Haemodialysis hypotension and nitric oxide production: Comparison of heparin with parnaparin


Arici M., Altun B., Dinler O., Kiykim A., Usalan C., Erdem Y., ...Daha Fazla

BLOOD PURIFICATION, cilt.20, sa.2, ss.145-149, 2002 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 20 Sayı: 2
  • Basım Tarihi: 2002
  • Doi Numarası: 10.1159/000047000
  • Dergi Adı: BLOOD PURIFICATION
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.145-149
  • Hacettepe Üniversitesi Adresli: Hayır

Özet

Background: There is increasing evidence for the role of nitric oxide (NO) in haemodialysis hypotension but the source of elevated NO is still controversial. Heparin has been reported to enhance NO production by cultured human endothelial cells. The aim of this study was to compare the role of unfractionated heparin and low molecular weight heparin (LMWH, parnaparin) on mean arterial pressure (MAP) and NO production in haemodialysis patients with hypotensive episodes. Patients and Methods: Ten maintenance haemodialysis patients with hypotensive episodes were involved in this study. Patients were anticoagulated with heparin for 3 weeks and then switched to parnaparin for 3 weeks. Serum NO levels were analysed before starting dialysis, at the nadir of MAP during a haemodialysis session and at the end of dialysis in the last haemodialysis session of the 3rd week of each anticoagulation treatment. Results; NO levels were 39.4 +/- 13.2 AM at the beginning of haemodialysis, 92.4 +/- 31.4 muM during hypotensive episode and 43.1 mu 25.1 muM the end of dialysis with heparin treatment (p < 0.05). In the parnaparin period, NO levels were 47.2 +/- 22.7 muM at the beginning, 80.7 +/- 46.5 uM during the hypotensive episode and 45.8 +/- 23.2 muM at the end of the session (p < 0.05). The percent increase in NO levels during the hypotensive period compared to that at the beginning of haemodialysis with heparin was significantly higher than that with parnaparin (140.2 μ 50.4 vs. 119.6 &PLUSMN; 44.8%; p < 0.05). The percent decrease in MAP with heparin use was also significantly higher than with parnaparin use (48.6 &PLUSMN; 6.4 vs. 39.6 &PLUSMN; 5.3% p < 0.05). Conclusion: We have observed that MAP decrements and NO increases were less manifest during hypotensive episodes with parnaparin treatment compared to heparin. This difference may be related to differences in endothelial binding capacity, thrombin affinity and/or effects on platelet functions of unfractionated heparin and LMWHs. Copyright © 2002 s. KargerAG, Basel.