scholarly journals Assessment of PEEP-Ventilation and the Time Point of Parallel-Conductance Determination for Pressure-Volume Analysis Under β-Adrenergic Stimulation in Mice

2019 ◽  
Vol 6 ◽  
Author(s):  
Lucas Bacmeister ◽  
Sebastian Segin ◽  
Rebekka Medert ◽  
Diana Lindner ◽  
Marc Freichel ◽  
...  
2005 ◽  
Vol 173 (4S) ◽  
pp. 390-390 ◽  
Author(s):  
Victor K. Lin ◽  
Shih-Ya Wang ◽  
Claus G. Roehrborn

2004 ◽  
Vol 43 (05) ◽  
pp. 143-149 ◽  
Author(s):  
N. Hamscho ◽  
C. Menzel ◽  
L. Neuss ◽  
A. F. Kovács ◽  
F. Grünwald ◽  
...  

Summary:Aim: For the evaluation of the diagnostic potential of dual time point FDG positron emission tomography (PET) in patients with suspicious focal abdominal up-take, dual time point PET imaging was compared with clinical findings. Patients, methods: In a prospective study, 56 patients exhibiting a solitary suspicious, intense abdominal FDG uptake, underwent dual time point PET imaging for staging or restaging of different malignant tumors, maximal standardized uptake value (SUVmax) measurements included. The first acquisition was started 64.8 ± 19.5, the second 211.3 ± 52.5 min after FDG injection. The final diagnosis based on CT or MRT imaging and a follow-up period of 12.6 ± 2.8 months. Additionally, colonoscopy was done in 6 patients. In another 6 patients histopathology was obtained from CT guided biopsy. Results: Malignant focal abdominal lesions with a SUVmax <2.5 (n = 4) showed an uptake increase of ≥30%. In the remaining malignant cases with an uptake of ≥2.5 (n = 11), up-take increased in 64% and decreased in 36%. Malignant lesions showing FDG uptake decrease (n = 4) had an initial SUVmax value ≥2.5 and remained with a SUVmax ≥2.5 in the second imaging. In benign lesions with an initial SUVmax ≥2.5 (n = 31), the uptake increased in 17 patients (55%) and decreased in 14 patients (45%). All lesions which changed configuration (33%) were confirmed as benign (n = 5). Conclusion: Using dual time point PET abdominal lesions show a very hetergenous uptake pattern regardless of their dignity. Malignancy can only be reliably excluded in lesions which change their configuration and in lesions with an initial SUVmax value <2.5 combined with an SUV decrease in the delayed imaging. Particularly abdominal lesions which show an initial SUVmax ≥2.5 combined with a SUV increase in the delayed imaging are suspicious for malignancy and need further clarification.


1992 ◽  
Vol 68 (05) ◽  
pp. 545-549 ◽  
Author(s):  
W L Chandler ◽  
S C Loo ◽  
D Mornin

SummaryThe purpose of this study was to determine whether different regions of the rabbit vascular system show variations in the rate of plasminogen activator (PA) secretion. To start, we evaluated the time course, dose response and adrenergic specificity of PA release. Infusion of 1 µg/kg of epinephrine stimulated a 116 ± 60% (SD) increase in PA activity that peaked 30 to 60 s after epinephrine administration. Infusion of 1 µg/kg of norepinephrine, isoproterenol and phenylephrine had no effect on PA activity. Pretreatment with phentolamine, an alpha adrenergic antagonist, blocked the release of PA by epinephrine while pretreatment with the beta blocker propranolol had no effect. This suggests that PA release in the rabbit was mediated by some form of alpha receptor.Significant arterio-venous differences in basal PA activity were found across the pulmonary and splanchnic vascular beds but not the lower extremity/pelvic bed. After stimulation with epinephrine, PA activity increased 46% across the splanchnic bed while no change was seen across the lower extremity/pelvic bed. We conclude that several vascular beds contribute to circulating PA activity in the rabbit, and that these beds secrete PA at different rates under both basal and stimulated conditions.


1970 ◽  
Vol 23 (03) ◽  
pp. 417-422 ◽  
Author(s):  
D. G McKay ◽  
J.-G Latour ◽  
Mary H. Parrish

SummaryThe infusion of epinephrine in high doses produces disseminated intravascular coagulation by activation of Hageman factor. The effect is blocked by phenoxybenz-amine and is therefore due to stimulation of α-adrenergic receptor sites.


Author(s):  
A Goßmann ◽  
C Bangard ◽  
A Mühler ◽  
K Krüger ◽  
M Zähringer ◽  
...  
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