21 research outputs found

    Diabetes and reactivity of isolated human saphenous vein

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    Helical strips of saphenous veins from diabetic ( n =8) and non-diabetic ( n = 18) humans were studied in vivo for their responsiveness to several vasoactive agents. Following application of passive force (˜20·0 mN), venous strips from non-diabetic humans often developed spontaneous phasic contractile activity (12 out of 18 patients; 2–5 contractions/min). These intrinsic changes in force were seen in venous strips from only one diabetic patient. The phasic contractions were not altered by treatment with phentolamine, whereas the calcium channel blocker, D-600, and calcium-free solution (1·0 mM EGTA) inhibited the phasic contractions. Saphenous veins from diabetic patients developed less maximal, active tension in response to norepinephrine than those from non-diabetic patients. Contractile responses to serotonin, angiotensin II, and elevated potassium concentration in saphenous veins from diabetic patients were not different from those in veins from non-diabetic patients. These observations demonstrate attenuated development of active tension in response to alpha-adrenergic receptor activation and reduced spontaneous contractile activity in venous smooth muscle from diabetic patients.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/74640/1/j.1475-097X.1984.tb00136.x.pd

    Characteristic Changes of Vascular Adrenergic Reactions in Diabetes Mellitus

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    Natural killer cell activity in families of patients with systemic lupus erythematosus: demonstration of a killing defect in patients

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    Natural killer (NK) cell cytotoxic activity and cell frequency, expressed as a percentage of total lymphocytes, have been determined in peripheral blood mononuclear cells from first-degree relatives of patients with systemic lupus erythematosus (SLE), the patients themselves, a group of rheumatoid arthritis (RA) patients and controls. Low levels of killing activity relative to controls were found in some members of all groups with the extent of depression falling into two ranges. Moderate reductions were seen in female (3/31, 10%) and male (4/14, 29%) relatives of SLE patients, female (12/60, 20%) and male (3/4, 75%) SLE patients and female RA patients (6/17, 35%). A more profound depression of killing activity was confined to other female SLE patients (15/60, 25%). There were strong correlations in all groups between killing activity and percentage of NK cells, but analysis of the ratio of these parameters and studies with purified preparations of NK cells suggest that the reduced activity in SLE frequently involves a defect in the killing capacity of the individual cells in addition to the reduced levels of NK cells. Azathioprine (AZA), which was used in treatment of 12 SLE patients, was invariably associated with low values of killing activity. It appears to substantially reduce the percentage of NK and B cells in an action unconnected with the NK cell abnormalities associated with SLE. The finding of low killing activity in relatives and a correlation between their activity and that of their patients support the view that NK cell deficiency is a genetic determinant of SLE. NK cells in SLE may produce insufficient levels of cytokines required for the regulation of IgG production
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