高压氧在治疗脊髓损伤伴截瘫及肢体慢性溃疡中的应用

本文报告了用高压氧治疗脊髓损伤伴截瘫患者１２例，肢体慢性溃疡８例。将患者置于２个大气压的单人氧舱内，每次９０ｍｉｎ。前者疗程为１周，每日２次。后者疗程为２周，每日１次。治疗结果：脊髓损伤伴截瘫患者中８例有明显而有意义的功能恢复，占６６．６％。慢性溃疡患者中有３例愈合，４例好转，有效率为８５％。作者认为：早期使用高压氧是治疗急性截瘫，尤其是不完全性截瘫的一种安全有效的方法。高压氧治疗可加速慢性溃疡创面的愈合，但不能取代溃疡面的局部处理。     

Suppressive effect of hyperbaric oxygenation on immune responses of normal and autoimmune mice.

We studied the effect of hyperbaric oxygenation (HBO) on immune responses in normal and autoimmune mice. Mice were exposed to HBO in an animal chamber at a pressure of 252.5 kPa for 1 h and once a day for 5 days. The immunization of C3H/He mice with sheep erythrocytes induced marked anti-sheep erythrocyte antibody response on day 7. However, this response was markedly suppressed in HBO-treated mice. The suppression is dependent on the duration of HBO and it works on the early and the late stage of antibody responses. HBO suppresses the development of both sheep erythrocyte-specific B cells and helper T cells after the immunization. Then, we tried to expose autoimmune mice to HBO. Spontaneous immunoglobulin production of NZB and MRL/lpr spleen cells was also significantly suppressed by HBO. Furthermore, long term HBO exposure results in the suppression of the development of autoimmune symptoms such as proteinuria, facial erythema and lymphadenopathy in MRL/lpr mice. All these results suggest that HBO is applicable for the treatment of autoimmune diseases.     

Hyperbaric oxygen therapy improves angiogenesis and bone formation in critical sized diaphyseal defects

Besides the use of autologous bone grafting several osteoconductive and osteoinductive methods have been reported to improve bone healing. However, persistent non‐union occurs in a considerable number of cases and compromised angiogenesis is suspected to impede bone regeneration. Hyperbaric oxygen therapy (HBO) improves angiogenesis. This study evaluates the effects of HBO on bone defects treated with autologous bone grafting in a bone defect model in rabbits. Twenty‐four New‐Zealand White Rabbits were subjected to a unilateral critical sized diaphyseal radius bone defect and treated with autologous cancellous bone transplantation. The study groups were exposed to an additional HBO treatment regimen. Bone regeneration was evaluated radiologically and histologically at 3 and 6 weeks, angiogenesis was assessed by immunohistochemistry at three and six weeks. The additional administration of HBO resulted in a significantly increased new bone formation and angiogenesis compared to the sole treatment with autologous bone grafting. These results were apparent after three and six weeks of treatment. The addition of HBO therapy to autologous bone grafts leads to significantly improved bone regeneration. The increase in angiogenesis observed could play a crucial role for the results observed. © 2015 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 33:513–520, 2015.     

不同细胞构筑在高压氧治疗迟发型脑病中的功能研究

目的：通过研究高压氧（ HBO）治疗急性CO中毒大鼠皮层不同细胞构筑在神经细胞凋亡中的差别,探讨HBO治疗急性CO中毒的机制及靶向定位。方法利用雄性SD大鼠,建立急性CO中毒模型。应用免疫组织化学以及免疫荧光的方法,测定在CO中毒和HBO治疗1 d、3 d、7 d、14 d和21 d后Caspase－3、NeuN和MMP－9的表达变化。结果急性CO中毒后,皮层神经细胞凋亡随中毒后时间延长而加重;不同细胞构筑发生凋亡程度不同,内颗粒层和内锥体细胞层最明显;Caspase－3与MMP－9在内颗粒层与内锥体细胞层变化最明显,在1 d开始增多,3 d达到最大值,7 d开始减少;HBO治疗后,MMP－9和Caspase－3降低,尤其以内颗粒层与内锥体细胞层最明显;且HBO治疗7 d后,降低最明显。结论急性CO中毒后,皮层各层神经细胞均发生凋亡现象,内颗粒层和内锥体细胞层最明显;凋亡可能与MMP－9降解神经细胞周围的基质, Caspase－3促进凋亡有关;HBO治疗可能是通过调控复杂的蛋白表达机制,调节MMP－9以及Caspase－3的表达水平,最终抑制神经细胞的凋亡;HBO治疗7 d对凋亡的作用最明显。     

高压氧辅助治疗对卒中后抑郁患者血清5-HT、NE及神经功能的影响

目的：观察高压氧（HBO）辅助治疗对卒中后抑郁（PSD）患者血清5-羟色胺（5-HT）、去甲肾上腺素（NE）及神经功能的影响。方法70例PSD患者根据数字表法随机分为2组,对照组（n=35例）采用常规措施治疗,观察组（n=35例）待确定活动性出血已稳定或已趋于稳定后,在对照组治疗基础上加用HBO治疗。两组疗程均为30d,比较两组患者治疗前后血清5-HT、NE表达水平及汉密尔顿抑郁量表（HAMD）、中国脑卒中量表（CSS）,改良Barthel指数（MBI）评分变化。结果两组患者治疗后血清5-HT、NE表达水平均明显升高（P<0.05）,且观察组升高较对照组更为显著（P<0.05）;两组患者治疗后HAMD、CSS评分明显降低（P<0.05）,而MBI评分明显升高（P<0.05）,且观察组降低或升高较对照组更为显著（P<0.05）。结论 HBO辅助治疗可明显升高PSD患者血清5-HT、NE表达水平,改善抑郁状态和神经功能。     

高压氧治疗对瘢痕疙瘩放疗后创面移植皮片成活的影响

痕疙瘩切除后创面皮片移植的成活有促进作用.     

Mitochondrial Injury in Human Acute Carbon Monoxide Poisoning: The Effect of Oxygen Treatment

The best oxygen therapy for acute carbon monoxide poisoning (ACOP) remains unestablished. Reported mitochondrial complex IV (mtCIV) inhibition, together with carboxyhaemoglobin (COHb)-induced hypoxia, may influence acute clinical symptoms and outcome. To “mitochondrially” evaluate treatment efficacy, we correlated intoxication severity and symptoms with mitochondrial function (mtCIV activity) and oxidative stress (lipid peroxidation) in 60 poisoned patients and determined ACOP recovery depending on either normobaric or hyperbaric oxygen therapy along a 3-month follow-up. In the present article we positively evaluate mtCIV as a good marker of ACOP recovery, treatment effectiveness, and late neurological syndrome development, which advocates for hyperbaric oxygen therapy as the treatment of choice. However, we discourage its usefulness as a severity marker because of its excessive sensitivity. We additionally evaluate oxidative stress role and prognostic factors for neurological sequelae development.