Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0264733 (ventricular dilatation)
 2,163 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Survivors of both human and animal bacterial shock develop a characteristic pattern of progressive changes in cardiovascular function over a period of 7-10 d. In this present study, we examined whether endotoxin (a product of Gram-negative bacteria) or TNF (a cytokine released from macrophages) could reproduce the same complex cardiovascular changes observed in septic shock over a period of 7-10 d. To test this hypothesis, we implanted a thrombin-fibrin clot containing purified endotoxin from E. coli into the peritoneal cavity of eight dogs, and infused TNF into eight different dogs. Over the next 10 d, serial simultaneous heart scans and thermodilution cardiac outputs were performed in these awake nonsedated animals. By day 2 after challenge with either endotoxin or TNF, animals developed a decrease (p less than 0.05) in both mean arterial pressure and left ventricular ejection fraction. With fluid resuscitation, animals manifested left ventricular dilatation (increased [p less than 0.05] end diastolic volume index), increased or normal cardiac index, and decreased or normal systemic vascular resistance index. In surviving animals, these changes returned to normal with 7-10 d. The time course of these changes was concordant (p less than 0.05) with that previously described in a canine model of septic shock using viable bacteria. During the 10-d study, control animals receiving sterile clots or heat-inactivated TNF had not significant changes in hemodynamics. The results from this canine model demonstrate that either endotoxin or TNF alone can produce many of the same hemodynamic abnormalities seen in human septic shock and in a canine septic shock model induced by live bacteria. These findings support the hypothesis that the action of endogenous mediators (TNF) responding to bacterial products (endotoxin) is the common pathway that produces the serial cardiovascular changes found in septic shock.
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PMID:Endotoxin and tumor necrosis factor challenges in dogs simulate the cardiovascular profile of human septic shock. 264 95

Binswanger's disease (BD) is a condition characterized by prominent brain atrophy with ventricular dilatation, diffuse white matter (WM) lesions and a scattering of lacunar infarcts. BD patients have dementia, and have vascular risk factors, focal cerebrovascular deficits and evidence of subcortical cerebral dysfunction. From our clinical studies, the most effective prophylaxis against the development of BD is to manage the hypertension, especially a high nocturnal blood pressure, in the early stage patients showing only a scattering of lacunes and/or mild WM lesions. The pathogenesis of BD is likely to be chronic cerebral ischemia due to hypertensive small artery disease with capillary collagenosis, which causes the multiple lacunes and the alterations in the glia and axons. In addition, arterial hypertension and a subsequent dysfunction of the blood-brain barrier (BBB) may cause the WM lesions. A compromised BBB will permit the entry of serum components, immunoglobulins, complements and fibrinogen into the perivascular neural parenchyma. These substances may subsequently activate both astro- and microglia and thus damage the myelin structures. Experimentally, immunosuppressants, cyclosporin A and FK 506 suppressed both the glial activation and WM changes after chronic cerebral hypoperfusion. The pro-thrombotic state of the microcirculation in BD patients may also contribute to local inflammation and the BBB dysfunction, because thrombin and prostanoids are involved in various tissue reactions including brain edema and glial activation. Therefore, novel therapeutic approaches using the administration of anti-thrombin and cyclo-oxygenase-2 inhibitors as well as immunosuppressants may be useful for preventing the progression of BD.
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PMID:Cytopathological alterations and therapeutic approaches in Binswanger's disease. 1951 55