| Cerebrovascular disease is one of the most frequent threats to elders in ourcountry. Its high incidence of a disease, moratality, incomplete not only distroyhealth and lives of its suffer, but also bring heavy economical burden to theirfamilies and society. Intercerebral hemorrhage occupies about 30% of acutecerebrovascular disease and its mortality in early stage is about 30%～40%.Effective treatments in early stage of intracerebral hemorrhage is now a hot spotin research field. Intracerebral hemorrhage, because of its threat to the humanbeings, has become the hot spot in the therapeutic field. If the long-timesecondary cerebral edema could be controlled efficiently, not only the course ofdisease would be shortened, also the living standard would be elevated. Recently,the escin, a kind of drug could prevent exudation and promote absorbability ofedema, the venous elasticity and cerebral circulation, has attracted more andmore interesting. This study was designed to observe the therapeutic effect ofescin in experimental intracerebral hemorrhagic edema rabbit modal, and thepossible mechanism. We tried to theorize the clinic application of escin.We established 54 experimental intracerebral hemorrhage rabbit models, byintracerebral injection of autologous nonheparinized blood in basal nucleus area.And we divided them into 3 groups at random, namely, the pseudosurgery group,the control group and the treatment group. Then each group was divided into 3subgroups according to 1d, 3d and 5d after surgery. We phlebotomize arterialblood from each rabbit at 8:00 am on the corresponding day and preserved theserum for next test. 2h before sacrificing the rabbit by 0.9% saline heart infusion,we injected EB through ear vein. After the execution, we measured the watercontent of brain by dry-wet measurement, the CORT content in serum and theIL-6 content in cerebral tissue by radioimmunoassay, the ACTH level in serumby ELISA and the EB quantity in cerebral tissue by atomic spectrophotometer. The result of the control group showed that the water weight in brainreached maximum level in 1d subgroup, gradually decreased in 3d subgroup andremained a higher level than that of the control group in 5d subgroup. Comparedwith the control group, the water weight index of the treatment group showedsignificant reduced in 3d subgroup and much less in 5d subgroup. So did theIL-6 content in cerebral tissue. On another hand, we found the CORT and ACTHlevel in serum reached the top in 1d subgroup, gradually decreased in 3dsubgroup and eventually reached the normal level in 5d subgroup. While in thetreatment group, both CORT and ACTH index dramatically increased bypair-analysis. However, there is no significant discrimination in EB contentamong 3 groups. In this study, we established the experimental intracerebral hemorrhagemodel by intracerebral injection of autologous nonhearinized blood. One reasonfor choicing this modle is that it's the easiest way to standardize the bleedingquantity and the location. Another reason is this model is similar to the clinicintracerebral hemorrhage patients. The experimental animal model fit our needto study the nature course of intracerebral hemorrhage and pathomorphologiccharacters. The cerebral edema variation paralleled IL-6 content variation incerebral tissue. This phenomenon indicated that, on the early stage ofintracerebral hemorrhage (especially 1d), the inflammatory reaction is the majorcause or inducement for edema. The efficient anti-inflammatory reagent couldreduce the cerebral edema and then protect the cerebral tissue. The escin hadbeen proved effective in decreasing IL-6 content and edema in brain. It alsocould stimulate the release of CORT and ACTH. We hypothesized the protectivemechanism of escin might be: Escin stimulated the release of CORT, whichup-regulated the sensitivity of vascular smooth muscle to catecholamine, andthen maintain the vascular tension, reduce the exudation; CORT could alsoprevent intracerebral NF-κbeta factor from activation, which decreased theIL-6 content in cerebral tissue, and eventually eliminate the inflammatoryreaction, ameliorate the shortage of blood and oxygen in perilesion. Escinpromoted the ACTH secretion, not only enhancing the CORT secretion, but alsothe estrogen and androgen. That, in turn, made up the high basic catabolism ofACTH by up-regulating anabolism. As the first messenger, ACTH couldspecifically bind to membrane receptor and catalyze the third messenger proteinkinase C through the second messenger camp. As a result of the chain reaction,the cellular synthesis or release of the protein, energy and neuromediator, theNa+ or Ca2+ pump function could be up regulated. Lastly, the escin was provedto improve patient's the psychotic status, memory, learn, attention, direction,motive, arousal and so on. However we didn't get the conclusive positive effectof escin in preventing blood brain barrier damage. We got the conclusion as followed: the intracerebral injection of autogolousnonheparinized blood can establish stable and well-repeated animal model ofexperimental intracerebral hemorrhage in basal nucleus area; 1d after theintracerebral hemorrhage, the cerebral edema reaches the top level and lasted atleast 5d; in the hemorrhagic lesion, IL-6 content dramatically increases, reaches... |
PDF Full Text Request