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Nitric oxide synthase inhibition attenuates cardiac response to hemodilution with viscogenic plasma expander.

Chatpun S, Cabrales P - Korean Circ J (2014)

Bottom Line: 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).

View Article: PubMed Central - PubMed

Affiliation: Institute of Biomedical Engineering, Faculty of Medicine, Prince of Songkla University, Songkhla, Thailand.

ABSTRACT

Background and objectives: 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.

Materials and 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).

Conclusion: 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.

No MeSH data available.


Related in: MedlinePlus

Cardiac function indices such as cardiac output (CO) (A), stroke volume (SV) (B), stroke work (SW) (C), and ejection fraction (EF) (D) present at baseline (BL), after N(G)-nitro-L-arginine methyl ester treatment (TM), at 0, 15, 30, and 60 minutes after hemodilution (HD). Values are relative to BL and presented as means±SD. *p<0.05 compared to BL, †p<0.05 compared between groups.
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Figure 4: Cardiac function indices such as cardiac output (CO) (A), stroke volume (SV) (B), stroke work (SW) (C), and ejection fraction (EF) (D) present at baseline (BL), after N(G)-nitro-L-arginine methyl ester treatment (TM), at 0, 15, 30, and 60 minutes after hemodilution (HD). Values are relative to BL and presented as means±SD. *p<0.05 compared to BL, †p<0.05 compared between groups.

Mentions: Fig. 4 shows the cardiac function indices for the control and treated groups. Cardiac output (CO) was significantly decreased in the treated group after L-NAME injection at all-time points compared to both, baseline and control group. Stroke volume (SV) was significantly decreased after hemodilution compared to the control group, but remained without significant changes compared to baseline. Stroke work (SW) remained with no significant changes between groups and relative to baseline up to 15 minutes after hemodilution. However, it was significantly increased in the control group at 30 minutes and 60 minutes after hemodilution, at this last time point it was significantly higher (p<0.05) for the control group compared to the treated group. The ejection fraction was not statistically different between groups or compared to baseline. However, it exhibited a trend to decrease (by 14%) in the treated group after L-NAME injection and to increase in the control group during hemodilution.


Nitric oxide synthase inhibition attenuates cardiac response to hemodilution with viscogenic plasma expander.

Chatpun S, Cabrales P - Korean Circ J (2014)

Cardiac function indices such as cardiac output (CO) (A), stroke volume (SV) (B), stroke work (SW) (C), and ejection fraction (EF) (D) present at baseline (BL), after N(G)-nitro-L-arginine methyl ester treatment (TM), at 0, 15, 30, and 60 minutes after hemodilution (HD). Values are relative to BL and presented as means±SD. *p<0.05 compared to BL, †p<0.05 compared between groups.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3958604&req=5

Figure 4: Cardiac function indices such as cardiac output (CO) (A), stroke volume (SV) (B), stroke work (SW) (C), and ejection fraction (EF) (D) present at baseline (BL), after N(G)-nitro-L-arginine methyl ester treatment (TM), at 0, 15, 30, and 60 minutes after hemodilution (HD). Values are relative to BL and presented as means±SD. *p<0.05 compared to BL, †p<0.05 compared between groups.
Mentions: Fig. 4 shows the cardiac function indices for the control and treated groups. Cardiac output (CO) was significantly decreased in the treated group after L-NAME injection at all-time points compared to both, baseline and control group. Stroke volume (SV) was significantly decreased after hemodilution compared to the control group, but remained without significant changes compared to baseline. Stroke work (SW) remained with no significant changes between groups and relative to baseline up to 15 minutes after hemodilution. However, it was significantly increased in the control group at 30 minutes and 60 minutes after hemodilution, at this last time point it was significantly higher (p<0.05) for the control group compared to the treated group. The ejection fraction was not statistically different between groups or compared to baseline. However, it exhibited a trend to decrease (by 14%) in the treated group after L-NAME injection and to increase in the control group during hemodilution.

Bottom Line: 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).

View Article: PubMed Central - PubMed

Affiliation: Institute of Biomedical Engineering, Faculty of Medicine, Prince of Songkla University, Songkhla, Thailand.

ABSTRACT

Background and objectives: 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.

Materials and 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).

Conclusion: 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.

No MeSH data available.


Related in: MedlinePlus