Observations on Edema Formation and Resolution in Gleich Syndrome: Essential Role of the Kidneys in Effective Arterial Blood Volume Regulation

2001 ◽  
Vol 21 (2) ◽  
pp. 154-161 ◽  
Author(s):  
Cagatay Oktenli ◽  
Fatih Bulucu ◽  
Murat Gurbuz ◽  
Ergün Bozoglu ◽  
Yusuf Oguz ◽  
...  
1977 ◽  
Vol 15 (1) ◽  
pp. 22-31 ◽  
Author(s):  
J. Weinman ◽  
A. Hayat ◽  
G. Raviv

Author(s):  
Zsolt Vajda ◽  
Dominique Promeneur ◽  
Tamás Dóczi ◽  
Endre Sulyok ◽  
Jørgen Frøkiær ◽  
...  

Author(s):  
Hikaru Takeuchi ◽  
Hiroaki Tomita ◽  
Yasuyuki Taki ◽  
Yoshie Kikuchi ◽  
Chiaki Ono ◽  
...  

1992 ◽  
Vol 262 (3) ◽  
pp. G537-G544
Author(s):  
J. G. Wood ◽  
Z. Y. Yan ◽  
L. Y. Cheung

This study examined the effects of platelet-activating factor (PAF) on the gastric microcirculation. We measured changes in vascular resistance and filtration during intra-arterial infusion of graded doses of PAF and its metabolite, lyso-PAF, to an ex vivo gastric segment of alpha-chloralose-anesthetized dogs. PAF produced dose-related sustained increases in vascular resistance (2-150 nM; n = 6). Filtration and venous hematocrit were also both significantly increased by PAF. In contrast, there were no statistically significant changes in these measurements with lyso-PAF (n = 6). Filtration and venous hematocrit were not significantly changed by norepinephrine at doses that increased perfusion pressure to the same degree as PAF (n = 4). PAF also increased filtration in the absence of changes in perfusion pressure (during maximal vasodilation induced with papaverine). Finally, removal of leukocytes from gastric arterial blood significantly attenuated these responses to PAF. Our results suggest that PAF-induced mucosal ischemia is primarily due to vasoconstriction and may involve edema formation due to increased filtration as well. In addition, these responses to PAF appear to be largely dependent on circulating leukocytes.


EMJ Urology ◽  
2021 ◽  
pp. 107-117
Author(s):  
Priyanka Jethwani ◽  
Namrata Krishnan

Oedema is a hallmark feature of nephrotic syndrome (NS) and can cause significant patient morbidity. The pathogenesis of oedema formation is complex and results from abnormalities in sodium retention, inter-play of neurohormonal factors, and changes in capillary filtration barrier. Salt retention is often primary (‘overfill’ theory) because of increased sodium-potassium adenosine triphosphatase activity in the collecting duct cells, increased direct epithelial sodium channel activation (ENaC) by urinary proteases (independent of aldosterone), and an overall increased effective arterial blood volume. However, a subset of patients with NS, especially children, demonstrate decreased effective arterial blood volume (‘underfill’ theory) and secondary sodium retention as the primary mechanism of oedema formation. Increased capillary permeability and vascular inflammation contributes as well. Loop diuretics with or without salt-poor albumin are the mainstay of therapy in adults, although no large clinical trials exist to guide diuretic choice or dosage. Combination diuretic therapy is recommended to achieve multi-site nephron blockade and overcome diuretic resistance, which is a frequent challenge. Use of direct ENaC inhibitors (amiloride) in combination with loop diuretics may be especially beneficial given the primary role of ENaC in sodium retention. Aquaretics such as vasopressin receptor antagonists may have a role in treatment as well. Well-designed clinical trials are essential to guide therapy of refractory oedema in NS. In this review, the authors discuss the pathogenesis of oedema formation in patients with NS and propose a treatment algorithm for management of resistant oedema based on the limited available evidence.


2010 ◽  
Vol 31 (2) ◽  
pp. 560-571 ◽  
Author(s):  
Yi-Ching Lynn Ho ◽  
Esben Thade Petersen ◽  
Ivan Zimine ◽  
Xavier Golay

Despite the different origins of cerebrovascular activity induced by neurogenic and nonneurogenic conditions, a standard assumption in functional studies is that the consequence on the vascular system will be mechanically similar. Using a recently developed arterial spin labeling method, we examined arterial blood volume, arterial-microvascular transit time, and cerebral blood flow (CBF) in the gray matter and in areas with large arterial vessels under hypercapnia, visual stimulation, and a combination of the two. Spatial heterogeneity in arterial reactivity was observed between conditions. During hypercapnia, large arterial volume changes contributed to CBF increase and further downstream, there were reductions in the gray matter transit time. These changes were not significant during visual stimulation, and during the combined condition they were moderated. These findings suggest distinct vascular mechanisms for large and small arterial segments that may be condition specific. However, the power relationships between gray matter arterial blood volume and CBF in hypercapnia (α = 0.69 ± 0.24) and visual stimulation (α = 0.68 ± 0.20) were similar. Assuming consistent capillary and venous volume responses across these conditions, these results offer support for a consistent total CBV–flow relationship typically assumed in blood oxygen-level dependent calibration techniques.


2011 ◽  
Vol 24 (4) ◽  
pp. 211-223 ◽  
Author(s):  
Danielle van Westen ◽  
Esben T. Petersen ◽  
Ronnie Wirestam ◽  
Roger Siemund ◽  
Karin Markenroth Bloch ◽  
...  

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