| Cerebrovascular disease is a common disease and frenquntlyoccurring that severely threatens human health and longevity. Recently,cerebrovascular disease is one of the three main causes for adult death.Intracerebral hemorrhage(ICH) is the severe multiple and death rate. Itis well known that the most important reason for death is herniationinduced by brain edema after ICH. So it has become hot spot how toinhibite the generate of brain edema. Clinical study has proved thatfocal mild hypothermia can reduce brain edema after ICH. But studiesof the mechanism have been few. Recently discoveried, aquaporin is amembrance protein that has intimate relation for water transport.Among aquaporin, aquaporin-4(AQP4) is the main content at brain.Cerebral distribution of AQP4 imply that it is a main leading to braintissue water transport. At physiologic and pathologic case, AQP4 of thebrain tissue plays important role in buffer kalium ion and maintainintermal fluid balance and adjusting center somotic pressure andforming cerebral edema. In addition, it can adjust formation ofcerebrospinal fluid. Along with AQP4 and hypothermia beinglucubrated about cerebral edema mechanism, we guess they may havevery important interaction. Therefore, to seek a method adjusting AQP4expressive, which make cerebral edema therapy at molecular level andmake brain demage lessen.Objective To observe local-brain mild hypothermia effect onrats ICH, observe the change brain tissue water content and AQP4expression, further analyze molecular mechanism of focal mildhypothermia therapy and provide rationale for clinical ICH.Methods Using rats cerebral hemorrhage model of autologousblood injection at left caudate nucleus. The 144 Wistar rats wererandomly divided into sham-operated contral group and normothermiagroup and focal mild hypothermia group. Each group is respectivelyfurther divided into 4 subgroups: 3h,6h,24h and 72h. The total ofevery subgroup are 6 rats. The rats are used to measure dye-wet weightand AQP4 of immunohistochemistry. Normothermia group ratsreceived no operation;sham-operated contral group rats werecompleted same operation process, but weren't injected blood;focalmild hypothermia group rats were sticked by hypothermia pat todesease the local temperation of brain. Focal mild hypothermia groupanaesthesia rats were binded and fixed at cystospiment dorsal positionafter postop 30 min(normothermia group rats were anaesthesia andfixed on cystosepiment same time). When cooling, temperature ofcooling equipment was set between 10.and 12℃ . Respectively measureanus temperature and drum temperature by spot-needle stylethermodetector, and use drum membrance temperature to representbrain temperature. Make brain temperature retained between 32 and34℃ and anus temperature retained between 35 and 36.5 ℃. At 3hgroup rats continually were cooled for 2 hours. At 6h and 24h grouprats continually were cooled for 4 hours. At 72h group rats continuallywere cooled 4 hours every day. To corresponding time spot the animalswere decapitated, the brains were removed carefully. One group rats'brain were used to measure brain tissue water content, the other grouprats were perfused, imbeded and bladed. Observed change of brainedema through HE stain by microscope and measured the masculinecell population of AQP4 around brain edema and opposite side caudatenucleus. The data were analyzed by one-way analysis of variance.Results It was thus evident that brain tissue edema of 3h ICHgroup rats wasn't obvious, brain tissue edema of 6h and 24h ICH grouprats was obvious, brain tissue edema of 72h ICH group rats was themost obvious and its periphery forms visible edema band, howeverbrain edema of mlid hypothermia group lessened than thenormothermia through light microscope at HE slice. At the same time,it was discovered that water content and AQP4 of cephalophymaperiphery 3h ICH group rats didn't visibly change, those of 6h ICHgroup rats and 24h ICH group rats visibly increased, those of 72h ICHgroup rats showed lightest increase. Compared focal mild hypothermiagroup rats with normothermia group rats, the former's water contentand AQP4 of 3h ICH group rats' cephalophyma periphery showed novisibly changed, 6h ICH group rats and 24h ICH group rats visiblydecreased, 72h ICH group rats obviously decreased.Conclusion Water content and AQP4 of cephalophymaperiphery 3h ICH group rats show no visible change, those of 6h ICHgroup rats and 24h ICH group rats change remarkably, those of 72hICH group rats showes most significant different. Which indicatedAQP4 participate brain edematization after ICH. Compared focal mildhypothermia group rats with normothermia group rats, the former'swater content and AQP4 of cephalophyma periphery visibly decrease.Which indicates focal mild hypothermia therapy can relieveencephaledema after ICH. The mechanism of action can be impactAQP4 expression which make encephaledema relieve. The mechanismof brain edema formation after intracerebral hemorrhage is verycomplex. It is impossible for simple focal mild hypothermia to inhibitbrain edema absolutely. But the study indicated that it can decreasebrain edema formation and had recreased AQP4 expression, this lendsa support to clinical using in ICH.From the study we can conclude that focal mild hypothermia hasthe effect of decreasing brain edema and helps to delay brain edemaformation after experimental ICH in rats. Focal mild hypothermia candecrease AQP4 expression at periphery encephaledema. Focal mildhypothermia can relieve encephaledema and adjust aquatic conveythough impacting AQP4, which might be one of the mechanisms of itin the treatment of ICH.
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