INT8662
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
Delayed elevation of plasma endothelin-1 during unilateral alveolar hypoxia without systemic hypoxemia in humans. | |||||||||||||||
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CONCLUSIONS: Tissue ischemia may increase venous ET-1 levels in humans. | |||||||||||||||
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Immediately after the initial release of the proximal and distal clamps, venous oxygen content dramatically decreased from 11.3 to 3.6 mL/dL (vol%) with significant increases in venous ET-1 concentration from 2.3 to 4.9 pg/mL. | |||||||||||||||
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CONCLUSIONS: We conclude that there might be an ischemic component in this patient with optic neuritis and hypothesize that this ischemic component is at least in part due to a temporarily increased endothelin-1 level.
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Infusion of HS-HES resulted in an increase in plasma endothelin concentration before and after CPB (from 3 to 6 pg/mL). | |||||||||||||||
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Thus, plasma endothelin level was elevated in patients with unstable angina pectoris and myocardial infarction and the increase persisted for several days after the onset of symptoms. | |||||||||||||||
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They point to the observation of significantly elevated ET-1 levels in vasospastic and systemic diseases such as multiple sclerosis, rheumatoid arthritis, fibromyalgia, and Susac syndrome. | |||||||||||||||
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Although animal models have suggested that increased levels of ET-1 by itself can lead to glaucoma via ischemia (Cioffi et al 2004), these same results have not been demonstrated in human population studies. | |||||||||||||||
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Several studies show that calcium channel antagonists reduce the effect of increased levels of ET-1 on ocular perfusion and improve visual field defects through induced vasodilation (Flammer et al 2001). | |||||||||||||||
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Grieshaber and Flammer (2005) suggest that the elevation of ET-1 in glaucoma represents an epiphenomenon rather than a distinctive mechanism. | |||||||||||||||
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Interestingly, the increase in CBV during selective ETA receptor blockade was more pronounced in type 2 diabetic patients with a high body mass index (BMI) and low levels of insulin-like growth factor binding protein-1 (IGFBP-1), supporting the existence of a close relationship between insulin resistance and increased ET-1 activity. | |||||||||||||||
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This supports the notion that the ET-1 system is upregulated in patients with type 2 diabetes and that ETA receptor blockade exerts hemodynamic effects only under such conditions. | |||||||||||||||
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Here we show that in a murine osteolytic 2472 sarcoma model of bone cancer pain, the 2472 sarcoma cells express high levels of ET-1, but express low or undetectable levels of endothelin A (ETAR) or B (ETBR) receptors whereas a subpopulation of sensory neurons express the ETAR and non-myelinating Schwann cells express the ETBR. | |||||||||||||||
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Additionally, we have recently demonstrated that ET-1 is significantly increased locally in OA cartilage and synovial membrane when compared with normal tissues. | |||||||||||||||
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RESULTS: The patient was found to have a temporary ocular blood flow dysregulation and increased plasma endothelin-1 levels which decreased after the acute phase of the optic nerve. | |||||||||||||||
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In venous plasma of patients with erectile dysfunction, significantly increased ET-1 and decreased NO levels were found [32]. | |||||||||||||||
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In addition, in postmenopausal women, long-term ERT decreased plasma ET-1 levels in the systematic circulation, associated with an increased NO-to-ET-1 ratio (Polderman et al 1993; Lieberman et al 1994). | |||||||||||||||
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Most patients with pulmonary artery hypertension have elevated EDN1 levels, and pharmacological blockage of EDN1 activity leads to clinical improvement and better prognosis [81]. | |||||||||||||||
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Aqueous humor levels of ET-1 are reportedly elevated in HTG (Noske et al 1997) and one study demonstrated a significant elevation of plasma ET-1 in HTG when the subjects were moved from the supine to upright position (Kaiser et al 1997). | |||||||||||||||
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To further support a role for vasospasm in endothelial dysfunction, Nicolela and colleagues (2003) reported an abnormal increase in plasma ET-1 in response to body cooling in OAG patients. | |||||||||||||||
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