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

Despite the rat heart having very low collateral flow, there are many reports of pharmacological limitation of infarct size in rats with permanent coronary occlusion. Investigating possible artefacts, cardiac function was measured in isolated rat hearts (n = 12/group) 1, 2, 4, 6, 12, 18, 24, or 48 h after permanent coronary occlusion. In sham operated controls, cardiac output was 63.8 +/- 3.8 ml/min; in rats with occlusion this fell to 37.7 +/- 3.3 ml/min after 1 h of occlusion and did not increase during the 48 h of study. Lumen areas, areas of underperfusion, and minimum wall thickness were unchanged after 4 h of occlusion. Between 4 and 12 h, substantial wall thinning occurred (midinfarct wall thickness decreased from 3.69 +/- 0.24 mm to 2.01 +/- 0.16 mm). After 12 h of occlusion, wall thinning and expansion of the infarct increased lumen volume by three- to fourfold. Wall thinning resulted in a progressive decrease in the volume of the zone of underperfusion (which decreased by almost 30% over 48 h). Tetrazolium negative tissue was not evident in the first 4 h of occlusion but by 12 h, 85.0 +/- 2.6% of the underperfused tissue was necrotic. Gross examination of sections often indicated apparently tetrazolium positive tissue within the zone of underperfusion. Microscopic examination of histological sections revealed this tissue to be necrotic but, in contrast to the tetrazolium negative tissue within the zone of underperfusion, not yet subject to white cell infiltration. "Apparent" infarct size limitation in the rat heart might be due to: (1) incorrect designation of tissue as tetrazolium positive within the severely ischaemic zone of underperfusion; (2) inappropriately equating the zone of underperfusion (measured at the end of ischaemia) to the risk zone (measured at the onset of ischaemia); (3) the possibility that some drugs might affect white cell infiltration, tetrazolium staining characteristics, wall thinning, and tissue remodelling.
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PMID:Evolving myocardial infarction in the rat in vivo: an inappropriate model for the investigation of drug-induced infarct size limitation during sustained regional ischaemia. 245 66

In utero inflammation may accelerate fetal lung maturation but may also play a role in the pathogenesis of chronic lung disease. We examined the impact of endotoxin, a potent proinflammatory stimulus, on structural and functional maturation of preterm sheep lungs. Date bred ewes received 20 mg Escherichia coli endotoxin or saline by ultrasound guided intra-amniotic injection at 119 d gestation. A comparison group of animals received 0.5 mg/kg betamethasone, a known maturational agent, at 118 d gestation. Lambs were delivered by cesarean section at 125 d (term = 150 d) and ventilated for 40 min. Lung function data are reported elsewhere. Total and differential white cell counts were performed on amniotic fluid and fetal lung fluid samples. Morphometric analyses were performed on inflation fixed right upper lobes. Total cell count increased slightly but not significantly in both amniotic fluid and fetal lung fluid. Both endotoxin and betamethasone had similar effects on alveolarization: average alveolar volume increased by approximately 20% and total alveolar number decreased by almost 30%. Both treatments led to thinning of alveolar walls, although this was statistically significant in the betamethasone-treated group only. Although antenatal endotoxin leads to striking improvements in postnatal lung function, this may be at the expense of normal alveolar development.
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PMID:Antenatal endotoxin and glucocorticoid effects on lung morphometry in preterm lambs. 1110 47