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)

Indomethacin has been shown to increase virus titers and to worsen cardiac injury in the acute phase of coxsackievirus B4 murine myocarditis. The authors evaluated the effects of indomethacin on the histopathologic changes in a later phase of this disease after virus clearance. Two-day old CD1 mice were infected with coxsackievirus B4. Ten days later, surviving animals were randomized to receive indomethacin or saline intraperitoneally for 10 days. They were then euthanatized, and their hearts were examined for the presence of inflammation, necrosis, scarring, and focal thinning. Mortality was slightly higher among treated animals (7/15 versus 2/12, p = 0.3). The index of inflammation (0.6 +/- 0.5 versus 0.7 +/- 0.5) necrosis and scarring (0.4 +/- 0.5 versus 0.3 +/- 0.5) among treated and control animals, respectively, was not significantly different, but the size of involved myocardium (149742 +/- 201982 versus 35300 +/- 45413 microns2) was remarkably larger (p less than 0.05), and focal ventricular thinning (5/12 versus 0/10, p = 0.03) was encountered among indomethacin recipients exclusively. These findings indicate that indomethacin treatment in the late phase of coxsackievirus B4 myocarditis enhances myocardial damage and increases the incidence of focal ventricular thinning.
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PMID:Focal ventricular thinning caused by indomethacin in the late phase of coxsackievirus B4 murine myocarditis. 131 98

The effects of the prostaglandin synthesis inhibitor, indomethacin, on the preovulatory morphology of apical follicle walls have been examined by transmission electron microscopy. Immature mice, superovulated with 5 IU pregnant mare serum (PMS) followed 40 hours later by 80 IU luteinizing hormone (LH) were treated with either 10 mg/kg indomethacin or an equivalent volume of the indomethacin vehicle 10 minutes prior to LH. Follicular apices from both groups were compared at 12 hours post-LH. Indomethacin treatment suppressed many of the morphological changes normally occurring in the apex during preovulatory development. Whereas apices from vehicle-treated animals demonstrated marked deterioration, dissociation, and thinning of tissue, the cell layers of apices from indomethacin-treated animals remained thickened and tightly packed, with limited signs of disruption. The results presented herein are consistent with the idea that prostaglandins are essential mediators of ovulation and suggest that these lipids augment apical rupture by mobilizing granulosa cells and stimulating the loss of connective tissue elements.
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PMID:An ultrastructural study of preovulatory apical development in mouse ovarian follicles: effects of indomethacin. 684 67

In order to demonstrate the possible role of prostaglandins in preovulatory follicular development, immature mice superovulated with pregnant mare serum followed 40 hours later by luteinizing hormone (LH) were treated with the prostaglandin-synthetase inhibitor, indomethacin. Indomethacin (10 mg/kg) injected at varying intervals prior to or following LH inhibited ovulation most effectively when administered within 2 hours of the ovulatory gonadotropin. This inhibition was accompanied by (1) suppression of the morphological changes normally occurring within the follicular wall during preovulatory development and (2) failure of germinal vesicle breakdown (GVBD) in two-thirds of the follicles examined. When GVBD occurred, indomethacin treatment appeared to delay meiotic maturation. Cumulus tissue was more compact than in control follicles and maintained a close association with the oocyte. These results suggest that alterations in the morphology of the follicle prior to ovulation--specifically, thinning of the apical follicular wall and meiotic maturation--are regulated by prostaglandins.
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PMID:Effects of indomethacin on preovulatory follicles in immature, superovulated mice. 712 57