Hemodialysis Hypotension: Interaction of Inhibitors, iNOS, and the Interdialytic Period

Kang, Ellen S.; Tevlin, Marjorie T.; Wang, Yu Bo; Chiang, Thomas M.; Cardenas, Raul; Myers, Linda K.; Acchiardo, Sergio R.

doi:10.1016/s0002-9629(15)40465-3

Cited by 20 publications

(10 citation statements)

References 26 publications

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“…It has been hypothesized that induction of inducible NO synthase, which is already upregulated by repeated stimulation of monocytes by the dialysis treatment, is primarily responsible for an increase in NO synthesis during dialysis. Moreover, a removal of endogenous inhibitors of NO, like asymmetric dimethylarginine (ADMA) during hemodialysis, has also been causally implicated [13,14,16,19,20,24]. On the other hand, the rapid increase in NO generation immediately after hemodialysis has been attributed to a stimulation of the constitutive form of NO synthase by activated platelets or white blood cells [21].…”

Section: Discussionmentioning

confidence: 99%

Nitric Oxide Synthetic Capacity in Relation to Dialysate Temperature

Beerenhout¹,

Noris

Kooman³

et al. 2004

Blood Purif

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Background: During hemodialysis, vascular reactivity is impaired, which can be corrected by lowering dialysate temperature. It has also been shown that nitric oxide (NO) is related to intradialytic hypotension. As NO synthesis may be temperature-dependent, this study addressed the influence of dialysate temperature on the NO synthetic capacity of plasma. Methods: NO synthetic capacity was studied during hemodialysis with a dialysate temperature of 37.5°C (dialysis-37.5°C) and programmed extracorporeal blood cooling (cool dialysis; Blood Temperature Monitor; Fresenius C) in 12 stable patients. NO synthetic capacity was assessed ex vivo by [³H]L-citrulline formation from [³H]L-arginine in cultured endothelial cells after incubation with plasma samples obtained during the respective sessions. Results: Core temperature decreased (–0.32 ± 0.10°C) and energy transfer rate was significantly lower (–27.5 ± 2.8 W; p < 0.05) during cool dialysis compared to dialysis-37.5°C (0.19 ± 0.06°C and –0.8 ± 1.2 W respectively; p < 0.05). Systolic blood pressure decreased during dialysis-37.5°C (–19 ± 4 mm Hg; p < 0.05), but not during cool dialysis (–6 ± 5 mm Hg). NO synthetic capacity increased during dialysis-37.5°C (55.5 ± 9.3 to 73.5 ± 10.2 pmol/10⁵ cells; p < 0.05), in contrast to cool dialysis (67.3 ± 11.1 to 66.2 ± 10.8 pmol/10⁵ cells). Conclusion: The stimulatory effect of uremic plasma on endothelial NO synthesis was augmented during dialysis-37.5°C but not during cool dialysis.

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Section: Discussionmentioning

confidence: 99%

Nitric Oxide Synthetic Capacity in Relation to Dialysate Temperature

Beerenhout¹,

Noris

Kooman³

et al. 2004

Blood Purif

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“…stock solutions of the GCs, to be stored at -20 ° C, were prepared in saline (0.9% NaCl) corresponding to the high range of reported uremic plasma concentrations ( table 1 ) [23][24][25][26][27][28] .…”

Section: General Experimental Set-upmentioning

confidence: 99%

Guanidino Compounds as Cause of Cardiovascular Damage in Chronic Kidney Disease: An in vitro Evaluation

Schepers

Glorieux²,

Dou³

et al. 2010

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Chronic kidney disease is considered a major cause of cardiovascular risk and non-traditional risk factors remain largely unknown. The in vitro toxicity of 10 guanidino compounds (GCs) was evaluated via a standardized approach on different cell systems of relevance in cardiovascular disease. The parameters evaluated were production of reactive oxygen species, expression of surface molecules, cell proliferation, cytotoxicity and calcification. Several GCs had a stimulatory effect on monocytes and granulocytes (SDMA, creatine and guanidinobutyric acid (GBA)). Some GCs (guandine (G), guanidinosuccinic acid (GSA) and SDMA) inhibited endothelial cell proliferation or reduced calcification in osteoblast-like human VSMC (ADMA, GSA and SDMA). Stimulation of osteoclastogenesis could be demonstrated for ADMA, G, guanidinoacetic acid and GBA in a RAW264.7 cell line. No compounds were cytotoxic to AoSMC or endothelial cells, nor influenced their viability. GCs, especially SDMA, likely contribute to cardiovascular complications in uremia, mainly those related to microinflammation and leukocyte activation.

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“…This can have profound effects on both the vasculature and myocardium. In end stage renal disease, not only is there in increase in baseline NO production, there is also an increase in inhibitors of NO, namely asymmetric dimethylarginine (ADMA) [36]. It turns out these inhibitors are dialyzable, which suggests that disturbances within the baseline interplay between specific activators and inhibitors during HD may contribute to hemodynamic instability [36,37].…”

Section: The Role Of Nitric Oxide In Intradialytic Hypotensionmentioning

confidence: 99%