Augmentation of systemic blood pressure during spinal cord ischemia to prevent postoperative paraplegia after aortic surgery in a rabbit model.
OBJECTIVE
Paraplegia from spinal cord ischemia remains an unresolved complication in thoracoabdominal aortic surgery, with high morbidity and mortality. This study investigated postoperative effects of systemic blood pressure augmentation during ischemia.


METHODS
Spinal cord ischemia was induced in rabbits by infrarenal aortic occlusion for 15 minutes with infused phenylephrine (high blood pressure group, n = 8) or nitroprusside (low blood pressure group, n = 8) or without vasoactive agent (control, n = 8). Spinal cord blood flow, transcranial motor evoked potentials, neurologic outcome, and motor neuron cell damage (apoptosis, necrosis, superoxide generation, myeloperoxidase activity) were evaluated.


RESULTS
Mean arterial pressures during ischemia were controlled at 121.9 +/- 2.8, 50.8 +/- 4.3, and 82.3 +/- 10.7 mm Hg in high blood pressure, low blood pressure, and control groups, respectively. In high blood pressure group, high spinal cord blood flow (P < .01), fast recovery of transcranial motor evoked potentials (P < .01), and high neurologic score (P < .05) were observed after ischemia relative to low blood pressure and control groups. At 48 hours after ischemia, there were significantly more viable neurons, fewer terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling-positive neurons, and less alpha-fodrin expression in high blood pressure group than low blood pressure and control groups. Superoxide generation and myeloperoxidase activity at 3 hours after ischemia were suppressed in high blood pressure group relative to low blood pressure group.


CONCLUSIONS
Augmentation of systemic blood pressure during spinal cord ischemia can reduce ischemic insult and postoperative neurologic adverse events.
Izumi
So
S
Department of Surgery, Division of Cardiovascular Surgery, Kobe University Graduate School of Medicine, Kobe, Japan.
Okada
Kenji
K
Hasegawa
Tomomi
T
Omura
Atsushi
A
Munakata
Hiroshi
H
Matsumori
Masamichi
M
Okita
Yutaka
Y
D000818:Animals; D001011:Aorta / Q000503:physiopathology*; D017209:Apoptosis; D001794:Blood Pressure / Q000187:drug effects*; D002352:Carrier Proteins / Q000378:metabolism; D002404:Catheterization / Q000009:adverse effects*; D004195:Disease Models, Animal; D004558:Electric Stimulation; D019054:Evoked Potentials, Motor; D007262:Infusions, Intravenous; D008840:Microfilament Proteins / Q000378:metabolism; D009046:Motor Neurons / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D009336:Necrosis; D009460:Neurologic Examination; D009599:Nitroprusside / Q000008:administration & dosage; D018384:Oxidative Stress / Q000187:drug effects; D010264:Paraplegia / Q000209:etiology / Q000473:pathology / Q000503:physiopathology / Q000517:prevention & control*; D009195:Peroxidase / Q000378:metabolism; D010656:Phenylephrine / Q000008:administration & dosage*; D011817:Rabbits; D012039:Regional Blood Flow / Q000187:drug effects; D013116:Spinal Cord / Q000098:blood supply / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D020760:Spinal Cord Ischemia / Q000188:drug therapy* / Q000209:etiology / Q000473:pathology / Q000503:physiopathology; D013481:Superoxides / Q000378:metabolism; D013997:Time Factors; D014662:Vasoconstrictor Agents / Q000008:administration & dosage*; D014665:Vasodilator Agents / Q000008:administration & dosage; D013049:Spectrin
D002352:Carrier Proteins; D008840:Microfilament Proteins; D009599:Nitroprusside; D009195:Peroxidase; D010656:Phenylephrine; D013481:Superoxides; D014662:Vasoconstrictor Agents; D014665:Vasodilator Agents; D013049:Spectrin