Evaluation of alveolo-capillary permeability in thyrotoxicosis using Tc-99m DTPA aerosol scintigraphy

2005 ◽  
Vol 19 (3) ◽  
pp. 193-196
Author(s):  
Aziz Gültekin ◽  
Mahmut Yüksel ◽  
Selva Mert ◽  
Şakir Berkarda
Diabetes ◽  
1995 ◽  
Vol 44 (10) ◽  
pp. 1209-1212 ◽  
Author(s):  
M. A. Hussain ◽  
K. Studer ◽  
E. P. Messmer ◽  
E. R. Froesch

Author(s):  
Nikolai Hulde ◽  
N. Rogenhofer ◽  
F. Brettner ◽  
N. C. Eckert ◽  
I. Fetz ◽  
...  

Abstract Purpose Controlled ovarian stimulation significantly amplifies the number of maturing and ovulated follicles as well as ovarian steroid production. The ovarian hyperstimulation syndrome (OHSS) increases capillary permeability and fluid extravasation. Vascular integrity intensely is regulated by an endothelial glycocalyx (EGX) and we have shown that ovulatory cycles are associated with shedding of EGX components. This study investigates if controlled ovarian stimulation impacts on the integrity of the endothelial glycocalyx as this might explain key pathomechanisms of the OHSS. Methods Serum levels of endothelial glycocalyx components of infertility patients (n=18) undergoing controlled ovarian stimulation were compared to a control group of healthy women with regular ovulatory cycles (n=17). Results Patients during luteal phases of controlled ovarian stimulation cycles as compared to normal ovulatory cycles showed significantly increased Syndecan-1 serum concentrations (12.6 ng/ml 6.1125th–19.1375th to 13.9 ng/ml 9.625th–28.975th; p=0.026), indicating shedding and degradation of the EGX. Conclusion A shedding of EGX components during ovarian stimulation has not yet been described. Our study suggests that ovarian stimulation may affect the integrity of the endothelial surface layer and increasing vascular permeability. This could explain key features of the OHSS and provide new ways of prevention of this serious condition of assisted reproduction.


Author(s):  
Gy. Boros ◽  
J. Sámik ◽  
Ljubov Gofman ◽  
Judit Nagv ◽  
Gy. Deák ◽  
...  

Blood coagulation, thrombocyte function and capillary resistance were studied in 21 adult patients with Schoenlein-Henoch’s syndrome. 20 different tests were carried out at different stages of the disease. In 2 cases skin, in 1 mesocolon and in 10 kidneys were examined histologicaly (light microscopy, immunofluorescence, electron microscopy).Capillary permeability was increased at least once in every patient. All patients but 2 were characterized by hypercoagulability. In addition to thrombotic changes, an increase in labile fibrinogen was detected in the serum of 12 patients, and thrombin time was prolonged in 11 patients on 31 occasions. Plasma fibrinolytic activity was increased in 11 patients. Fibrin deposition was demonstrable in the skin of 2 in the mesocolon of 1 and in the kidneys of 7 patients.It is suggested that besides the capillaropathy a coagulation defect, resembling consumption coagulopathy is a characteristic of Schoenlein-Henoch’s syndrome.


Biomedicines ◽  
2021 ◽  
Vol 9 (3) ◽  
pp. 320
Author(s):  
Thaís Pereira da Silva ◽  
Fernando Jacomini de Castro ◽  
Larissa Vuitika ◽  
Nayanne Louise Costacurta Polli ◽  
Bruno César Antunes ◽  
...  

Phospholipases-D (PLDs) found in Loxosceles spiders’ venoms are responsible for the dermonecrosis triggered by envenomation. PLDs can also induce other local and systemic effects, such as massive inflammatory response, edema, and hemolysis. Recombinant PLDs reproduce all of the deleterious effects induced by Loxosceles whole venoms. Herein, wild type and mutant PLDs of two species involved in accidents—L. gaucho and L. laeta—were recombinantly expressed and characterized. The mutations are related to amino acid residues relevant for catalysis (H12-H47), magnesium ion coordination (E32-D34) and binding to phospholipid substrates (Y228 and Y228-Y229-W230). Circular dichroism and structural data demonstrated that the mutant isoforms did not undergo significant structural changes. Immunoassays showed that mutant PLDs exhibit conserved epitopes and kept their antigenic properties despite the mutations. Both in vitro (sphingomyelinase activity and hemolysis) and in vivo (capillary permeability, dermonecrotic activity, and histopathological analysis) assays showed that the PLDs with mutations H12-H47, E32-D34, and Y228-Y229-W230 displayed only residual activities. Results indicate that these mutant toxins are suitable for use as antigens to obtain neutralizing antisera with enhanced properties since they will be based on the most deleterious toxins in the venom and without causing severe harmful effects to the animals in which these sera are produced.


1990 ◽  
Vol 259 (5) ◽  
pp. H1351-H1356 ◽  
Author(s):  
V. H. Huxley ◽  
D. J. Meyer

Perfusion of exchange microvessels with the vasoactive hormone, atrial natriuretic peptide (AP), acutely and reversibly elevates hydraulic conductivity (Lp) by mechanisms that are, as yet, unknown. This, the first of two studies to characterize AP responses when perfusate composition was altered, specifically focuses on the action of AP when perfusate albumin was lowered to change the transcapillary barrier properties for water by passive mechanisms (protein effect). Perfusion of frog (Rana pipiens) mesenteric microvessels with 1 nM AP in 10 mg/ml bovine serum albumin (BSA) elevated Lp by a median 2.1-fold (range 1.2-2.7, n = 13) from control levels (10 mg/ml BSA). Reduction of perfusate albumin from 10 to 1 mg/ml elicited a small rise in Lp (1.8-fold, n = 10); Lp rose a further 2.1-fold (n = 6) when 1 nM AP was added to 1 mg/ml BSA. Likewise, protein-free perfusion elevated Lp from a median 2.2 to 5.1 X 10(-7) cm.s-1.cmH2O-1 (n = 11); 1 nM AP in protein-free perfusate elevated Lp a further 2.1-fold (n = 8). Thus, regardless of protein content, the response to the peptide was a consistent, twofold increase in exchange vessel Lp (n = 27). These data are consistent with the suggestion that the AP-activated rise in Lp (twofold) occurs via an increase in the effective area of the transcapillary pathway for water without influencing the selectivity properties of the paracellular, albumin-sensitive portion of the barrier.


1960 ◽  
Vol 198 (3) ◽  
pp. 543-546 ◽  
Author(s):  
S. A. Kabins ◽  
J. Fridman ◽  
J. Neustadt ◽  
G. Espinosa ◽  
L. N. Katz

A localized pulmonary infarction was produced by injecting a starch suspension into the pulmonary artery wedge position of one lung lobe in pentobarbitalized dogs, and the effect of three so-called antiserotonins on the ensuing pulmonary edema was determined. Edema was inhibited in the nonembolized lung lobes in 88% of the B.A.S. (1-benzyl-2-methyl-5-methoxytryptamine HCl), 45% of the DHE (dihydroergotamine), and 12% of the BOL (2-brom- d-lysergic acid diethylamide) dogs. Reasons are given for assuming that the actions of B.A.S. and DHE are due to their antiadrenergic rather than to any antiserotonin properties which they may have. Serotonin, therefore, at most has a slight role in the pulmonary edema formation caused by starch emboli. It is postulated that the emboli by producing an infarct and setting up a reflex mediated through the sympathetic nervous system, cause the release in turn of catecholamines and of histamine, the latter being immediately responsible for the capillary permeability change leading to pulmonary edema.


1996 ◽  
Vol 112 (1) ◽  
pp. 85-93 ◽  
Author(s):  
Masayuki Haniuda ◽  
Seiki Hasegawa ◽  
Takeshi Shiraishi ◽  
Carolyn M. Dresler ◽  
Joel D. Cooper ◽  
...  

1981 ◽  
Vol 61 (3) ◽  
pp. 2P-2P ◽  
Author(s):  
M. Kanazawa ◽  
S. Van Schaick ◽  
A. Hussein ◽  
M. Scott ◽  
G. De J. Lee

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