Spinal cord perfusion pressure in dogs after control of proximal aortic hypertension during thoracic aortic cross-clamping with esmolol or sodium nitroprusside.
BACKGROUND
Spinal cord perfusion pressure may be reduced when sodium nitroprusside is used to control proximal aortic hypertension during thoracic aortic clamping. The effect of esmolol infusion on spinal cord perfusion pressure during thoracic aortic clamping is unknown. This study compares spinal cord perfusion pressure following control of proximal hypertension with either sodium nitroprusside or esmolol during thoracic aortic clamping.


METHODS
The thoracic aorta was cross-clamped for 30 min in 18 dogs anesthetized with halothane. A control group (n = 6) received no treatment of proximal hypertension during cross-clamping. In two other groups, proximal arterial pressure was controlled (100 mmHg) by infusion of either sodium nitroprusside (n = 6) or esmolol (n = 6). Brachial and femoral arterial pressures, spinal cord perfusion pressure, pulmonary artery occlusion, central venous pressures, and cardiac output were monitored. Neurologic assessment was performed 24 h following surgery.


RESULTS
Femoral arterial pressure was lower with nitroprusside (14 +/- 3 mmHg) compared to esmolol (24 +/- 4 mmHg) after 15 min of aortic cross-clamping. Cerebrospinal fluid pressure increased during aortic cross-clamping in the sodium nitroprusside group (from 7 +/- 5 to 16 +/- 6 mmHg) but not in esmolol or control groups. Spinal cord perfusion pressure was lower with nitroprusside at 15 min of aortic cross-clamping (2 +/- 4 mmHg) compared to control (15 +/- 7 mmHg) and esmolol groups (17 +/- 11 mmHg). Esmolol infusion reduced cardiac output and increased ventricular filling pressures compared to control and nitroprusside groups.


CONCLUSIONS
Esmolol was associated with greater spinal cord perfusion pressure, but adverse hemodynamic effects, when compared with nitroprusside during thoracic aortic cross-clamping. When only surviving dogs (4 control, 5 esmolol, 6 nitroprusside) are considered, the incidence of neurologic deficit was greater in nitroprusside-treated dogs than in either control or esmolol-treated dogs. No difference in outcome was present when all dogs are considered.
Ryan
T
T
Department of Anesthesia, Royal College of Surgeons, Ireland.
Mannion
D
D
O'Brien
W
W
Grace
P
P
Bouchier-Hayes
D
D
Cunningham
A J
AJ
D000319:Adrenergic beta-Antagonists / Q000627:therapeutic use*; D000818:Animals; D001013:Aorta, Thoracic / Q000502:physiology*; D001018:Aortic Diseases / Q000503:physiopathology / Q000517:prevention & control*; D015170:Cerebrospinal Fluid Pressure / Q000502:physiology; D003250:Constriction; D004285:Dogs; D006973:Hypertension / Q000503:physiopathology / Q000517:prevention & control*; D009599:Nitroprusside / Q000627:therapeutic use*; D011412:Propanolamines / Q000627:therapeutic use*; D013116:Spinal Cord / Q000502:physiology*
D000319:Adrenergic beta-Antagonists; D011412:Propanolamines; D009599:Nitroprusside; C036604:esmolol