HSH injection infusion on acute intracranial hypertension associated with hemorrhagic shock in dogs brain tissue pathology and the impact of oxygen free radicals

[Abstract] Objective To observe the hypertonic saline hydroxyethyl starch 40 injection (HSH) in dogs with acute intracranial hypertension associated with hemorrhagic shock model in the recovery cycle of blood volume, reduced brain edema and reduce the brain tissue content of oxygen free radicals effect. Methods 20 healthy dogs, using epidural balloon method of water injection and arterial bleeding associated with the acute intracranial hypertension model of hemorrhagic shock. Animals were randomly divided into group of hydroxyethyl starch solution (HES group), lactate Ringer's solution group (RL group), 7.5% sodium chloride solution group (HS group) and hypertonic saline hydroxyethyl starch 40 injection group (HSH group), respectively, in the shock 1h Enter the appropriate liquid. Monitoring of mean arterial pressure (MAP), central venous pressure (CVP), heart rate (HR), intracranial pressure (ICP), detection of brain tissue malondialdehyde (MDA) content, superoxide dismutase (SOD) activity, brain tissue for histopathologic examination. Results 4 groups after resuscitation fluid can effectively increased MAP (P <0.05), but the HES group and RL group, ICP increased significantly (P <0.05), recovery after 2h, HS group, MAP started to decline (P <0.05). To recover after 4h, only to maintain a favorable HSH group MAP and lower ICP, HSH group of brain tissue content of oxygen free radicals compared with other groups decreased (P <0.05). Pathological examination showed that the recovery after 4h, HSH group of brain tissue damage compared with other groups of light. Conclusion hypertonic saline hydroxyethyl starch 40 injection can effectively recover hemorrhagic shock, reduced ICP and oxygen free radical generation, reducing cerebral ischemia-reperfusion injury. [Keywords:] Hypertonic hydroxyethyl starch 40 sodium chloride injection in dogs with acute intracranial hypertension intracranial pressure after hemorrhagic shock and brain tissue superoxide dismutase MDA Effect of HSH on oxygen free radicals and histopathological change of brain tissue in acute intracranial hypertension and hemorrhagic shock model of dog XU Xiang, GU Miao-ning, XIAO Jin-fang, XIAO Hua-ping, ZHAO Zhen-long, LIU Gao-wang. Department of Anesthesiology Nan Fang Hospital, Nan Fang Medicai college, Guang Zhou, 510515, China. [Abstract] Objective To observe the effect of hypertonic sodium chloride hydroxyethyl starch 40 injection (HSH) on oxygen free radicals and morphological change of brain tissue in acute intracranial hypertension and hemorrhagic shock model of dog. Methods 20 healthy dogs were randomly divided into group HES, group RL, group HS and group HSH. Balloon epidural injection and arterial bleeding model was prepared.Corresbonding liquids were infused separately 1h after shock.The level of mean arterial blood pressure (MAP), central venous pressure (CVP), heart rate (HR) and intracranial pressure (ICP) were monitored, and the level of superoxide dismutase (SOD) and malondialdehyde (MDA) were determined.Samples of brain tissue were removed for Pathological examination. Results After resuscitation, liquids of 4 groups can effectively increase MAP (P <0.05), but group HES and group RL significantly increased ICP (P <0.05). 2 hours after resuscitation, MAP of group HS begin to decrease and 4 hours after resuscitation only group HSH can maintain a ideal MAP and lower ICP. MDA and SOD levels were statistically significant different between group HSH and other groups 4 hours after resuscitation (P <0.05). Pathological examination revealed less injury in group HSH. Conclusion HSH can effectively resuscite hemorrhagic shock, decrese ICP , reduce oxygen free radicals levels in brain and relieve tissue ischemia / reperfusion injury. [Key Words] HSH; dog; acute intracranial hypertension; hemorrhagic shock; brain tissue; SOD; MDA. craniocerebral trauma is one of the most serious injuries, while the hemorrhagic shock with severe traumatic brain injury mortality is very high (1). Control of brain edema, reducing brain cell injury is a neurosurgical treatment of peri-operative period of an important means of determining the prognosis of patients with the key issue. Shock is often a large number of fluid infusion to maintain blood pressure stability, but often results in brain edema, caused by secondary injury; ischemia-reperfusion produce large amounts of oxygen free radicals, often causing irreversible damage to brain cells; while the conventional application of dehydrating diuretics treatment of cerebral edema to reduce intracranial pressure (intracranial pressure, ICP), there would be less effective blood volume, increased shock. In this study, the main observation of hypertonic sodium chloride hydroxyethyl starch 40 injection (hypertonic sodium chloride hydroxyethyl starch 40 injection, HSH) recovery of hemorrhagic shock reduced the role of intracranial pressure, brain tissue by detecting malondialdehyde (MDA) content, super - oxide dismutase (SOD) activity on the HSH brain ischemia - reperfusion injury in the impact of key areas to make some research into brain tissue were observed in the corresponding morphology changes to assess the HSH in the brain protection application. 1. Materials and methods 1.1 Animals and groups: 20 healthy mongrel dogs, male and female informal, weight 10-20kg, from Nanfang Hospital, Southern Medical University Experimental Animal Center. Were randomly divided into groups of hydroxyethyl starch solution (HES group), lactate Ringer's solution group (RL group), 7.5% sodium chloride solution group (HS group) and hypertonic saline hydroxyethyl starch 40 injection group (HSH group). Each group of five animals. 1.2 Animal model and resuscitation: peripheral venipuncture, intravenous 3% pentobarbital sodium (1ml/kg) induction of anesthesia. anesthesia after the sit-fixed smooth operation of the stage, on the 9th through the mouth into the trachea tube, connect anesthesia machines, fixed, adjust respiratory parameters (respiratory rate 15-30bpm, tidal volume 250-430ml to ETCO2 maintained at (32-37) mmHg. Intravenous infusion of vecuronium bromide (0.08mg/kg/h), inhalation of 1% isoflurane and oxygen to maintain anesthesia. OK right jugular vein incision, insert a 18G intravenous catheter, connection monitor, monitor central venous pressure (CVP ). the left femoral artery incision, insert a 20G heparin tube, monitoring arterial blood pressure. OK bladder puncture, indwelling catheter. dogs head at the top to the hair, skin, the middle longitudinal line of the scalp incision exposed the parietal bone. in the left parietal bone drilling, diameter 6-10mm, will be water balloon and sent into the epidural space, fixed balloon, suture the scalp. the right parietal bone drilling for intraventricular catheter, when the cerebrospinal fluid gradually filled with plastic tubes, fixed, and then L-type piezometer measuring cerebral ventricular pressure, regulation 0:00 and left parallel to the external auditory canal. both sides of the skull with bone wax hole defects were closed, to ensure the reliability of manometry. to the available water within the water balloon, so that the basis of intraventricular pressure ratio pressure increases 10 mmHg and maintained. right femoral artery puncture, 15min bleeding inside the uniform, so that MAP reduced to 40mmHg, and adjust the amount of blood loss so that blood pressure to maintain this level, continue to 60min to complete acute intracranial hypertension with hemorrhagic shock model making, the subsequent recovery. HSH group respectively 8ml/kg, HES group by an equivalent amount of blood loss, RL Group by three times the amount of blood loss, HS Group by 6ml/kg input, all the liquid inside the losers are in the 20min. craniotomy on the recovery of 240min take temporal lobe brain tissue of full thickness, in part for the measurement of malondialdehyde (MDA) content, superoxide dismutase (SOD) activity, and the other for the morphological study. 1.3 OUTCOME MEASURES: 1.3.1 Continuous Measurement of MAP recovery process , CVP, HR, ICP, respectively, before fetching water balloon (T02), after fetching water balloon (T01), bleeding after (T0), shock to maintain 1h (T60), the recovery after 20min (T80), the recovery after 40min (T100), the recovery after 1min (T120), the recovery after 2h (T180), the recovery after 3h (T240), the recovery after 4h (T300) data collection. 1.3.2 brain tissue malondialdehyde (MDA) Determination: The thio - barbituric acid (TBA) method. The principle is that lipid peroxide degradation product of malondialdehyde (MDA) with thiobarbituric acid (TBA) condensation to form a red product of the maximum absorption peak at 532nm with a spectrophotometer measured absorbance. MDA kit from Nanjing Jiancheng Bio-engineering Institute, determination kit according to instructions. 1.3.3 brain tissue superoxide dismutase (SOD) activity assay: use of xanthine oxidase France. The principle is that by xanthine and xanthine oxidase reaction system to produce superoxide anion radical (O2 -