OBJECTIVES: We investigated the effect of inhaled nitric oxide and infused acetylcholine in patients with pulmonary hypertension undergoing cardiac catheterization before cardiopulmonary transplantation. BACKGROUND: The fate of patients under consideration for transplantation of the heart or lungs, or both, is influenced by the evaluation of their pulmonary vascular reactivity. METHODS: We evaluated 11 patients who were classified into two groups on the basis of mean left atrial pressure > 15 mm Hg (group I, n = 6) or < or = 15 mm Hg (group II, n = 5). All patients inhaled nitric oxide at 80 ppm. This was preceded by an infusion of 10(-6) mol/liter of acetylcholine in seven consecutive patients (n = 3 in group I, n = 4 in group II). RESULTS: In group I, inhaled nitric oxide decreased pulmonary artery pressure from (mean +/- SE) 71 +/- 13 to 59 +/- 10 mm Hg (p < 0.05), pulmonary vascular resistance from 14.9 +/- 3.8 to 7.6 +/- 1.7 Um2 (p < 0.05) and intrapulmonary shunt fraction from 17.8 +/- 3.6% to 12.7 +/- 2.1% (p < 0.05). Left atrial pressure tended to increase from 27 +/- 4 to 32 +/- 5 mm Hg (p = 0.07). In group II pulmonary vascular resistance decreased in response to nitric oxide from 36.4 +/- 9.0 to 31.1 +/- 7.9 Um2 (p < 0.05). Cardiac index, systemic pressure and resistance did not change in either group. Seven patients who received acetylcholine had no significant alteration in pulmonary hemodynamic variables. CONCLUSIONS: These preliminary observations suggest that nitric oxide is a potent pulmonary vasodilator with minimal systemic effects. It may be useful in discriminating patients needing combined heart and lung transplantation from those requiring exchange of the heart alone.
OBJECTIVES: We investigated the effect of inhaled nitric oxide and infused acetylcholine in patients with pulmonary hypertension undergoing cardiac catheterization before cardiopulmonary transplantation. BACKGROUND: The fate of patients under consideration for transplantation of the heart or lungs, or both, is influenced by the evaluation of their pulmonary vascular reactivity. METHODS: We evaluated 11 patients who were classified into two groups on the basis of mean left atrial pressure > 15 mm Hg (group I, n = 6) or < or = 15 mm Hg (group II, n = 5). All patients inhaled nitric oxide at 80 ppm. This was preceded by an infusion of 10(-6) mol/liter of acetylcholine in seven consecutive patients (n = 3 in group I, n = 4 in group II). RESULTS: In group I, inhaled nitric oxide decreased pulmonary artery pressure from (mean +/- SE) 71 +/- 13 to 59 +/- 10 mm Hg (p < 0.05), pulmonary vascular resistance from 14.9 +/- 3.8 to 7.6 +/- 1.7 Um2 (p < 0.05) and intrapulmonary shunt fraction from 17.8 +/- 3.6% to 12.7 +/- 2.1% (p < 0.05). Left atrial pressure tended to increase from 27 +/- 4 to 32 +/- 5 mm Hg (p = 0.07). In group II pulmonary vascular resistance decreased in response to nitric oxide from 36.4 +/- 9.0 to 31.1 +/- 7.9 Um2 (p < 0.05). Cardiac index, systemic pressure and resistance did not change in either group. Seven patients who received acetylcholine had no significant alteration in pulmonary hemodynamic variables. CONCLUSIONS: These preliminary observations suggest that nitric oxide is a potent pulmonary vasodilator with minimal systemic effects. It may be useful in discriminating patients needing combined heart and lung transplantation from those requiring exchange of the heart alone.
Authors: Prashant Bobhate; Long Guo; Shreepal Jain; Richard Haugen; James Y Coe; Dominic Cave; Jennifer Rutledge; Ian Adatia Journal: Pediatr Cardiol Date: 2015-01-11 Impact factor: 1.655
Authors: Duncan J Macrae; David Field; Jean-Christophe Mercier; Jens Møller; Tom Stiris; Paolo Biban; Paul Cornick; Allan Goldman; Sylvia Göthberg; Lars E Gustafsson; Jürg Hammer; Per-Arne Lönnqvist; Manuel Sanchez-Luna; Gunnar Sedin; Nim Subhedar Journal: Intensive Care Med Date: 2004-01-13 Impact factor: 17.440