardial infarction in rats. 1265 65

After atraumatic birth, three neonates presented with muscle hypotonia and weakness. Flaccid paresis of the upper extremities, spasticity of the lower extremities, dissociate sensory loss and autonomic dysfunction developed later. This ruled out the initial, tentative diagnoses of cerebral palsy, spinal muscular atrophy or hereditary neuropathy. Diagnostic imaging revealed marked thinning of the cervical spinal cord in all patients. The possible aetiology of these lesions is considered. In all cases, an antenatal or perinatal infarction is thought to be the most probable cause. Different clinical pictures following intrauterine spinal cord ischemia are discussed. Spinal cord lesion must be considered even after atraumatic birth.
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PMID:Cervical spinal cord atrophy in the atraumatically born neonate: one form of prenatal or perinatal ischaemic insult? 1269 May 68

Immediately after an acute myocardial infarction (AMI) or in models of ischemia-reperfusion injury, cardiac endothelin (ET) system is markedly activated, and plasma levels of ET are increased. In the heart, expression of the main components of the ET system (ET-1 peptide, both receptor subtypes ETA and ETB, though not endothelin converting enzyme) are increased both at the gene level and protein level, in the viable myocardium, and--even more substantially--in the necrotic area. Despite these conspicuous abnormalities, the role of ET in this setting remains unclear. In the absence of human data, most short-term studies in animals (in terms of hours to up to 8 days post-AMI) and in the reperfused ischemic heart, have found beneficial effects of ET receptor blockade on survival rate, incidence of arrhythmias, cardiac function, and morphology. In contrast, many studies in which a long-term ET inhibition was started immediately post-infarction and the late effects were examined in animals with ensuing chronic heart failure (14-100 days postinfarction), adverse effects were also observed, such as scar thinning, further ventricular dilation, or even a worse survival rate. It appears that the ET system plays a dual role during the early post-AMI period. At present, it is not clear whether the short-term beneficial effects or long-term adverse effects of ET receptor blockade would prevail. Acute use of short-acting ET receptor antagonists in patients with AMI complicated by an acute heart failure is an attractive possibility that also remains to be investigated.
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PMID:The endothelin system and its role in acute myocardial infarction. 1283 71

This study investigates whether retinal ischemia/reperfusion leads to alterations in the expression of AMPA-type glutamate receptor (AMPAR) subunits GluR1-4. In ischemia-vulnerable hippocampal neurons, a subunit-specific downregulation of GluR2 precedes the actual neurodegeneration. Our purpose was to study whether retinal ischemia induces a similar downregulation of GluR2 preceding the loss of ganglion and amacrine cells. A 60-min ischemic period was followed by reperfusion lasting between 2 h and 7 days. Changes in the expression patterns of GluR1-4 were assessed using immunocytochemistry. In the same sections, alterations in cell density, thickness of retinal layers, and density of apoptotic cells were investigated. Two-hour post-ischemia, GluR1 immunoreactivity was nearly absent from the inner plexiform layer (IPL). Thereafter, labeling intensity recovered slowly and was close to control levels at 7 days, albeit in a thinner IPL. The decrease in GluR2/3 labeling intensity was most profound at 4 h. The recovery of GluR2/3 staining intensity was slow, and staining was still decreased at 7 days. GluR2 immunoreactivity was not attenuated after ischemia. GluR4 labeling showed a similar time course as observed for GluR1, but the decrease in immunoreactivity was less profound and the recovery was nearly complete. The immunostaining of PKCalpha, a rod bipolar cell marker, was unaffected at all reperfusion times. The reduction of GluR staining preceded both the typical thinning of the IPL and the peak of cell loss, but coincided with a significant swelling of the IPL. In conclusion, retinal ischemia/reperfusion leads to differential changes in the expression of the different AMPA-type GluR subunits, which may affect excitatory synaptic transmission in the inner retina. However, no evidence was found for a preferential loss of GluR2 immunoreactivity that could account for selective neurodegeneration of amacrine and ganglion cells after retinal ischemia.
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PMID:Ischemia-induced alterations of AMPA-type glutamate receptor subunit. Expression patterns in the rat retina--an immunocytochemical study. 1470 73

The most premature motion change after coronary occlusion is early diastolic thinning of the ischemic left ventricular (LV) wall, with concomitant thickening of the normoperfused wall. We aimed 1). to demonstrate that these early changes are the result of the absence of fluid within the ischemic myocardium (hydraulic skeleton) rather than to cell anoxia and 2). to quantitate the contribution of the lack of hydraulic skeleton to left ventricular asynergy of contraction in seven anesthetized dogs submitted to acute, short-lasting circumflex artery (Cx) occlusion (ischemia) and to perfusion of the Cx with an oxygen-free solution (anoxia). We analyzed the time course of regional work index (WI, area of the LV pressure-wall thickness loop) and regional efficiency (defined as the ratio of WI to the maximum possible work). Interwall asynergy was defined as the difference between the regional efficiency of the anterior and posterior walls. After 9-10 s, posterior wall efficiency decreased 37 +/- 6% with anoxia and 72 +/- 3% with ischemia (P < 0.025), and interwall asynergy was 0 +/- 6% with anoxia and 32 +/- 5% with ischemia (P < 0.05). The contribution of absent hydraulic skeleton to interwall asynergy (calculated as the difference between %asynergy in anoxia and %asynergy in ischemia) was 30 +/- 8% (P < 0.05). In conclusion, the earliest wall motion change observed after acute coronary occlusion, namely ischemic wall thinning concomitant with normoperfused wall thickening during isovolumic relaxation, is the result of the absence of intracoronary fluid. The lack of hydraulic skeleton within the myocardium contributes approximately 30% to interwall asynergy.
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PMID:Contribution of myocardium hydraulic skeleton to left ventricular wall interaction and synergy in dogs. 1503 Nov 22


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