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Vincent JL, Sarot J, Unger P, et al. Afterload reduction in the critically ill: nicergoline versus sodium nitroprusside. J Cardiovasc Pharmacol. 1987;9(5):546-50doi: 10.1097/00005344-198705000-00007.
Vincent, J. L., Sarot, J., Unger, P., & Kahn, R. J. (1987). Afterload reduction in the critically ill: nicergoline versus sodium nitroprusside. Journal of cardiovascular pharmacology, 9(5), 546-50. https://doi.org/10.1097/00005344-198705000-00007
Vincent, J L, et al. "Afterload reduction in the critically ill: nicergoline versus sodium nitroprusside." Journal of cardiovascular pharmacology vol. 9,5 (1987): 546-50. doi: https://doi.org/10.1097/00005344-198705000-00007
Vincent JL, Sarot J, Unger P, Kahn RJ. Afterload reduction in the critically ill: nicergoline versus sodium nitroprusside. J Cardiovasc Pharmacol. 1987 May;9(5):546-50. doi: 10.1097/00005344-198705000-00007. PMID: 2439835.
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J Cardiovasc Pharmacol. 1987 May;9(5):546-50. doi: 10.1097/00005344-198705000-00007.

Afterload reduction in the critically ill: nicergoline versus sodium nitroprusside.

Journal of cardiovascular pharmacology

J L Vincent, J Sarot, P Unger, R J Kahn

PMID: 2439835 DOI: 10.1097/00005344-198705000-00007

Abstract

We investigated the potential value of vasodilating therapy in critically ill patients with inappropriately low cardiac output during acute illness. In seven patients with low flow state during septic or postoperative state, sodium nitroprusside (20-100 micrograms/min) was compared with nicergoline (NIC) (0.5 to 2.5 mg/min), a new selective alpha 1-blocking agent with negative chronotropic action. Sodium nitroprusside (NP) decreased arterial pressure (from 90 +/- 5 to 68 +/- 5 mm Hg, p less than 0.01) and pulmonary artery balloon-occluded pressure from 20.3 +/- 3.1 to 15.4 +/- 2.8 mm Hg, p less than 0.01) and increased heart rate (from 110 +/- 11 to 120 +/- 13 beats/min, p less than 0.05) but failed to increase stroke volume (from 24.7 +/- 4.8 to 23.4 +/- 4.4 ml, NS). During NIC administration, a comparable decrease in systemic vascular resistance was associated with a significant increase in stroke volume (from 21.6 +/- 3.3 to 25.6 +/- 3.2 ml/m2, p less than 0.01) and cardiac output (CO) (from 2.4 +/- 0.3 to 2.7 +/- 0.3 L/min/m2, p less than 0.025), whereas the decrease in arterial pressure was less significant (from 91 +/- 8 to 84 +/- 7 mm Hg, p less than 0.05). Because NIC has no positive inotropic action, the most likely mechanism is that a baroreceptor-mediated increase in heart rate with NP was prevented by the negative chronotropic action of NIC. Both drugs adversely affected arterial blood oxygenation. By its unique property to decrease heart rate, NIC could represent a valuable vasodilating agent, especially in acute conditions.

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