| The patient of persistent vegetation state (PVS), commonly called plant person. Its essential clinical features are loss of brain function. The patients are wakefulness and have sleeping cycle, but have not any meaningful cognitive responsiveness. It is very complicated and difficult to diagnosis and treatment clinically. With the rapid development of technique and method of emergency medicine on heart and brain, the incidence rate of PVS increases by degrees year by year. It causes greatest hazardous for patient physically and mentally and bring larger trouble to family and social. PVS is widely payed attention to . Clinical data mostly come from magnetic resonance imaging(MRI) and computed tomography (CT) scan of the brains of PVS resulted from various cause, these findings mainly show significance pathologic alteration in brain. But little is known about the physiology and biochemistry mechanisms of the pathogenesis of PVS. We firstly investigate the changes of physiology and biochemistry in PVS, and further study the mechanisms of genetic background of PVS.At First, we have observed the-concentrations of endothelin(ET), nitrogen monoxide(NO), Ca2+, monoamine and amino acid neurotransmitters in plasma (serum) and cerebrospinal fluid(CSF) in PVS. We found that the level of ET, NO, GABA, Ser, Trp, Tyr, Lys in CSF of patients with PVS was significantly elevated compared with that of control ( P<0. 001, P<0. 05, P<0. 01, P<0. 01, P<0. 05, P<0. 05, P<0. 05) ; the level of 5-HT, Cyst, Ca2* was significantly decreased compared with that of control ( P<0. 05, P<0.01, P<0.001), and that the level of NO, ET, DA,Glu and Arg in plasma(serum) was significantly elevated compared with that of control ( P<0. 01, P<0. 005, P<0. 05, P<0. 01, P<0. 01).The brain of PVS incurs impairment by ischemia or hypoxia. High ET causes the vasoconstriction augmentation, meanwhile high NO causes the augmentation of vasodilatation. The synergistic interaction of ET and NO may play an important role on maintenance of the normal blood circulation of other undamaged tissue of brain. We think ET and NO were involved in the pathogenesis of PVS.The significant increase of GABA in CSF of PVS and its unchanged precursor Glu are likely to reflect the excessive or damage of the GABA nervous cells in the brain of PVS, these GABA releases into CSF and inhibit the neuron. Itmay be main cause of the pathogenesis of PVS.We found that the high GLU but unchanged GABA in plasma may reflect the damage or compensatory hyperplasia of brain tissue of high GLU, such as cerebra cortex, cerebella and corpus striatum. The GLU from these cells releases into blood and result in the increase of GLU in plasma.According to our results, 5-HT level in CSF of PVS dropped significantly, its procedure TRP significantly increased (P<0. 05, P<0.05). We think that the 5-hydroxytryptaminergic neurons (mainly are rapheal nuclei masses) were destroyed or the activities of the limited velocity enzyme, tryptophan (TP) hydroxylase, might decrease in the process of conversion from TRP to 5-HT. These resulted in the level of 5-HT in CSF of PVS dropped significantly.In PVS plasmas, DA level increased significantly than that of the control (P<0. 05). DA can stimulate the smooth muscle of blood vessel, enhance cAMP, and cause vasodilation, thus improve the blood circulation of PVS patient.Ca2* decreases significantly in the CSF of PVS P<0. 001), but there is not any change in plasma, this indirectly clarify the calcium influx into nerve cell, increase intracellular calcium levels of nerve cell to make Ca2* decrease in CSF. The possible pathway is the high ET and No in brain. Overloading of Ca2+ in nerve cell may reinforce the lesion of nerve cell further.The pathogenesis mechanism of PVS may be involved in alteration of many neurotransraitters, and the injury of cerebral vessels of PVS is not only in stress, but also may be damage in nature or permanent.Based on neurotransmitters, we study the relationship between the pathogenesis of PVS and genetic backgroun...
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