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目的和方法：用致失血性休克（ＨＳ）的放血量和平衡动脉血压（ＡＢＰ）２ｈ过程的剩余血量差作标准测得 ＨＳ的 ＡＢＰ５．３ ｋＰａ为代偿型，４．０ ｋＰａ为失代偿型。比较两型 ＨＳ血中 Ｎａ＋、Ｋ＋、蛋白总量（ＴＰ）和醛固酮的含量及血中葡萄糖、乳酸、血尿素氮（ＢＵＮ）、乳酸脱氢酶（ＬＤＨ）水平的变化，并观察用血管紧张素转换酶抑制剂疏甲丙脯酸（Ｃａｐｔ．）降低血管紧张素Ⅱ（Ａｎｇ－Ⅱ）形成后上述指标的变化，以了解Ａｎｇ－Ⅱ在ＨＳ发病过程中的意义。结果：Ｃａｐｔ．可使失代偿性 ＨＳ的剩余血量从接近零值明显回升，机体状态改善。两型 ＨＳ均有血液稀释且不受Ｃａｐｔ．的影响；有血Ｋ＋和醛固酮升高但血Ｎａ＋无变化，预先应用Ｃａｐｔ．可使前二者回降而对后者无影响。Ａｎｇ－Ⅱ促进醛固酮分泌从而加强排Ｋ＋保Ｎａ＋的现象未检出。两型ＨＳ均有血中乳酸、ＬＤＨ、ＢＵＮ升高，失代偿性 ＨＳ相对严重，Ｃａｐｔ．均可使之回降。代偿性 ＨＳ有血糖升高，而失代偿性 ＨＳ则见血糖显著降低， Ｃａｐｔ．对前者无影响却可使后者的血糖明显回升。结论：ＡＢＰ在５．３ｋＰａ水平为代偿性ＨＳ，在４．０ｋＰａ为失代偿性ＨＳ，后者血中各项指标变化均较前者明显严重，Ｃａｐｔ．?
PURPOSE AND METHODS: ABP5.3 kPa HS was compensated with the standard of the difference between the amount of bleeding induced by hemorrhagic shock (HS) and the remaining blood volume during 2 hours of equilibration arterial pressure (ABP). 4.0 kPa Decompensated. The levels of Na +, K +, total protein (TP), aldosterone and blood glucose, lactate, BUN, LDH in two types of HS were compared. Capt., A hormone - converting enzyme inhibitor, decreases these changes after angiotensin Ⅱ (Ang-Ⅱ) formation, so as to understand the significance of Ang-Ⅱ in the pathogenesis of HS. Result for: Capt. Can make the remaining blood loss of decompensated HS significantly rose from near zero, the body condition improved. Both types of HS are hemodiluted and are not Capt. Of the impact; blood K + and aldosterone increased blood Na + no change, pre-Capt. Can make the former two fall back and have no effect on the latter. Ang-Ⅱ promote the secretion of aldosterone thereby enhancing row K + Paul Na + phenomenon was not detected. Both types of HS have blood lactic acid, LDH, BUN increased, decompensated HS is relatively serious, Capt. Can make it back down. Compensatory HS has elevated blood glucose, while decompensated HS see a significant decrease in blood glucose, Capt. No effect on the former can make the latter’s blood sugar rose significantly. CONCLUSION: The ABP is compensated HS at 5.3kPa and decompensated HS at 4.0kPa. The indexes of blood in the latter are obviously more serious than the former. ?