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慢性呼吸衰竭病人红细胞内酸碱变化机制的研究 被引量:2

Study on Mechanism of Erythrocytic Acid-base changes in Patients With Chronic Respiratory Failure
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摘要 本文对肺心病Ⅰ型呼吸衰竭组40例,Ⅱ型呼吸衰竭组40例和对照组37例的红细胞(RBC)内外血气和RBC膜带3蛋白(band3protein)阴离子交换功能进行了研究。结果表明:肺心病Ⅱ型呼吸衰竭病人红细胞内呈偏碱状态,其产生机制可能为①血红蛋白(Hb)浓度升高,缓冲容量增大;②还原Hb增多;③RBC内外阴离子交换受限。肺心病Ⅱ型呼吸衰竭病人RBC内pH(pHi)增高,使氧离曲线左移,可增加血液携氧能力,这种氧亲和力升高为肺心病患者氧转运的进一步代偿。 atients were divided into 3 groups,i.e. respiratory fairlure type Ⅰ(n=40),respiratory fail-ure type Ⅱ (n=40)and control group(CG,n=37).The changes of plasma and RBC blood gasesand band 3 protein anion transport function were investigated.The results demonstrated that therelative intraerythrocyte alkolosis was results from the increase of HCO_3 of the patients with res-piratory failure type Ⅱ. This appeared to be related to ① increased Hb and the strengthenedbuffer capacity;② the increase of deoxygenated Hb;③ anion exchange restriction between plasmaand RBC. Alkalosis in the RBC might increase the oxygencarrying capacity of blood,which mightfurther compensate for the low oxygen transportation in the patients with cor pulmonale.
出处 《基础医学与临床》 CSCD 1995年第4期60-63,共4页 Basic and Clinical Medicine
基金 国家自然科学基金
关键词 慢性 呼吸衰竭 红细胞 酸碱代谢紊乱 Cor pulmonale respiratory failuer acid-base imbalance band 3 protein
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  • 1周汉清,生物化学与生物物理学报,1993年,25卷,111页
  • 2张志鸿,Biochim Biophys Acta,1992年,1106卷,31页
  • 3许红,生物物理学报,1992年,8卷,481页

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