| Background:Carbon monoxide(CO) is a common asphyxial gas in our life. The population of carbon monoxide poisoning and the dead after acute carbon monoxide poisoning (ACOP) lists the first place among all acute poisoning in our country. Especially delayed encephalopathy after acute carbon monoxide poisoning(DEACMP) will happen to some people after ACOP .Because the clear pathogenesis has not been discovered, there`s no effective way in clinical treatment of DEACMP and reversing the happening trend. In recent years, some schoolers put forward the option about microthrombus after ACOP. And high incidence rate of cerebral infarction has been noticed. Thromboxane A2 (TXA2) is synthesized on platelets using arachidonic acid. It contracts blood vessle fiercely, making blood pressure rising, reducing cyclic AMP (cAMP) of platelets, having blood platelets congregate and resulting thrombosis. Prostacyclin(PGI2) is synthesized in vascular endothelial cells. It dilates blood vessel fiercely and restrain the congregation of platelets. In physiological condition, TXA2 and PGI2 keep the balance of regulating the tension of blood vessel and hematoblastic activity. If the balance is broken, blood vessel will lose tension and platelets congregate, simultaneously inflammatory factors are released and result in a series of pathophysiologic process. Objective:To study the pathogenesis of ACOP and DEACMP in terms of vascular mechanism, we study the cerebral vascular endothelial cells on the basis of animal experiments, observing TXB2 and 6-k-PGF1αlevel of plasma in rats in order to provide theoretical evidence for the treatment of ACOP and DEACMP. Meanwhile we observe cerebral vascular endothelial cell ultrastructure alteration and situation of blood brain barrier (BBB). Methods:56 healthy Sprague-Dawley rats, male and female taking a half part separately, were divided into control group and operated group(the moment, 1st day, 4th day, 7th day, 14th day, 21st day group), 8 rats in every group. Carbon monoxide poisoning model of rat was established with absorbing CO poisoning gas. The control group inhaled the atmosphere. We obtain the venous blood sample at the certain time according the different group to determine TXB2 and 6-k-PGF1αlevel. At the same time, prepare pathological slice. Result: 1.Compared with the control group, the TXB2 level of operated group elevated. From the 4th day to the 21st day, the TXB2 level rose generously. 2.The 6-k-PGF1αlevel rose up at the poisoning moment, then returned to usual level, and ascended again at 7th day and reached the max at the 21st day. 3.There's statistical difference of TXB2/6-k-PGF1αbetween control group and 7th day and 14th day group. 4.It was observed that there was swelled around blood vessel and neurons, erythrocyte went out of vessel and neurons programmed cell death (PCD), capillary vessel joint of rats'tissue became slack, mitochondrial swelled, the blood vessel crimpled and was transfigured. Conclusion 1.The research evidenced that thrombus come into being and cerebral capillary vessel endothelial cell was hurt. BBB was damaged after ACOP.The pathologic variety maybe the result of alteration of TXB2 and 6-k-PGF1α. 2.In clinical treatment, inhibitor of blood platelet can be used to restrain thrombosis and defend DEACMP, because the ascending of TXB2 level after ACOP 3.The TXB2 level rose up continuously, and reached the max at the 21st day. It was possible that the rising of TXB2 was related with DEACMP. |
PDF Full Text Request