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Ann Thorac Surg 1997;63:298-299
© 1997 The Society of Thoracic Surgeons
King Faisal Specialist Hospital Research Centre, Box 3354, Riyadh 11211, Saudi Arabia, e-mail:alhalees{at}kfshrc.edu.sa
To the Editor:
We read with great interest the review article about the use of nitric oxide (NO) in cardiothoracic surgery [1]. We have used NO for the past 2 years, in nearly 75 cases so far. One problem we infrequently encounter is weaning NO. In some patients a sort of dependence on NO can develop. We had a 1-year-old boy in whom type I truncus arteriosus with absent left pulmonary artery and severe truncal valve regurgitation was diagnosed who exhibited this type of dependence. The patient's anomaly was totally corrected and the truncal valve was replaced with a size 16 Carbomedics mechanical valve. The patient showed suprasystemic pulmonary artery pressure despite full sedation, paralysis, hyperventilation, 100% oxygen, and prostaglandin E1; finally, pulmonary artery pressure was controlled with inhaled NO. With each attempt to wean NO a sharp increase in pulmonary artery pressure occurred. Serum magnesium (Mg2+) level was elevated by administering magnesium sulfate (MgSO4), 100 mg/kg intravenously (=0.81 mEq/kg) until a serum level ranging from 2.5 to 3.2 mmol/L was achieved. This decision was based on our institute's experience with the use of MgSO4 as a pulmonary vasodilator in both animal trials and clinical studies [2, 3]. Subsequently, NO was completely weaned off and the patient was extubated with a serum Mg2+ level of 3 mmol/L. The patient was discharged home a week later and continued to do well at 6-month follow-up. Magnesium activates adenylate cyclase, causing an increase in the cyclic adenosine monophosphate level in vascular smooth muscles. High levels of cellular cyclic adenosine monophosphate enhance relaxation by depressing intracellular free calcium concentrations necessary for contraction. Also, MgSO4 may act through increasing the production of endogenous NO [4, 5]. Therefore, it may be advantageous to use MgSO4 in cases of difficulty in weaning from NO, which might be encountered more frequently in the future with the rapidly increasing use of NO.
References
Division of Cardiothoracic Surgery, Northwestern University Medical School, 251 E Chicago Ave, Suite 1030, Chicago, IL 60611
Department of Surgery, University of Colorado Health Sciences Center, 4200 E 9th Ave, Denver, CO 80262
To the Editor:
We thank Dr Al-Halees and associates for their interest in our review article. Doctor Al-Halees and his colleagues should be congratulated for such successful care in such high-risk patients. Clearly, persistent and refractory pulmonary hypertension may be a very vexing problem.
We also have noticed several patients from whom it was difficult to wean inhaled nitric oxide in the management of pulmonary hypertension. We have typically approached such patients by slowly dropping the dose of administered inhaled nitric oxide to as low as 1 to 2 ppm and with time have been able to successfully wean patients from inhaled nitric oxide using this strategy. We were, however, very interested to learn of the effective use of intravenous magnesium therapy to control pulmonary vascular resistance.
We will soon publish an article [1] on a study in which magnesium was found to be essential for endothelium-dependent but not endothelium-independent cyclic guanosine monophosphate--mediated mechanisms of pulmonary vascular smooth muscle relaxation. Magnesium was likewise essential for cyclic adenosine monophosphate--mediated pulmonary vascular smooth muscle relaxation [1]. We therefore share the opinion that magnesium is important in control of pulmonary vascular smooth muscle tone. However, our data would suggest that magnesium is not essential for the effects of inhaled nitric oxide to be manifest, because nitric oxide is an endothelium-independent cyclic guanosine monophosphate--mediated pulmonary vasorelaxant.
Nonetheless, we are very interested in the observations of Dr Al-Halees and colleagues. The management of pulmonary hypertension can be very difficult, and it is important that the cardiothoracic surgeon be familiar with a variety of techniques to manipulate pulmonary vascular smooth muscle tone. A therapy that works in one circumstance may fail in another circumstance, and it therefore behooves the cardiothoracic surgeon to have a familiarity with a variety of therapeutic strategies. We therefore congratulate Dr Al-Halees and his colleagues on their success.
Reference
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