摘要
失血性休克过程的缺氧是低动力型、等张性。本文证实,随着休克的发展,由于细胞受损,用氧障碍,进而继发组织性“缺氧”。细胞用氧障碍则无需进一步动用血氧解离代偿的贮备力,从而表现出在静脉血氧饱和度较高水平上氧供求平衡的假象,而且出现PvO_2和PvCO_2相对恒定而pH进行性下降的分离现象。细胞氧供不足的重要性已让位于用氧障碍,后者决定着休克的进一步发展。分析诸器官静脉血气和pH的变化还显出,不同器官变化各有特点。将诸器官在休克过程静脉血气变化的均值相比,肝PvO_2最低而PvCO_2最高,反映出肝是主要代谢器官的特点;肾是主要排泄器官而且血供丰富,所以它的变化则恰好和肝相反。pH的变化和血气变化是相适应的。血气和pH的变化还反映出肾功在休克3h后开始受损。
The classical conception in hypoxia of hemorrhagic shock is hypokinctic and isotonic. In this paper we demonstrated that a secondary 'histotoxic hypoxia' would company with the development of hemorrhagic shock, because the cell was injured and unable to use oxygen sufficiently. Hence, mobilizing of compensatory storage of HbO_2 dissociation would not be required continaously, a pseudo-equilibrium between supplying and requiring was established on a higher level of HbO_2 saturation and PvO_2 and PvCO_2 kept on a constant level but the pH decreased continuously, the later was part companying with the former. Then the important significance of hypokinetic hypoxia gave place to the inability of utilizing oxygen, upon which the development of hemorrhagic shock depended. Each organ possessed its characteristie changes, the hepatic PvO_2 was lower and the PvCO_2 was higher than the others, but the renal PvO_2 was higher and its PvCO_2 was lower than the others. Functional disturbance of kidney would occur 3 h after shock.
关键词
失血性
休克
中毒性
缺氧
肝
肾
hemorrhagic shock
histotoxic shock
oxygen deficit
liver
kidney
