Eyraud Daniel, Richard Olivier, Borie Dominique C, Schaup Barbara, Carayon Alain, Vézinet Corinne, Movschin Marie, Vaillant Jean-Christophe, Coriat Pierre, Hannoun Laurent
Department of Anesthesiology and Critical Care, Groupe Hospitalier Pitié-Salpêtrière, Assistance Publique-Hôpitaux de Paris, University Pierre et Marie Curie, 47 Boulevard de l'Hôpital, 75013 Paris, France.
Anesth Analg. 2002 Nov;95(5):1173-8, table of contents. doi: 10.1097/00000539-200211000-00008.
Hepatic vascular exclusion (HVE) combines portal triad clamping and occlusion of the inferior vena cava. Although HVE has been performed for major liver resections during the last 2 decades, little is known about the mechanisms that explain its satisfactory hemodynamic tolerance. Consequently, we performed a comprehensive study of both hemodynamic and hormone responses to HVE. Twenty-two patients who underwent liver resection for secondary tumors developed in noncirrhotic livers were prospectively studied. Heart rate, arterial blood pressure, pulmonary artery pressure, mixed venous saturation, cardiac output, and left ventricular dimensions determined by transesophageal echocardiography were monitored in HVE patients. Blood concentrations of arginine vasopressin (AVP), epinephrine, norepinephrine, dopamine, and atrial natriuretic peptide and plasma renin activity (PRA) were measured before clamping; 5, 15, and 30 min after clamping; and 15 min after unclamping. Hemodynamic response to HVE was characterized by a significant (P < 0.05) decrease in left ventricular dimensions, fractional area change, and pulmonary artery pressure. We also observed a marked decrease in cardiac output (50%) and an increase in heart rate and systemic vascular resistance. After unclamping, there was peripheral vasodilation, assessed by a significant decrease in systemic vascular resistance from the preclamping value to unclamping. An acute and sustained increase in AVP and norepinephrine that returned to baseline after unclamping and the absence of modification in PRA concentrations were noted. The marked decrease in venous return that characterizes HVE is compensated for by an increase in vascular resistance secondary to an important activation of the AVP and sympathetic systems. The PRA system does not play an important role in maintaining arterial blood pressure during HVE.
Hemodynamic and hormonal responses to the acute interruption of caval venous return to the heart were investigated in patients undergoing liver resection with hepatic vascular exclusion. A compensatory role for arginine vasopressin and sympathetic systems that provoked increased vascular resistance was demonstrated.
肝血管阻断术（HVE）联合门静脉三联钳夹和下腔静脉闭塞。尽管在过去20年中HVE已用于主要肝脏切除术，但对其令人满意的血流动力学耐受性的解释机制知之甚少。因此，我们对HVE的血流动力学和激素反应进行了全面研究。对22例因非肝硬化肝脏中出现继发性肿瘤而接受肝切除术的患者进行了前瞻性研究。在HVE患者中监测心率、动脉血压、肺动脉压、混合静脉饱和度、心输出量以及经食管超声心动图测定的左心室尺寸。在钳夹前、钳夹后5、15和30分钟以及松开钳夹后15分钟测量精氨酸加压素（AVP）、肾上腺素、去甲肾上腺素、多巴胺和心房利钠肽的血药浓度以及血浆肾素活性（PRA）。HVE的血流动力学反应表现为左心室尺寸、面积变化分数和肺动脉压显著（P<0.05）降低。我们还观察到心输出量显著降低（50%）以及心率和全身血管阻力增加。松开钳夹后，出现外周血管舒张，表现为全身血管阻力从钳夹前值到松开钳夹时显著降低。注意到AVP和去甲肾上腺素急性持续增加，松开钳夹后恢复至基线水平，且PRA浓度无变化。HVE特征性的静脉回流显著减少通过AVP和交感神经系统重要激活继发的血管阻力增加得到代偿。PRA系统在HVE期间维持动脉血压方面不起重要作用。
对接受肝血管阻断术肝切除术的患者，研究了腔静脉回心血量急性中断时的血流动力学和激素反应。证实了精氨酸加压素和交感神经系统具有引发血管阻力增加的代偿作用。
