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CONFLICTING RESULTS ABOUT THE ROLE OF NITRIC OXIDE IN DIALYSIS INDUCED HYPOTENSION

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206-210

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Abstract (Original Language): 
Hemodiyaliz seansı sırasında gözlenen akut hipotansiyonda endojen nitrik oksidin olası rolünü araştırmak amacıyla bu çalışma planlanmıştır. Çalışmaya daimi olarak haftada üç gün 4 saat hemodiyalize giren, normal kan basıncına sahip ve herhangi bir antihipertansif ilaç kullanımı olmayan 27 son dönem böbrek yetmezlikli hasta alındı. Hemodiyaliz işlemi hemofan dializer ve bikarbonattı solüsyon ile yapıldı. Hastaların diyaliz öncesi 12 saat ve diyaliz seansı boyunca aç kalmaları sağlandı. Vakaların diyaliz boyunca saat başı kan basıncı ölçümleri yapıldı. Plazma nitrat düzeyi ölçümleri için tüm vakalardan diyaliz öncesinde, diyalizin 2. saati sonunda ve diyaliz bitiminde kan örnekleri alındı. Hemodiyaliz seansı boyunca kan basınçlarında görülen değişimlere göre hastalar iki gruba bölündüler: Birinci gruba, hemodiyaliz süresince ortalama arter basıncı (OAB) 10 mmHg ve üstünde azalma gösteren 16 hasta; ikinci gruba ise OAB değerleri bu düzeyden daha az değişim gösteren 11 hasta dahil edildi. Birinci grubda diyaliz öncesi ortalama OAB 83.8±16.2 mmHg iken diyaliz sonunda 65.8 ± 15.2 mmHg olarak bulundu (p=0.001). ikinci grubta ise diyaliz öncesi ortalama OAB 88.9±8.9 mmHg, diyaliz sonunda 87.8±9 mmHg ölçüldü (p=0.43). Ultrafiltrasyon hızı açısından iki grup farklı değildi (p=0.34). Hemodiyaliz öncesi plazma nitrat düzeyleri hipotansif grupta 76.4±69.7mmol/L, normotansifgrupta 63.2±34.9 mmol/L idi (p=0.9). Diyaliz bitiminde ölçülen nitrat düzeyleri ise her iki grupta anlamlı olarak azalarak hipotansif grupta 32.6±19.3 mmol/L'ye (p=0.000); normotansif grupta ise 33.8±13 mmol/L'ye (p=0.006) geriledi. Plazma nitrat düzeyleri ile OAB değişimleri arasında herhangi bir korelasyon bulunamadı (p=0.2). Bizim sonuçlarımız, diyalizin indüklediği hipotansiyonda artmış nitrik oksid düzeylerinin rolü olduğunu bildiren daha önceden yapılmış çalışmalarla çelişki içindedir. Vaka sayılarımız yeterli olmamakla birlikte diyalizin indüklediği hipotansiyonda nitrik oksidin olası rolünün hala tartışmalı olduğu kanaatindeyiz.
Abstract (2. Language): 
This study was planned to investigate the possible role of endogenous nitric oxide (NO) in acute hypotension during hemodialysis. Twenty-seven patients who had normal blood pressure before hemodialysis(HD) were included in this study. None of the patients was receiving antihypertensive drugs. The patients were dialysedfor 4 hour three times a week using hemophane membranes and a bicarbonate-based dilysate in our hemodialysis centre. The participants did not eat during dialysis. In all cases, blood pressures were recorded at every hour and for the measurement of plasma nitrate, blood samples were collected before the start of dialysis, at 2 hours after the start of dialysis (middialysis) and after the end of dialysis. On the basis of their blood pressure responses during hemodialysis, the patients were divided into two groups: 16 patients who had hypotensive episodes during hemodialysis were defined as those in whom mean arterial pressure (MAP) decreased more than 10 mmHg. The remain patients (n=11) were included in the other group named normotensive patients. In thefirst group, MAP were 83.8±16.2 mmHg and 65.8 ± 15.2 mmHg before and after hemodialysis respectively (p=0.001 ). In the second group, MAP were 88.9±8.9 mmHg and 87.8±9 mmHg before and after dialysis, respectively (p=0.43 ). Ultrafiltration rate was not differ between hypotensive and normotensive groups (p=0.34). Plasma nitrate levels at the initiation of hemodialysis did not differ significantly between hypotensive (76.4±69.7mmol/L) and normotensive (63.2±34.9 mmol/L) patients (p=0.9). In addition, nitric oxide production markedly decreased during hemodialysis into each groups (from 76.4±69.7 to 32.6±19.3 p=0.000 in the first group, from 63.2±34.9 to 33.8±13, p=0.006 in the second group) and did not found any correlation between NO production and MAP after hemodialysis (p=0.2). Our present results appear to conflict with previous studies showing that enhanced NO biosynthesis may contribute to hemodialysis induced hypotension. Although the number of patients is not enough, we suggest that the role of NO in dialysis-induced hypotension is still unclear.

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REFERENCES

References: 

1) Kitamura M., Saito A.: Dialysis hypotension: a rewiew of recent studies of causative factors; Nephrology 2001 ;6 (3): 109-112,
2) Schreiber M.J. Clinical dilemmas in dialysis: Managing the hypotensive patient setting the stage; Am J Kidney Dis 2001;38(4), Suppl 4: 1-10.
3) Perazella MA. Pharmacologic options available to treat symptomatic intradialytic hypotension; Am J Kidney Dis 2001;38 (4) Suppl 4 : 26-36.
4) Schreiber MJ. Clinical case-based approach to understanding intradialytic hypotension; Am J Kidney Dis 2001;38(4) Suppl 4: 37-47.
5) Kang E. S., Acchiardo S. R., Wang Y., Tevlin M. T., Hughes T., Cardoso S. Hypotension during hemodialysis: role for nitric oxide; Am J Medical Sci
1997; 313 (3):138-146.
6) Beasley D, Brenner BM. Role of nitric oxide in hemodialysis hypotension; Kidney Int. 1992;42: 96-100.
7) Nishimura M, Takahashi H, Maruyama K et al. Enhanced production of nitric oxide may be involved in acute hypotension during maintenance hemodialysis. Am J
Kidney Dis. 1998;31:809-817
8) Braman RS, Hendrix SA. Nanogram nitrite and nitrate determination in environmental and biological materials by vanadium (III) reduction xith chemiluminescence detection.
Analytcal Chemistry,1989;61:2715-2718
9) Port F. K., VanDeKerkhove K. M, Kunkel S. L., Kluger
M. J. The role of dialysate in the stimulation of interleukin-1 production during clinical hemodialysis; Am. J Kidney Dis 1987; 10(2):l 18-122
10)
Türkme
n M., Kavukçu S., Apaydın Ş., Soylu A.
Çocuklarda hemodiyaliz sırasında ortaya çıkan hipotansiyonda nitrik oksidin rolü; çocuk sağlığı ve
hastalıkları dergisi 1999;42:27-35.
11) Yokokawa K, Mankus R, Saklayen MG et al. Increased nitric oxide production in patients pith hypotension during hemodialysis. Ann Intern Med 1995;123:35-7
12) Nakayama M, Kawaguchi Y, Numata M, Hasegawa T, Hosoya T. Role of nitric oxide in hypotension during
hemodialysis. Nephron 1998;79:490-491
13) Nishimura M. Role of NO in hemodialysis hypotension.
Int J Artif Organs 1999;22:789-790
14) Daugirdas JT. Dialysis hypotension. A hemodynamic
analysis. Kidney Int 1991 ;39 :233-246
15) Cases A., Esforzado N., Lario S., Vera M., Pedret J. L., Fillat F. R., Jimenez W. Increased plasma adrenomedullin levels in hemodialysis patients with sustained hypotension; Kidney Int 2000;57: 664-670.
16) Blum M., Yachnin T., Wollman Y., Chernihovsky T., Peer G., Grosskopf I., Kaplan E., Silverbeg D., Cabili S., Iaina A. Low nitric oxide production in patients with
chronic renal failure; Nephron 1998;79:265-268.
17) Wilcox C.S., Deng X., Doll A.H, Snellen H., Welch
WJ. Nitric oxide mediates renal vasodilation during erythropoietin induced polycythemia; Kidney Int. 1993;44:430-435
18) Yamasaki H., Nagake Y., Akagi S., Sugimoto T., Ichikawa H., Makino H. Plasma adrenomedullin levels in patients on hemodialysis; Nephron 2001;89:20-25.
19) Letizia C, Mazzaferro S., Chicca S., Cerci S., Subioli S., Cinotti GA., D'Erasmo E. Changes in adrenomedullin plasma concentrations during haemodialysis in patients with chronic renal failure;
Nephrol Dial Transplant 1999;14:519-520.
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