中华劳动卫生职业病杂志
中華勞動衛生職業病雜誌
중화노동위생직업병잡지
CHINESE JOURNAL OF INDUSTRIAL HYGIENE AND OCCUPATIONAL DISEASES
2011年
5期
338-342
,共5页
目的 评价不同氧疗技术(常压下不同浓度吸氧及高压氧)对急性硫化氢(H2S)中毒大鼠的心肌、肺、肝组织形态学的影响.方法 雄性健康Wistar大鼠100只随机分为5组:正常对照组(吸入空气)、染毒组(H2S静式染毒60 min)、33%氧疗组及50%氧疗组(染毒结束后20 min内,将大鼠移置常压下含氧浓度为33%、50%的密闭透明罐中,吸氧100 min)、高压氧组[染毒结束后20 min内,将大鼠置于婴儿高压氧舱内,纯氧洗舱10 min,升压10 min至0.2 MPa(2 ATA)后稳压给氧60 min,减压20 min,共100 min],每组20只.各组在实验结束后立即解剖,取肺、心、肝组织,进行光学显微镜和电子显微镜观察.结果 光学显微镜下可见,染毒组心肌肌丝断裂,排列不规则,胞质水肿,细胞核固缩.33%氧疗组、50%氧疗组、高压氧组心肌肌丝排列逐渐趋于规则、整齐,且肌细胞横纹渐显清晰.染毒组肺泡上皮细胞水肿,肺泡腔边缘不光滑,肺泡腔内可见炎性细胞渗出,33%、50%氧疗组肺泡间隔欠光滑,偶见肺泡水肿;高压氧组肺泡腔内未见渗出.染毒组肝板走形紊乱,细胞间隙增宽,偶见胞质水肿.33%、50%氧疗组肝板走行仍欠规则,其中33%氧疗组可见气球样变.高压氧组肝板放射状排列,胞浆均匀.电子显微镜下可见,染毒组心肌细胞线粒体肿胀,嵴模糊、断裂、自溶;高压氧组线粒体结构清晰,基本修复.染毒组肺泡上皮细胞细胞核中期凋亡,细胞器空泡化;高压氧组细胞核相对正常,仍有空泡化.染毒组肝细胞的胞质结构稀松,核膜不清,染色质结块、边集,线粒体轻度肿胀,出现吞噬体;氧疗各组均未见明显改善.结论 H2S可引起心肌、肺泡上皮细胞、肝细胞的广泛而严重的损害,立即氧疗可明显减轻中毒引起的心肌损伤,对肺组织损伤有一定程度的改善,且高压氧疗对于受损组织的恢复优于常压给氧.但不同给氧方式对肝组织损害的治疗作用均有限.
目的 評價不同氧療技術(常壓下不同濃度吸氧及高壓氧)對急性硫化氫(H2S)中毒大鼠的心肌、肺、肝組織形態學的影響.方法 雄性健康Wistar大鼠100隻隨機分為5組:正常對照組(吸入空氣)、染毒組(H2S靜式染毒60 min)、33%氧療組及50%氧療組(染毒結束後20 min內,將大鼠移置常壓下含氧濃度為33%、50%的密閉透明罐中,吸氧100 min)、高壓氧組[染毒結束後20 min內,將大鼠置于嬰兒高壓氧艙內,純氧洗艙10 min,升壓10 min至0.2 MPa(2 ATA)後穩壓給氧60 min,減壓20 min,共100 min],每組20隻.各組在實驗結束後立即解剖,取肺、心、肝組織,進行光學顯微鏡和電子顯微鏡觀察.結果 光學顯微鏡下可見,染毒組心肌肌絲斷裂,排列不規則,胞質水腫,細胞覈固縮.33%氧療組、50%氧療組、高壓氧組心肌肌絲排列逐漸趨于規則、整齊,且肌細胞橫紋漸顯清晰.染毒組肺泡上皮細胞水腫,肺泡腔邊緣不光滑,肺泡腔內可見炎性細胞滲齣,33%、50%氧療組肺泡間隔欠光滑,偶見肺泡水腫;高壓氧組肺泡腔內未見滲齣.染毒組肝闆走形紊亂,細胞間隙增寬,偶見胞質水腫.33%、50%氧療組肝闆走行仍欠規則,其中33%氧療組可見氣毬樣變.高壓氧組肝闆放射狀排列,胞漿均勻.電子顯微鏡下可見,染毒組心肌細胞線粒體腫脹,嵴模糊、斷裂、自溶;高壓氧組線粒體結構清晰,基本脩複.染毒組肺泡上皮細胞細胞覈中期凋亡,細胞器空泡化;高壓氧組細胞覈相對正常,仍有空泡化.染毒組肝細胞的胞質結構稀鬆,覈膜不清,染色質結塊、邊集,線粒體輕度腫脹,齣現吞噬體;氧療各組均未見明顯改善.結論 H2S可引起心肌、肺泡上皮細胞、肝細胞的廣汎而嚴重的損害,立即氧療可明顯減輕中毒引起的心肌損傷,對肺組織損傷有一定程度的改善,且高壓氧療對于受損組織的恢複優于常壓給氧.但不同給氧方式對肝組織損害的治療作用均有限.
목적 평개불동양료기술(상압하불동농도흡양급고압양)대급성류화경(H2S)중독대서적심기、폐、간조직형태학적영향.방법 웅성건강Wistar대서100지수궤분위5조:정상대조조(흡입공기)、염독조(H2S정식염독60 min)、33%양료조급50%양료조(염독결속후20 min내,장대서이치상압하함양농도위33%、50%적밀폐투명관중,흡양100 min)、고압양조[염독결속후20 min내,장대서치우영인고압양창내,순양세창10 min,승압10 min지0.2 MPa(2 ATA)후은압급양60 min,감압20 min,공100 min],매조20지.각조재실험결속후립즉해부,취폐、심、간조직,진행광학현미경화전자현미경관찰.결과 광학현미경하가견,염독조심기기사단렬,배렬불규칙,포질수종,세포핵고축.33%양료조、50%양료조、고압양조심기기사배렬축점추우규칙、정제,차기세포횡문점현청석.염독조폐포상피세포수종,폐포강변연불광활,폐포강내가견염성세포삼출,33%、50%양료조폐포간격흠광활,우견폐포수종;고압양조폐포강내미견삼출.염독조간판주형문란,세포간극증관,우견포질수종.33%、50%양료조간판주행잉흠규칙,기중33%양료조가견기구양변.고압양조간판방사상배렬,포장균균.전자현미경하가견,염독조심기세포선립체종창,척모호、단렬、자용;고압양조선립체결구청석,기본수복.염독조폐포상피세포세포핵중기조망,세포기공포화;고압양조세포핵상대정상,잉유공포화.염독조간세포적포질결구희송,핵막불청,염색질결괴、변집,선립체경도종창,출현탄서체;양료각조균미견명현개선.결론 H2S가인기심기、폐포상피세포、간세포적엄범이엄중적손해,립즉양료가명현감경중독인기적심기손상,대폐조직손상유일정정도적개선,차고압양료대우수손조직적회복우우상압급양.단불동급양방식대간조직손해적치료작용균유한.
Objective To evaluate the effects of different oxygen therapy technique (different concentrations of normobaric oxygen and the hyperbaric oxygen) on the ultrastructure of cardiac muscle, lung and liver in rats with acute hydrogen sulfide intoxication. Methods One hundred healthy male Wistar rats were randomly divided into five groups: normal control group (A), poisoned group (B), oxygen therapy group (C), oxygen therapy group (D) and oxygen therapy group (E). After the exposure to 300 ppm H2S for 60 min in a static exposure tank (1 m3) , the rats were treated with oxygen therapy, C, D and E groups were given 33% oxygen, 50% oxygen of atmospheric oxygen and hyperbaric oxygen therapy for 100 min, respectively. The rats in normal control group inhaled air under the same environment. After exposure and therapy, the tissues of lung, heart and liver were observed under light microscope and electron microscope. Results The results of light microscope examination showed that the broken and not well aligned cardiac myofilaments, cytoplasmic edema and pyknosis could be seen in group B. The well aligned and clear cardiac myofilaments appeared in group C, D and E. The alveolar hemorrhage, edema and inflammatory cells exudation could not be seen in group A. Alveolar epithelial cell edema, unsmooth alveolar edge and alveolar inflammatory cells exudation could be found in group B. The unsmooth alveolar septal borders and pulmonary edema could be seen occasionally in group C and D, the alveolar inflammatory cells exudation could not be seen in group E. The regular hepatic boards and the uniform hepatic cellular nuclei were found in group A. The disordered hepatic boards, widened cellular gaps and cytoplasmic edema could be seen occasionally in group B. The irregular hepatic boards and ballooning degeneration could be seen in group C and D. The regular hepatic boards and uniform cytoplasm could be found in group E. The results of electron microscope examination indicated that the mitochondrial swelling, autolyzing, fuzzy and breakage of myocardial cells were observed in group B; the clear mitochondrial structure appeared in group E. The apoptosis and organelle vacuole of alveolar epithelial cells could be observed in group B. The relatively normal nuclei of alveolar epithelial cells could be seen in group E. The lax cytoplast structure of hepatocytes, unclear nuclear membrane, lumped chromatin, slightly swelled mitochondria and phagosomes were observed in group B. However, no improved change was observed in group C, D and E. Conclusion Hydrogen sulfide could induce the extensive and severe damage of myocardial mitochondria , alveolar epithelial cells and hepatocytes, the oxygen therapy in good time could reduce significantly the myocardial injury, and improve the lung injury to some extent. High-pressure oxygen therapy is better than the normobaric oxygen therapy.
