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J Thorac Cardiovasc Surg 2006;131:250-251
© 2006 The American Association for Thoracic Surgery
Letter to the Editor |
Division of Thoracic and Cardiovascular Surgery, Ribeirão Preto Faculty of Medicine, University of São Paulo, São Paulo, Brazil
Recently, Taylor and Holtby
1
have presented a case of refractory hypotension in a child with native mitral valve endocarditis with cerebral complications in whom methylene blue (MB) was less effective than previously described.
2,3
We have been using MB to treat refractory vasoplegias since 1994, and our experience is corroborated by the specialized medical literature. Most of our experience involved adults who had hypotension during cardiopulmonary bypass (CPB) or after the operation, situation in which, like sepsis, nitric oxide plays a primordial role.
4,5
In this milieu two prospective and randomized studies reached positive conclusions about the efficacy of MB to treat
6
or prevent
7
the vasoplegic syndrome in patients having cardiac surgery with the aid of CPB.
Recently, we operated on a drug-addicted young man with native aortic valve endocarditis. The patient received a bileaflet valve prosthesis (St Jude Medical, Inc, St Paul, Minn). A high dose of norepinephrine was necessary to maintain a reasonable blood pressure during CPB. After weaning from CPB he was hypotensive and had a high cardiac output, low systemic vascular resistance, and pulmonary edema. The arterial oxygen saturation was below 80%, even though he was being ventilated with 100% oxygen and positive end-expiratory pressure. We started MB in a continuous infusion in a way quite similar to that used by Dr Taylor, followed by a bolus of 3 mg/kg (in 100 mL of 5% glucose in water) twice a day. Even though the mean arterial pressure did not increase, even with norepinephrine, the cardiac output gradually decreased, and the systemic vascular resistance increased. In addition, the rapid resolution of lung edema resulting in higher arterial oxygen saturation was astonishing.
Although Drs Taylor and Holtby seemed disappointed with the effect of the MB on blood pressure, we believe that their case had an impressive evolution despite of its severity. We disagree that "obvious clinical improvement using MB was not evident in this case," since most of the pharmacologic support to the circulation was necessary for a short time. In our opinion, the controversy about the use of MB to treat similar cases arises when one uses MB merely as a kind of "last-minute vasopressor." MB sometimes seems to work for this purpose and sometimes it does not, perhaps due the fact that, unlike many vasopressors, MB does not act through a membrane receptor. We believe the pivotal action of MB is not exclusively the guanylyl cyclase blockage resulting in a reduction in cyclic guanosine monophosphate (cGMP). This blockage also enhances the "crosstalk" between cyclic adenosine monophosphate (cAMP) and cGMP pathways, which facilitates the effect of the cAMP-dependent vasopressors. Many clinical reports in the medical literature, including sepsis treatment, substantiate that the guanilyl cyclase blockage seems to improve the effect of the vasopressors, shortening the length of pharmacologic cardiovascular support. Another quite advantageous effect of MB is its capacity to reduce vascular permeability.
8,9
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