Neurogenic Pulmonary Edema Associated with Ruptured Spinal Cord Arteriovenous Malformation

Neurosurgery ◽  
1983 ◽  
Vol 12 (6) ◽  
pp. 691-693 ◽  
Author(s):  
Don S. Lee ◽  
Arthur Kobrine
Keyword(s):  
Spinal Cord ◽  
Arteriovenous Malformation ◽  
Pulmonary Edema ◽  
Neurogenic Pulmonary Edema ◽  
Spinal Cord Arteriovenous Malformation

Abstract A case of neurogenic pulmonary edema (NPE) associated with a ruptured spinal cord arteriovenous malformation (AVM) is presented. The mechanisms involved in the development of NPE are discussed briefly. The possible role of preganglionic sympathetic fibers in the spinal cord in the etiology of NPE is suggested.

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

2009 ◽  
Vol 297 (4) ◽  
pp. R1111-R1117 ◽  
Author(s):  
Jiří Šedý ◽  
Josef Zicha ◽  
Jaroslav Kuneš ◽  
Aleš Hejčl ◽  
Eva Syková
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Spinal Cord ◽  
Heart Rate ◽  
Pulmonary Edema ◽  
No Synthase ◽  
Neurogenic Pulmonary Edema ◽  
Therapeutic Effects ◽  
Cord Injury

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 N G-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.

The role of catecholamines in the pathogenesis of neurogenic pulmonary edema associated with subarachnoid hemorrhage

2012 ◽  
Vol 154 (12) ◽  
pp. 2179-2185 ◽  
Author(s):  
Joji Inamasu ◽  
Keiko Sugimoto ◽  
Yasuhiro Yamada ◽  
Tsukasa Ganaha ◽  
Keisuke Ito ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Pulmonary Edema ◽  
Neurogenic Pulmonary Edema

Spinal cord arteriovenous malformation in a neonate

1986 ◽  
Vol 64 (2) ◽  
pp. 322-324 ◽  
Author(s):  
T. S. Park ◽  
Wayne S. Cail ◽  
Johnny B. Delashaw ◽  
John Kattwinkel
Keyword(s):  
Spinal Cord ◽  
Arteriovenous Malformation ◽  
Clinical Manifestation ◽  
Neurological Deterioration ◽  
Ischemic Damage ◽  
Aneurysmal Dilatation ◽  
Content Type ◽  
Spinal Cord Arteriovenous Malformation ◽  
Fine Print

✓ A 2-day-old neonate with a spinal cord arteriovenous malformation developed severe paraparesis. The abrupt neurological deterioration was not associated with hemorrhage or aneurysmal dilatation. Ischemic damage of the spinal cord is suggested as the cause of the clinical manifestation.

scholarly journals Rapid but not slow spinal cord compression elicits neurogenic pulmonary edema in the rat

2009 ◽  
pp. 269-277 ◽  
Author(s):  
J Šedý ◽  
J Zicha ◽  
J Kuneš ◽  
P Jendelová ◽  
E Syková
Keyword(s):  
Spinal Cord ◽  
Heart Rate ◽  
Pulmonary Edema ◽  
Slow Rate ◽  
Systemic Blood Pressure ◽  
Cord Compression ◽  
Neurogenic Pulmonary Edema ◽  
Balloon Inflation ◽  
Thoracic Spinal Cord ◽  
Thoracic Spinal

The development of neurogenic pulmonary edema (NPE) can be elicited by an immediate epidural balloon compression of the thoracic spinal cord. To evaluate whether a slower balloon inflation could prevent NPE development, we examined the extent of NPE in animals lesioned with a rapid (5 μl - 5 μl - 5 μl) or slow rate (3 μl - 2 μl - 2 μl - 2 μl - 2 μl - 2 μl - 2 μl) of balloon inflation. These groups were compared with the NPE model (immediate inflation to 15 μl) and with healthy controls. Slow balloon inflation prevented NPE development, whereas the pulmonary index and histology revealed a massive pulmonary edema in the group with a rapid rate of balloon inflation. Pulmonary edema was preceded by a considerable decrease in heart rate during the inflation procedure. Moreover, rapid inflation of balloon in spinal channel to either 5 μl or 10 μl did not cause NPE. Thus, a slow rate of balloon inflation in the thoracic epidural space prevents the development of neurogenic pulmonary edema, most likely due to the better adaptation of the organism to acute circulatory changes (rapid elevation of systemic blood pressure accompanied by profound heart rate reduction) during the longer balloon inflation period. It should be noted that spinal cord transection at the same level did not cause neurogenic pulmonary edema.

scholarly journals Neurogenic Pulmonary Edema Induced by Spinal Cord Injury in Spontaneously Hypertensive and Dahl Salt Hypertensive Rats

2011 ◽  
pp. 975-979 ◽  
Author(s):  
J. ŠEDÝ ◽  
J. KUNEŠ ◽  
J. ZICHA
Keyword(s):  
Spinal Cord ◽  
Pulmonary Edema ◽  
Baroreflex Sensitivity ◽  
Experimental Hypertension ◽  
Neurogenic Pulmonary Edema ◽  
Protective Effects ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Isoflurane Anesthesia ◽  
Cord Injury

Neurogenic pulmonary edema (NPE), which is induced by acute spinal cord compression (SCC) under the mild (1.5 %) isoflurane anesthesia, is highly dependent on baroreflex-mediated bradycardia because a deeper (3 %) isoflurane anesthesia or atropine pretreatment completely abolished bradycardia occurrence and NPE development in rats subjected to SCC. The aim of the present study was to evaluate whether hypertension-associated impairment of baroreflex sensitivity might exert some protection against NPE development in hypertensive animals. We therefore studied SCC-induced NPE development in two forms of experimental hypertension – spontaneously hypertensive rats (SHR) and salt hypertensive Dahl rats, which were reported to have reduced baroreflex sensitivity. SCC elicited NPE in both hypertensive models irrespective of their baroreflex sensitivity. It is evident that a moderate impairment of baroreflex sensitivity, which was demonstrated in salt hypertensive Dahl rats, does not exert sufficient protective effects against NPE development.

Sign in / Sign up

Export Citation Format

Share Document