Ullman J E, Hjelmqvist H, Lundberg J M, Rundgren M
Department of Physiology, Karolinska Institute, Stockholm, Sweden.
Acta Physiol Scand. 1992 Dec;146(4):457-65. doi: 10.1111/j.1748-1716.1992.tb09447.x.
The effect of separate and combined blockade of vasopressin (AVP) V1-receptors and angiotensin II formation on resistance to a slow venous haemorrhage (0.7 ml kg-1 min-1) was studied in six conscious adult sheep by bleeding to the point of an abrupt fall in the mean systemic arterial pressure (MSAP). Intravenous administration of the V1-receptor antagonist [d(CH2)5Tyr(Me)AVP] (10 micrograms kg-1) and/or the angiotensin I converting enzyme inhibitor captopril (20 mg + 1 mg h-1) did not cause any significant haemodynamic changes in the normovolaemic animal. The volume of haemorrhage necessary to induce acute hypotension (MSAP < 50 mmHg) was significantly smaller after AVP blockade alone (13.8 +/- 0.7 ml kg-1; P < 0.01) but not after captopril treatment (14.7 +/- 1.6 ml kg-1; n.s.) compared to control animals receiving no drug treatment (16.8 +/- 0.6 ml kg-1). The combined treatment with the AVP antagonist and captopril caused a further decrease in tolerance to haemorrhage (9.4 +/- 1.2 ml kg-1; P < 0.001). Blockade of AVP V1-receptors was associated with an attenuated increase in systemic vascular resistance immediately after the end of haemorrhage, concomitant with an accentuated lowering of the central venous pressure. In contrast, captopril treatment decreased the degree of vasoconstriction mainly during the second half of the posthaemorrhage observation period of 1 hour. It is concluded that both AVP and angiotensin II contribute to the maintenance of the MSAP during haemorrhage in conscious sheep.(ABSTRACT TRUNCATED AT 250 WORDS)
在六只清醒成年绵羊中，研究了单独和联合阻断血管加压素（AVP）V1受体及血管紧张素II生成对抵抗缓慢静脉出血（0.7 ml·kg-1·min-1）的影响，出血直至平均体循环动脉压（MSAP）突然下降。静脉注射V1受体拮抗剂[d(CH2)5Tyr(Me)AVP]（10 μg·kg-1）和/或血管紧张素I转换酶抑制剂卡托普利（20 mg + 1 mg·h-1），在血容量正常的动物中未引起任何显著的血流动力学变化。与未接受药物治疗的对照动物（16.8 ± 0.6 ml·kg-1）相比，单独阻断AVP后诱发急性低血压（MSAP < 50 mmHg）所需的出血量显著减少（13.8 ± 0.7 ml·kg-1；P < 0.01），但卡托普利治疗后未减少（14.7 ± 1.6 ml·kg-1；无显著性差异）。AVP拮抗剂和卡托普利联合治疗导致对出血的耐受性进一步降低（9.4 ± 1.2 ml·kg-1；P < 0.001）。阻断AVP V1受体与出血结束后立即出现的全身血管阻力增加减弱有关，同时中心静脉压明显降低。相反，卡托普利治疗主要在出血后1小时观察期的后半段降低血管收缩程度。结论是，AVP和血管紧张素II在清醒绵羊出血期间均有助于维持MSAP。（摘要截短至250字）
