Third place winner of the Conrad Jobst Award in the gold medal paper competition. Prevention of spinal cord dysfunction in a new model of spinal cord ischemia.
Paraplegia or paraparesis caused by temporary cross-clamping of the aorta is a devastating sequela in patients after surgery of the thoracoabdominal aorta. No effective clinical method is available to protect the spinal cord from ischemic reperfusion injury. A small animal (rat) model of spinal cord ischemia is established to better understand the pathophysiological events and to evaluate potential treatments. Eighty-one male Sprague-Dawley rats weighing 300 g to 350 g were used for model development (45) and treatment evaluation (36). The heparinized and anesthetized rat was supported by a respirator following tracheostomy. The thoracic aorta was cannulated via the left carotid artery for post-clamping intra-aortic treatment solution administration. After thoracotomy, the aorta was freed and temporarily clamped just distal to the left subclavian artery and just proximal to the diaphragm for different time intervals: 0, 5, 10, 15, 20, 25, 30, 35, and 40 minutes (five animals per group). The motor function of the lower extremities postoperatively showed consistent impairment after 30 minutes clamping (5/5 rats were paralyzed), and this time interval was used for treatment evaluation. For each treatment, six animals per group were used, and direct local intra-aortic infusion of physiologic solution (2 mL) at different temperatures with or without buffer substances was given immediately after double cross-clamp to protect the ischemic spinal cord. Arterial blood (2 mL) was infused in the control group. The data indicate that the addition of HCO3-(20 mM) to the hypothermic (15 degrees C) solution offered complete protection of the spinal cord from ischemic injury.(ABSTRACT TRUNCATED AT 250 WORDS)
Lopez
S
S
Department of Surgery, East Tennessee State University, Johnson City 37614-0575.
Manahan
E
E
Evans
J R
JR
Kao
R L
RL
Browder
W
W
D000085:Acetates / Q000627:therapeutic use; D000818:Animals; D001011:Aorta / Q000601:surgery*; D002314:Cardioplegic Solutions / Q000627:therapeutic use; D004195:Disease Models, Animal; D004353:Drug Evaluation, Preclinical; D005942:Gluconates / Q000627:therapeutic use; D006531:HEPES / Q000627:therapeutic use; D007036:Hypothermia, Induced / Q000379:methods*; D015636:Magnesium Chloride / Q000627:therapeutic use; D008297:Male; D010264:Paraplegia / Q000175:diagnosis / Q000209:etiology / Q000503:physiopathology / Q000517:prevention & control*; D011183:Postoperative Complications / Q000175:diagnosis / Q000209:etiology / Q000503:physiopathology / Q000517:prevention & control*; D011189:Potassium Chloride / Q000627:therapeutic use; D051381:Rats; D017207:Rats, Sprague-Dawley; D015424:Reperfusion / Q000379:methods*; D015427:Reperfusion Injury / Q000175:diagnosis / Q000209:etiology / Q000503:physiopathology / Q000517:prevention & control*; D015203:Reproducibility of Results; D019346:Sodium Acetate; D017693:Sodium Bicarbonate / Q000627:therapeutic use*; D012965:Sodium Chloride / Q000627:therapeutic use; D013116:Spinal Cord / Q000098:blood supply*; D013997:Time Factors
D000085:Acetates; D002314:Cardioplegic Solutions; D005942:Gluconates; C012499:Plasma-lyte 148; D015636:Magnesium Chloride; D012965:Sodium Chloride; D019346:Sodium Acetate; D011189:Potassium Chloride; D017693:Sodium Bicarbonate; D006531:HEPES