血管紧张素转换酶抑制剂疏甲丙脯酸对失血性休克的影响  

Influence of angiotensin converting enzyme inhibitor captopril on hemorrhagic shock in rabbit

作　　者：岳峰[1] 江明[2] 郭炯[3] 王海燕[3] 

机构地区：[1]新疆医科大学一附院神经内科,新疆维吾尔自治区乌鲁木齐830054 [2]新疆医科大学一附院血液科,新疆维吾尔自治区乌鲁木齐830054 [3]新疆医科大学一附院病理生理教研室,新疆维吾尔自治区乌鲁木齐830054

出　　处：《中国病理生理杂志》2000年第4期308-311,共4页Chinese Journal of Pathophysiology

基　　金：国家自然科学基金资助(No.39160035)

摘　　要：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．?AIM and METHOD: In terms of difference value between bleeding blood volume that caused hemorrhagic shouk (HS) and residual blood volume at 2 h after HS, showed that HS at 5.3 kPa level was compen- satory and at 4.0 kPa level was decompensatory. Comparing some blood changes between HS two levels and their changes while pretreated with captopril (Capt. ) to reduce the release of angiotensin Ⅱ (Ang-Ⅱ), so as to inveshgate the significance of Ang - Ⅱ during HS. RESULTS: The residual blood volume in 4.0 kPa HS + Capt. group are again from near 'zero' value in simple 4.0 kPa HS group. In both two HS level groups found blood dilution and was not influenced by pretreating with Capt.; contents of K+ and aldosterone increased, but Na+ had no changes, in Capt. + HS group, the former two contents reduced and Na+ had no changes comparing with each HS group. In two HS groups, the bind lactate, lactic dehydrogenase (LDH), blood urea nitrogen (BUN) increased and had more increment in 4.0 kPa HS group. All these changes could be prevented by pretreating with Capt. The blood glucose in 5.3 kPa HS group increased markedly and Capt. had no influence on it, but decreased extremely in 4.0 kPa HS group and Capt. could make it re - increased. CONCLUSIONS: Artery blood pressure (ABP) at 5 .3 kPa level was compensatory HS and ABP at 4 .0 kPa level was decompensatory HS, some changes on decompensatory HS were more serious and severe than compensatory HS, Capt. has protective effects on some changes during HS and could prolong the survival time of decompensatory HS, all that indicated the increment of Aug - Ⅱ is an important pathogenetic factor during HS.

关 键 词：失血性休克 巯甲丙脯酸 血管紧张素 转换酶 

分 类 号：R631.402[医药卫生—外科学]