Experimental Study On The Alteration Of Permeability Of Blood-brain Barrier Following Decompressive Craniotomy

Object: Lots of clinical studies have shown that the standard large traumacraniotomy can reduce the mortality or disability rate of patients withuncontrollable intracranial hypertension. However, it was also found in someclinical cases that brain edema got worse and intracranial pressure may keep onrising even patients had decompressive craniotomy treatment. It has been provedthat the permeability of blood brain barrier was related to brain edema andintracranial pressure after trauma. The brain edema after trauma was mostly causedby the permeability of BBB. The effects of decompressive craniotomy on thealteration of brain Edema and BBB still remain unclear. In the present study, weestablished a rabbit model of uncontrollable intracranial hypertension to observethe alteration of permeability of BBB and brain edema following decompressivecraniotomy by using Evans blue tracer method and lanthanum nitrate tracer method.Methods: The model of uncontrollable intracranial hypertension was establishedby pushing compression in rabbit's epidural space. 54 New Zealand rabbits wereequally randomized to a control group(n=8), non decompressive craniotomygroup(group NDC, n=24) and decompressive craniotomy group(group DC, n=24).Theexperimental groups were divided into three time points: 3 h, 24 h and 72 h. Therewere 8 rabbits at each time point, 6 were used for testing the content of brainedema and EB, and 2 were used for observing permeability of BBB by lanthanum nitratetracer method.Results:1. In control group, there was not blue-stain on hemicerebrum brain tissues, butthere was obvious blue-stain in experimental group. The blued area of brain tissuesin group DC was smaller than the group NDC.2. The content of brain water was lower in control group, and higher in group NDC.The difference was significant at 3 h(p＜0.05), and was highly significant at 24h, 72 h(p＜0.01).The content of brain water in group DC was between that in controlgroup and in group NDC, and compared with that in control group, the differenceswere significant at 3 h and 24 h (p＜0.05)but insignificant at 72 h(p＞0.05); compared with that in group NDC, the difference were significant at 3 h,24 h(p＜0.05),andhighly significant at 72 h.3. The content of EB was lower in control group. There was significant differencebetween control group and experiential group(p＜0.05).The content of EB in groupDC was lower than that in group NDC, and the differences were highly significantat 3 h, 24 h and 72 h(p＜0.01).4. The BBB was intact in control group, lanthanum nitrate only appeared in capillarylumen, and the tight junction of endotheliocyte was closed. There were nopinocytotic vesicles and lanthanum nitrate in endotheliocyte. The disruption ofBBB was seen in experimental groups. The tight junction of endotheliocyte wasopened and the number of pinocytotic vesicles in endotheliocyte greatly increased.Lanthanum nitrate diffused into brain tissues. There was not difference betweengroup DC and group NDC at 3 h, but the diffusion in group DC was lower than thatin group NDC at 24 h and 72 h.Conclusion:1. The rabbit model of uncontrollable intracranial hypertension can easilysimulate the situation of haematoma eliminating and decompressive craniotomy withgood applicability and repeatability.2. Decompressive craniotomy can protect the BBB from disruption and alleviate brainedema. The brain edema after trauma was related to the opening of BBB.