title: Nitric oxide synthase inhibition attenuates cardiac response to hemodilution with viscogenic plasma expander.
abstract: OBJECTIVE
  Increased vascular wall shear stress by elevated plasma viscosity significantly enhances the endothelial nitric oxide synthase (eNOS) activity during an acute isovolemic hemodilution. Also the modulation of plasma viscosity has effects on the cardiac function that were revealed if a left ventricular (LV) pressure-volume (PV) measurement was used. The aim of this study was to assess cardiac function responses to nitric oxide synthase (NOS) inhibitors with the presence of an elevated plasma viscosity but a low hematocrit level. Furthermore, systemic parameters were monitored in a murine model.
  
  
  METHODS
  As test group five anesthetized hamsters were administered with N(G)-nitro-L-arginine methyl ester (L-NAME), NOS inhibitor, whereas five other hamsters were used as control group without L-NAME infusion. The dosage of L-NAME was 10 mg/kg. An isovolemic hemodilution was performed by 40% of estimated blood volume with 6% w/v dextran 2000 kDa, high viscosity plasma expanders (PEs) with viscosity 6.34 cP. LV function was measured and assessed using a 1.4 Fr PV conductance catheter.
  
  
  RESULTS
  The study results demonstrated that NOS inhibition prevented the normal cardiac adaptive response after hemodilution. The endsystolic pressure increased 14% after L-NAME infusion and maintained higher than at the baseline after hemodilution, whereas it gradually decreased in the animals without L-NAME infusion. The admission of L-NAME significantly decreased the maximum rate of ventricular pressure rise (+dP/dtmax), stroke volume and cardiac output after hemodilution if compared to the control group (p<0.05).
  
  
  CONCLUSIONS
  This finding supports the presumption that nitric oxide induced by an increased plasma viscosity with the use of a high viscosity PE plays a major role in the cardiac function during an acute isovolemic hemodilution.
authors.affiliation: Institute of Biomedical Engineering, Faculty of Medicine, Prince of Songkla University, Songkhla, Thailand.
authors.forename: Surapong
authors.initials: S
authors.lastname: Chatpun
authors.affiliation: Department of Bioengineering, University of California, San Diego, CA, USA.
authors.forename: Pedro
authors.initials: P
authors.lastname: Cabrales
keywords: Blood viscosity; Endothelial nitric oxide synthase; Hemodilution; Nitric oxide; Ventricular function