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Biomedical subjects

M Prager

Publications and source records attributed to M Prager.

43 records · Page 3Linked to original sources
PubMed1986

[Right atrial and ventricular thrombus formation in advanced left-side hypernephroma].

Hypernephromas may give rise to extensive thrombus formation in the inferior vena cava. In a 70-year-old female patient, two-dimensional echocardiography revealed a well-defined mass (2 X 2 cm in dimension) in the right atrium with occlusion of the tricuspid valve and thrombo-embolic material spreading from the inferior vena cava to the right atrium. This finding was confirmed by computed tomography and cavography. Computed tomography of the abdomen detected a large left-sided renal tumour and thrombotic occlusion of the whole vena cava. The patient was not willing to undergo surgery and the masses of thrombo-tumorous material in the right atrium and ventricle spread rapidly. Meanwhile a spontaneous recanalization of the oval foramen occurred. The patient died from massive pulmonary embolism. Only the signs and symptoms of right heart failure with confirmed thrombus formation in the right atrium led to the diagnosis of hypernephroma.

Aged↗
PubMedDate not supplied

Development of 'no-reflow' phenomenon in ischemia/reperfusion injury: failure of active vasomotility and not simply passive vasoconstriction.

BACKGROUND/AIM: Local blood flow failure (no-reflow phenomenon) during ischemia/reperfusion (I/R) injury may be mediated by interstitial edema formation (passive vasoconstriction) and/or microvascular spasm (active vasoconstriction). The development of the no-reflow phenomenon in the rabbit hind limb I/R model and the influence of treatment with L-arginine and/or antioxidative vitamins were investigated. METHODS: Untreated rabbits were compared with those treated with L-arginine (4 mg/kg/min) or antioxidative vitamins (0.4 ml/kg) alone or in combination during hind limb I/R (2.5/2 h). Interstitial edema formation and microvessel diameter alterations were measured morphometrically. Capillary blood perfusion was measured continuously with laser Doppler flowmetry. RESULTS: I/R injury was expressed by interstitial edema formation (interstitial space increase by 80%), microvascular constriction (microvessel cross-sectional area decrease by 30%), and development of no-reflow phenomenon (blood flow reduction by 60%). Treatment with antioxidative vitamins alone or L-arginine alone reduced interstitial edema by 22 and 31%, consequently, while combined L-arginine/antioxidative vitamin treatment showed a more pronounced edema reduction by 40%. Treatment with only antioxidative vitamins failed to influence the development of no-reflow, although interstitial edema formation was reduced. L-Arginine treatment alone or in combination with antioxidative vitamins prevented microvascular constriction and preserved blood flow after reperfusion without development of no-reflow despite still apparent interstitial edema. CONCLUSIONS: Affections of active vasomotility and not merely passive changes of external pressure (i.e., interstitial edema formation) should be considered important in the development of microvascular constriction during 'no-reflow' phenomenon.

Animals↗
PubMedDate not supplied

Positive effect of treatment with synthetic steroid hormone tibolon on intimal hyperplasia and restenosis after experimental endothelial injury of rabbit carotid artery.

BACKGROUND: Arterial intimal hyperplasia and following restenosis may be inhibited by estrogens. We investigated the effect of a synthetic steroid hormone, Tibolon: (a) on intima hyperplasia and restenosis in vivo, and (b) on production of endothelial nitric oxide synthase (eNOS), vascular endothelial growth factor (VEGF), endothelial cell proliferation and apoptosis in vitro. METHODS: Influence of Tibolon treatment (0.1 mg/kg body weight, during 3 days before and 3 weeks after the operation as a drinking solution once daily) on neointimal formation (measured by morphometry) and arterial wall damage (by qualitative histology) were investigated in vivo using an animal model of balloon injury of carotid artery. In human umbilical vein endothelial cells (HUVEC) and human microvascular endothelial cells (HMEC-1), the effect of Tibolon (0.1 microg/ml) on eNOS and VEGF was assessed by ELISA. Cell proliferation was induced by VEGF(165) and measured by BrdU incorporation assay, cell apoptosis was detected colorimetrically measuring DNA fragmentation. RESULTS: Balloon injury resulted in neointima formation and prominent damage of the carotid artery wall. Treatment with Tibolon increased luminal area, decreased intimal area and intima to media ratio, and promoted better reparation of damaged vessel wall. In vitro, Tibolon treatment did not influence the expression of eNOS protein in HUVEC as well as cell proliferation rate but reduced apoptosis of endothelial cells by about 40%. Additionally, this treatment suppressed basal and IL-1beta-stimulated synthesis of VEGF in HMEC-1. CONCLUSIONS: Tibolon treatment suppressed neointimal formation and promoted better reparation of damaged vessel wall in carotid artery after balloon injury. This positive effect seems to be associated with improved endothelial cell survival resulting possibly in increased NO production. It might be also related to the decrease of VEGF generation.

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