Excessively high systemic blood pressure in the early phase of reperfusion exacerbates early-onset paraplegia in rabbit aortic surgery.
OBJECTIVE
We have demonstrated that therapeutic augmentation of systemic blood pressure during spinal cord ischemia plays an important role in minimizing spinal cord injury in both experimental and clinical aortic surgery. However, there remain concerns that excessively high blood pressure during spinal cord reperfusion may aggravate the reperfusion injury. The purpose of this study is to investigate the effect of high blood pressure during spinal cord reperfusion on postoperative neurologic outcomes after aortic surgery in rabbits.


METHODS
Experiments were performed using a rabbit spinal cord ischemia-reperfusion model in 2 randomly divided groups: (1) In the HR group, the mean blood pressure was maintained at a high level (121 +/- 1.3 mm Hg) during reperfusion with intravenously administered phenylephrine; and (2) in the CR group, the mean blood pressure was not medically controlled (75 +/- 9.1 mm Hg) during reperfusion. Neurologic and histologic assessments and evaluation of early reperfusion injury were performed.


RESULTS
In the HR group, slow and incomplete recovery of transcranial motor-evoked potentials (P = .02) and low neurologic scores (P < .005) were observed during spinal cord reperfusion compared with the CR group. At 48 hours of reperfusion, there were significantly fewer viable neuron cells, more apoptosis, and more perivascular edema with gray matter vacuolation in the HR group (P < .001 for each). At 3 hours, myeloperoxidase activity (P = .0021), vascular permeability (P = .0012), and superoxide generation (P < .0001) were significantly increased in the HR group.


CONCLUSIONS
Excessively high blood pressure in the early phase of spinal cord reperfusion increased reperfusion injury in the spinal cord, leading to exacerbation of early-onset paraplegia. Avoidance of spinal cord reperfusion with high blood pressure may be one management strategy in thoracoabdominal aortic surgery.
Department of Surgery, Division of Cardiovascular Surgery, Kobe University Graduate School of Medicine, Kobe, Hyogo, Japan.
Bishow
B
Pokhrel
Tomomi
T
Hasegawa
So
S
Izumi
Atsushi
A
Ohmura
Hiroshi
H
Munakata
Yutaka
Y
Okita
Kenji
K
Okada
D000818:Animals; D001011:Aorta / Q000503:physiopathology / Q000601:surgery*; D017209:Apoptosis; D001794:Blood Pressure / Q000187:drug effects; D002199:Capillary Permeability; D002470:Cell Survival; D004195:Disease Models, Animal; D019054:Evoked Potentials, Motor; D009046:Motor Neurons / Q000378:metabolism / Q000473:pathology; D009460:Neurologic Examination; D010264:Paraplegia / Q000209:etiology* / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D009195:Peroxidase / Q000378:metabolism; D010656:Phenylephrine / Q000008:administration & dosage; D011817:Rabbits; D020127:Recovery of Function; D015427:Reperfusion Injury / Q000209:etiology* / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D013116:Spinal Cord / Q000098:blood supply* / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D020760:Spinal Cord Ischemia / Q000209:etiology* / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D013481:Superoxides / Q000378:metabolism; D013997:Time Factors; D014656:Vascular Surgical Procedures / Q000009:adverse effects*; D014662:Vasoconstrictor Agents / Q000008:administration & dosage
D014662:Vasoconstrictor Agents; D013481:Superoxides; D010656:Phenylephrine; D009195:Peroxidase