RESUMO
Objective To investigate the effects of propofol on neuronal apoptosis in anterior horn of spinal cord in rabbits with spinal cord ischemia-reperfusion (IR) injury. Methods Sixty New Zealand white rabbits aged 4-6 months weighing 2.0-2.5 kg were randomized to receive normal saline (group C), 10% intralipid (group F) and propofol 30 mg/kg (group P1 ), 40 mg/kg (group P2), 50 mg/kg (group P3) and60 mg/kg (group P4 ). 10% intralipid was added to propofol solution to make the fluid infused equal in volume between the 6 groups ( n = 10 each). Spinal cord ischemia was induced by occlusion of abdominal aorta distal to the left renal arteries combined with simultaneous occlusion of bilateral common iliac arteries for 30 min. A catheter was inserted into abdominal aorta close to the site of occlusion via left femoral artery. Normal saline, 10% intralipid or different doses of propofol was infused through the catheter as soon as aorta was clamped at the rate of 12 ml·kg-1·h-1 for 30 min. The aorta and bilateral iliac arteries were then declamped. The L4-6 of spinal cord was removed at 48 h of reperfusion for microscopic examination and the total number of normal motor neurons in the anterior horn of spinal cord was counted. The total number of neurons and apoptosis neurons in the anterior horn of spinal cord was counted by TUNEL and the apoptosis index of neurons was calculated. The expression of caspase-3 in the anterior horn of spinal cord was determined by immunohistochemical technique. Results The number of normal motor neurons was significantly higher, and the apoptosis index and expression of caspase-3 were significantly lower in group P1-4 than in group C and F ( P < 0.05). Compared with group P1, the number of normal motor neurons was significantly increased and the apoptosis index was significantly decreased in group P2-4 and the expression of caspase-3 was down-regulated in group P3 and P4 ( P < 0.05). Compared with group P2, the number of normal motor neurons was significantly increased in group P3 while decreased in group P4, and the apoptosis index was significantly decreased and the expression of caspase-3 was down-regulated in group P3 and P4 ( P < 0.05). Compared with group P3, the number of normal motor neurons was significantly decreased and the apoptosis index was significantly increased and the expression of easpnse-3 was up-regulated in group P4 ( P < 0.05) . Conclusion Propofol 30-60 mg/kg infused through aorta during occlusion can inhibit the neuronal apoptosis and attenuate IR injury to spinal cord dose-dependently in rabbits. The underlying mechanism may be related to the down-regulation of caspase-3 expression.
RESUMO
A patent cardiac support system which is used as a bridge treatment for acute myocardial infarction has been designed and tested in vitro and in two dogs in vivo. This is an easy-to-use intelligentized pulsatile flow cardiopulmonary bypass device to replace the function of heart. The device consists of two identical pumps and perfusion chambers, a sensing and control system, a gas exchanger between the vein and pump, two one way valves between pump and veins or arteries. Arterial pressure and EKG feedback mechanisms are used for maintaining blood pressure and coordinating the pumping activity with heart contraction. A prototype of the device was built to perform hydraulic in vitro tests with aims of verifying the new device's pumping behavior. Functional evaluation of the device was carried out by using it in a model circuit made with standard CPB components plus a mock hydraulic pipeline. This system demonstrated easy manipulation, good controllability, and provided a 65+/-2ml x beat(-1) flow volume. There was a linear correlation between peak pressure value and pulsatile frequency. In the two in vivo experiments, the primary objective was to determine whether the device could work well in dog, whether physiologic pulsatility could be achieved and whether the blood supply to heart should be sufficient during asystole status by drugs. The results suggest that all the goals have been achieved.