Hepatitis in young drug users.
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Biomedical subjects
Publications and source records attributed to C Ott.
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The nature of the activity of vasopressin which is responsible for the inhibition of renin secretion was studied by comparing the effects of vasopressin (AVP) and analogs of AVP in anesthetized water-loaded dogs. Infusion of AVP (1.0 ng/kg/min) increased mean arterial pressure (MAP) and decreased heart rate (HR) and free water clearance (CH2O). Plasma renin activity (PRA) decreased from 11.9 +/- 4.7 to 3.8 +/- 1.7 ng/ml/3 hr (p less than 0.05). A selective antidiuretic agonist, 1-deamino-8-D-arginine vasopressin (1.0 ng/kg/min), which had no effect on MAP or HR but was effective as AVP in decreasing CH2O, decreased PRA from 13.5 +/- 4.6 to 7.0 +/- 2.9 ng/ml/3 hr (p less than 0.05). Infusion of a selective vasoconstrictor agonist, 2-phenylalanine-8-ornithine oxytocin (1.0 ng/kg/min), increased MAP and decreased HR but did not decrease CH2O or PRA. A vasoconstrictor antagonist, d(CH2)5Tyr(Me)AVP (10 micrograms/kg), completely blocked the MAP and HR responses to AVP but did not block the decrease in CH2O or PRA (5.9 +/- 1.8 to 2.9 +/- 1.6 ng/ml/3 hr) (p less than 0.001). Infusion of the 0.45% saline vehicle had no significant effect on MAP, HR, CH2O or PRA. These results indicate that the inhibition of renin secretion by vasopressin in anesthetized water-loaded dogs is due to its antidiuretic activity.
Malondialdehyde (MDA) plasma concentrations (marker of lipid free radical peroxidation) and the unfractionated leucocyte and erythrocyte filterability rates (through 5 micron Nuclepore filters in a positive pressure filtration system) were determined during a partial ischaemia induced by two consecutive treadmill tests in 64 stage II peripheral vascular disease (PVD) patients and in 32 matched controls. Transcutaneous oxygen pressure (tcPO2) was monitored constantly throughout the walking tests and recovery periods. In the PVD patients impairments in the flow properties of leucocytes and erythrocytes were associated with increases in MDA plasma concentrations which correlated significantly with a lengthening of the tcPO2 half recovery times--index of the worsening of ischaemia. Patients could be divided into two sub-groups on the basis of these impairments and their half recovery times, suggesting this experimental model may provide a means to identify those stage II PVD patients most likely to develop critical limb ischaemia.
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Before and after a physical training programme a treadmill exercise was used to stress leg circulation and induce ischaemia in 20 patients affected by peripheral arterial occlusive disease (PAOD). Transcutaneous oxygen pressure (TcPO2) was monitored constantly and blood samples drawn at baseline, the onset of calf pain, the maximum walking time, the minimum TcPO2 value, and when the TcPO2 recovered half its basal value. The mononuclear and polymorphonuclear leucocyte subfractions were separated by density and their filterability rates (through 5 microns pore diameter Nuclepore filters) measured using a positive pressure filtration system. The mononuclear filterability rate was significantly impaired throughout the ischaemic event and inversely correlated with the TcPO2 values. Physical training while delaying the onset and progress of ischaemia did not modify this pattern, implying that regular exercise does not affect the rheological properties of leukocytes--impairments in which are markers of ischaemia.
Some markers of inflammation were monitored, and whole blood filterability was measured using a low shear positive pressure nuclepore filtration system in 21 patients at the onset of an acute bacterial infection and again after full clinical recovery 4 weeks later and compared to the filterability of 40 matched healthy controls. Impairments in whole blood filterability persisted even after convalescence.
Transcutaneous oxygen pressure (tcPO2), the unfractionated leukocyte filterability rate (ULFR), and plasma oxydant activity (POA) were monitored during a standard treadmill exercise test (2 km/h, 12 degrees slope) in two groups of stage-II peripheral vascular disease patients: one middle-aged group with an average age of 55 +/- 3 s.d. years, the other group elderly (average age 68 +/- 4 s.d. years). The results were compared to a healthy control group of 20 volunteers (average age 52 +/- 4 s.d. years). At the maximum walking time, the ULFR was significantly (p less than 0.001) impaired in both groups of patients compared to controls, and the level of plasma oxidant activity increased significantly (p less than 0.001). When the tcPO2 recovered half its basal value, the level of plasma oxidant activity approached basal values but the ULFR remained significantly (p less than 0.001) impaired. Inter-group analysis showed the total walking time was significantly (p less than 0.05) shorter in the elderly patients, and at the tcPO2 half recovery time the ULFR was significantly (p less than 0.01) more impaired.
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