Low dose of nitroglycerin failed to improve splanchnic hemodynamics in patients with cirrhosis: Evidence for an impaired cardiopulmonary baroreflex function
✍ Scribed by Richard Moreau; Dominique Roulot; Alain Braillon; Christophe Gaudin; Antoine Hadengue; Yannick Bacq; Dr. Didier Lebrec
- Publisher
- John Wiley and Sons
- Year
- 1989
- Tongue
- English
- Weight
- 580 KB
- Volume
- 10
- Category
- Article
- ISSN
- 0270-9139
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✦ Synopsis
High doses of nitroglycerin may decrease portal pressure in patients with cirrhosis with untoward effects such as arterial hypotension and a decrease in systemic O2 uptake. In the present study, low doses of nitroglycerin (7 to 15 wg per min, i.v.) were administered in 11 patients with cirrhosis in order to unload cardiopulmonary baroreceptor-one of the possible mechanisms by which nitroglycerin may improve splanchnic hemodynamics-and moreover to avoid deleterious systemic effects. Nitroglycerin significantly decreased right atrial pressure (-35%) and pulmonary wedged pressure (-27%) with significant increase in plasma norepinephrine concentration (+23%), which indicated that cardiopulmonary baroreceptor unloading was achieved. Changes in systemic hemodynamics were slight, although significant, with a decrease in arterial pressure (-8%) and an increase in heart rate (+8%); this indicates a minimal effect on high-pressure baroreflexes. In contrast, no significant change was observed in hepatic venous pressure gradient, hepatic blood flow and azygos blood flow. However, the fraction of cardiac output reaching the azygos system significantly increased by 18%. Plasma renin activity did not change significantly. Moreover, Oa transport and uptake were significantly decreased. These findings show that low doses of nitroglycerin failed to improve splanchnic hemodynamics in patients with cirrhosis. These results suggest an impaired cardiopulmonary baroreflex function which is probably located on the efferent arch.
Nitroglycerin may decrease portal pressure in patients with cirrhosis (1-3). Several mechanisms have been proposed to explain this effect (1). The reduction in portal pressure may result from a diminution in portal tributary blood flow due to a baroreflex-mediated increase in splanchnic arteriolar resistance (1): low-pressure (cardiopulmonary) as well as high-pressure (arterial) baroreceptors exert a control on splanchnic arteriolar tone (4-6). Moreover, nitroglycerin, which is a venodilator (7), may also reduce portal pressure by relaxing venous smooth