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PubMed · 5536948

Proptosis.

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J E Wright. 1970. Proptosis.. https://pubmed.ncbi.nlm.nih.gov/5536948/

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This study was conducted to examine segmental differences in vasodilatation caused by the basal release of nitric oxide (NO) in the serially connected pulmonary vessels and to estimate the relative contributions of endothelial and neuronal NO synthase (NOS), and inducible NOS to the vasodilatation. Using an X-ray TV system on in vivo cat lungs, we measured internal diameter (ID) changes in resistance (100-400 microm ID), small conduit (600-1000 microm) and large conduit (1200-1700 microm) arteries, and veins of the same size. Non-selective NOS inhibitors, L-NAME (30-50 mg/kg i.v.) and L-NMMA (40-60 mg/kg i.v.), decreased the ID of all vessels studied, although their D-isomers had no effect. The decrease was larger in conduit arteries than in resistance arteries, with maximum response of small conduit arteries (25 +/- 2%), while venous segments displayed relatively uniform response (10-12%). L-Arginine completely abolished the ID decrease but hexamethonium bromide and phentolamine had no effect. Selective inhibitors of inducible NOS, L-canavanine (100 mg/kg i.v.) and S-methylisothiourea (10 mg/kg i.v.) did not affect any of the vessels. The data suggest that basal release of NO chiefly derived from endothelial NOS serves to dilate cat pulmonary arteries and veins, particularly small conduit arteries.

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Normal D-dimer levels in patients with pulmonary embolism.

BACKGROUND: Pulmonary embolism (PE) is frequently evaluated in acute care settings. Despite this, the clinical diagnosis of PE is difficult. Results of ventilation-perfusion (V/Q) scans may be inconclusive, and pulmonary angiograms (PAGs) are cumbersome, involve risk, and are often unavailable. Using PAG as the standard criterion, we evaluated the relationship between PE, V/Q scans, and semiquantitative latex agglutination (LA) D-dimer levels. METHODS: Ninety-eight patients who underwent V/Q scanning for suspected PE were enrolled; based on the results of the scans, the patients were scheduled for PAG. Blood samples were drawn for LA D-dimer assays during the PAGs at Saint Joseph Hospital, Denver, Colo, from January 1, 1996, to February 1, 1997. A detailed medical record review was performed for all enrollees. RESULTS: The mean+/-SEM patient age was 56.6+/-1.9 years; 52 (53%) were men, 13 (13%) had cancer, 23 (23%) had undergone surgery within 30 days of their PAG, and 13 (13%) were receiving warfarin sodium. There were no differences in warfarin therapy, hypercoaguable state, or cancer prevalence between patients with negative and positive PAGs (P = .53). Ventilation-perfusion scan results were available for all study patients. Eight (27%) of 30 patients who had positive angiogram results had LA D-dimer levels less than 250 ng/mL. Patients with positive PAGs (n = 30) had the following V/Q scan results: normal, 0; low probability, 7; intermediate or indeterminate probability, 22; and high probability, 1. In patients with low-probability V/Q scan results (n = 34), a positive D-dimer result for PE (>250 ng/mL) had a sensitivity of 71.4% (95% confidence interval, 0.29-0.97) and a negative predictive value of 87.5% (95% confidence interval, 0.62-0.98). We found a significant difference in D-dimer levels in patients with an abnormal angiogram result (mean, 750 ng/mL) compared with patients with a normal angiogram result (mean, 250 ng/mL) (P= .01, chi2 test). CONCLUSIONS: Eight patients had normal D-dimer levels with angiographic evidence of PE. Algorithms in acute care settings have been proposed; they exclude PE with normal D-dimer levels using the enzyme-linked immunosorbent assay technique. These cannot be extrapolated to the more widely used LA assays. A normal LA D-dimer level alone or with V/Q scan results is not recommended to preclude the treatment of PE.

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