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Objective To determine whether reduction in central pressure augmentation and central systolic blood pressure by nitroglycerine (NTG) results from effects on pre-load or is due to arterial dilation. Methods We compared effects of NTG with those of lower body negative pressure (LBNP). Hemodynamic measurements were made at rest,during LBNP (10,20 and 30 mmHg,each for 15 min) and after NTG (10,30 and 100 μg/min,each dose for 15 min) in ten healthy volunteers. Cardiac pre-load,stroke volume and cardiac output were assessed by echocardiography. Central pressure augmentation and central systolic pressure were obtained by radial tonometry using a transfer function. Results LBNP (20 mmHg) and NTG (30 μg/min) reduced pre-load (as measured by the peak velocity of the S wave in the superior vena cava) to a similar degree [by (26.8±3.8)% and (23.9±3.4)%,respectively]. Compared to LBNP,NTG reduced systemic vascular resistance [by (32.9±7.5)%,P<0.01],decreased peripheral and central pressure augmentation [by (20.8±3.4)% units and (12.9±2.9)% units,respectively,each P<0.01]. Conclusion These results suggest that a reduction in pre-load does not explain reduction in pressure augmentation and central systolic blood pressure by NTG and that these effects are mediated through arterial dilation.
Objective To determine whether reduction in central pressure augmentation and central systolic blood pressure by nitroglycerine (NTG) results from effects on pre-load or is due to arterial dilation. Methods We compared effects of NTG with those of lower body negative pressure (LBNP). Hemodynamic measurements were made at rest, during LBNP (10,20 and 30 mmHg, each for 15 min) and after NTG (10,30 and 100 μg / min, each dose for 15 min) in ten healthy volunteers. Cardiac pre-load , stroke volume and cardiac output were assessed by echocardiography. Central pressure augmentation and central systolic pressure were obtained by radial tonometry using a transfer function. Results LBNP (20 mmHg) and NTG (30 μg / min) reduced pre-load (as measured by the peak velocity of the S wave in the superior vena cava to a similar degree [by (26.8 ± 3.8)% and (23.9 ± 3.4)%, respectively]. Compared to LBNP, NTG reduced systemic vascular resistance [by 7.5)%, P <0.01], decreased peripheral and central pressure au Conclusion These results suggest that a reduction in pre-load does not explain reduction in pressure augmentation and central systolic blood pressure (g) [by (20.8 ± 3.4)% units and (12.9 ± 2.9)% units, respectively, each P <0.01] by NTG and that these effects are mediated through arterial dilation.