We studied the effects of the electrolyte composition (K, Ca, Na) and prostaglandin E₁ of the extra-cellular fluid on the tension development of isolated canine coronary arterial strips. In 20mEq/l potassium solution, 4.7mEq/l calcium produced coronary artery contraction. This Ca-induced contraction was partially inhibited dose-dependently (between 10^-15M and 10^-12M) by prostaglandin E₁. Above 10^-11M, intensity of the inhibition did not change. In the presence of 20mEq/l potassium, the reduction of sodium concentration to 12mEq/l increased the tension of coronary artery. Prostaglandin E₁ did not affect this tension development. After 5min perfusion of prostaglandin E₁, Ca-induced contraction was not inhibited. It is concluded that low calcium, high sodium cardioplegic solution may relax the canine coronary artery. Addition of prostaglandin E₁ to cardioplegic solution may reduce the coronary artery contraction partially.

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Recently, oxygen free radical has been considered to be a cause of reperfusion injury in ischemic organs. It was thus thought that oxygen free radical must also be concerned with myonephropathic metabolic syndrome (MNMS). The present study shows the every efficacy of ascorbic acid (500mg/kg) as an oxygen radical scavenger. In this study, heparin (120U/kg) was used as an anticoagulant, gabexate mesilate (100mg/kg) as a protease inhibitor, and saline solution (500ml) as a control to measure CPK, GOT, LDH, and ALD, in the mongrel dog model of MNMS. The abdominal aorta of the MNMS model was clamped at the infra renal artery level, and released after 24h. Every medicine in 500ml saline solution was perfused through the external jugular vein for 200min, 20min before declamping and 180min after declamping. Ascorbic acid produced less serum CPK, ALD, and GOT after declamping, and a higher level of superoxide dismutase activity as measured by electron spin resonance, after perfusion, than other group. In conclusion, a large quantity of ascorbic acid was very effective in MNMS for both tissue protection and raising of SOD activity.

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A 61-year-old man underwent an emergency operation for a ruptured infrarenal abdominal aortic aneurysm. Operations included bifurcated graft replacement of the abdominal aorta, oversewing of five lumbar arteries between L3 and L5, and ligation of the occluded inferior mesenteric artery. Because of the severe adhesions and arteriosclerotic changes over the bifurcation of the abdominal aorta and both common iliac arteries, prolonged aortic cross-clamp time was needed. In spite of stable his postoperative general condition, he suffered paresthesia and complete sensory loss on the left lower leg and the right sole. Moreover he was found to have paresis on the left leg and the right thigh. Knee and ankle deep-tendon reflexes were absent on the left. Lasègue's sign was positive bilaterally, which was more brisk on the left. There was no incontinence of urine and feces. EMG showed neurogenic polyphasic potentials on the lower extremities. MRI of the thoracolumbar spine and sacrum showed no evidence responsible for this neurological deficit, but IV-DSA revealed complete occlusion of the left common and internal iliac arteries. Following the active rehabilitation, he was able to walk unaided, but remained to have residual paresthesia on the left lower leg at his discharge. It was concluded that ischemic injuries to the cauda equina resulted in this rare complication, which seemed to be secondary to oversewing of critical lumbar arteries, prolonged aortic cross-clamp time, and the acute occlusion of the left common and internal iliac arteries.

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