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.

Systemic and regional hemodynamics after nitric oxide synthase inhibition: role of a neurogenic mechanism

1994 ◽  
Vol 267 (1) ◽  
pp. R84-R88 ◽  
Author(s):  
M. Huang ◽  
M. L. Leblanc ◽  
R. L. Hester
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Cardiac Output ◽  
No Synthase ◽  
Before And After ◽  
Regional Hemodynamics ◽  
Autonomic Blockade ◽  
Infusion Of Norepinephrine ◽  
Oxide Synthase

The study tested the hypothesis that the increase in blood pressure and decrease in cardiac output after nitric oxide (NO) synthase inhibition with N omega-nitro-L-arginine methyl ester (L-NAME) was partially mediated by a neurogenic mechanism. Rats were anesthetized with Inactin (thiobutabarbital), and a control blood pressure was measured for 30 min. Cardiac output and tissue flows were measured with radioactive microspheres. All measurements of pressure and flows were made before and after NO synthase inhibition (20 mg/kg L-NAME) in a group of control animals and in a second group of animals in which the autonomic nervous system was blocked by 20 mg/kg hexamethonium. In this group of animals, an intravenous infusion of norepinephrine (20-140 ng/min) was used to maintain normal blood pressure. L-NAME treatment resulted in a significant increase in mean arterial pressure in both groups. L-NAME treatment decreased cardiac output approximately 50% in both the intact and autonomic blocked animals (P < 0.05). Autonomic blockade alone had no effect on tissue flows. L-NAME treatment caused a significant decrease in renal, hepatic artery, stomach, intestinal, and testicular blood flow in both groups. These results demonstrate that the increase in blood pressure and decreases in cardiac output and tissue flows after L-NAME treatment are not dependent on a neurogenic mechanism.

Diurnal Blood Pressure Variation in Quadriplegic Chronic Spinal Cord Injury Patients

1991 ◽  
Vol 80 (3) ◽  
pp. 271-276 ◽  
Author(s):  
Henry Krum ◽  
William J. Louis ◽  
Douglas J. Brown ◽  
Graham P. Jackman ◽  
Laurence G. Howes
Keyword(s):  
Blood Pressure ◽  
Spinal Cord ◽  
Heart Rate ◽  
Spinal Cord Injury ◽  
Ambulatory Monitoring ◽  
Pressure Variation ◽  
Night Time ◽  
Cord Injury ◽  
Blood Pressure Variation ◽  
Neurologically Intact

1. Measurement of blood pressure and heart rate over a 24 h period was peformed in 10 quadriplegic spinal cord injury patients and 10 immobilized, neurologically intact orthopaedic subjects by using the Spacelabs 90207 automated ambulatory monitoring system. 2. Systolic and diastolic blood pressure fell significantly at night in orthopaedic subjects but not in quadriplegic patients, and night-time blood pressures were similar in both groups. 3. Cumulative summation of differences from a reference value (cusum analysis) confirmed a markedly diminished diurnal blood pressure variation in the quadriplegic patients. 4. These findings could not be accounted for on the basis of blood pressure variations during chronic postural change. 5. Heart rate fell significantly at night in both groups. 6. The findings suggest that the increase in blood pressure during waking hours in neurologically intact subjects is a consequence of a diurnal variation in sympathetic activity (absent in quadriplegic patients with sympathetic decentralization) which is independent of changes in physical activity.

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.

Characterization of the role of endogenous nitric oxide in myogenic vascular oscillations during cooling-evoked hemodynamic perturbations of rats

2017 ◽  
Vol 95 (7) ◽  
pp. 803-810 ◽  
Author(s):  
Yi-Hsien Lin ◽  
Yia-Ping Liu ◽  
Yu-Chieh Lin ◽  
Po-Lei Lee ◽  
Che-Se Tung
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Heart Rate ◽  
Cold Stress ◽  
Low Frequency ◽  
Sympathetic Activation ◽  
Nitric Oxide Synthase Inhibitor ◽  
Dicrotic Notch ◽  
Endogenous Nitric Oxide

Rapid immersion of a rat’s limbs into 4 °C water, a model of cold stress, can elicit hemodynamic perturbations (CEHP). We previously reported that CEHP is highly relevant to sympathetic activation and nitric oxide production. This study identifies the role of nitric oxide in CEHP. Conscious rats were pretreated with the nitric oxide synthase inhibitor L-NAME (NG-nitro-l-arginine methyl ester) alone or following the removal of sympathetic influences using hexamethonium or guanethidine. Rats were then subjected to a 10 min cold-stress trial. Hemodynamic indices were telemetrically monitored throughout the experiment. The analyses included measurements of systolic blood pressure; heart rate; dicrotic notch; short-term cardiovascular oscillations and coherence between blood pressure variability and heart rate variability in regions of very low frequency (0.02–0.2 Hz), low frequency (0.2–0.6 Hz), and high frequency (0.6–3.0 Hz). We observed different profiles of hemodynamic reaction between hexamethonium and guanethidine superimposed on L-NAME, suggesting an essential role for a functional adrenal medulla release of epinephrine under cold stress. These results indicate that endogenous nitric oxide plays an important role in the inhibition of sympathetic activation and cardiovascular oscillations in CEHP.

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.

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