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Am J Physiol Regul Integr Comp Physiol 297: R1111-R1117, 2009. First published August 12, 2009; doi:10.1152/ajpregu.00251.2009
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Articles

The role of nitric oxide in the development of neurogenic pulmonary edema in spinal cord-injured rats: the effect of preventive interventions

Jirí Sedy,1,2,3 Josef Zicha,2,4 Jaroslav Kunes,2,4 Ales Hejcl,1 and Eva Syková1,5

1Institute of Experimental Medicine and 2Institute of Physiology, Academy of Sciences of the Czech Republic, Prague, Czech Republic; 3Institute of Dental Research, First Faculty of Medicine, Charles University and General University Hospital, Prague, Czech Republic; 4Center for Cardiovascular Research, Prague, Czech Republic; and 5Center for Cell Therapy and Tissue Repair and Department of Neuroscience, Second Faculty of Medicine, Charles University, Prague, Czech Republic

Submitted May 11, 2009 ; accepted in final form August 6, 2009

Neurogenic pulmonary edema (NPE) is an acute life-threatening complication following an injury of the spinal cord or brain, which is associated with sympathetic hyperactivity. The role of nitric oxide (NO) in NPE development in rats subjected to balloon compression of the spinal cord has not yet been examined. We, therefore, pretreated Wistar rats with the NO synthase inhibitor NG-nitro-L-arginine methyl ester (L-NAME) either acutely (just before the injury) or chronically (for 4 wk prior to the injury). Acute (but not chronic) L-NAME administration enhanced NPE severity in rats anesthetized with 1.5% isoflurane, leading to the death of 83% of the animals within 10 min after injury. Pretreatment with either the ganglionic blocker pentolinium (to reduce blood pressure rise) or the muscarinic receptor blocker atropine (to lessen heart rate decrease) prevented or attenuated NPE development in these rats. We did not observe any therapeutic effects of atropine administered 2 min after spinal cord compression. Our data indicate that NPE development is dependent upon a marked decrease of heart rate under the conditions of high blood pressure elicited by the activation of the sympathetic nervous system. These hemodynamic alterations are especially pronounced in rats subjected to acute NO synthase inhibition. In conclusion, nitric oxide has a partial protective effect on NPE development because it attenuates sympathetic vasoconstriction and consequent baroreflex-induced bradycardia following spinal cord injury.

blood pressure; heart rate; atropine


Address for reprint requests and other correspondence: J. Sedy, Institute of Experimental Medicine, Academy of Sciences of the Czech Republic, Vídenská 1083, Prague 4, 142 20 (e-mail: jirisedy{at}hotmail.com).






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