Sun Lena S, Dominguez Carmen, Mallavaram Navin A, Quaegebeur Jan M
Department of Anesthesiology, College of Physicians and Surgeons, Columbia University, 630 West 168th Street, New York, NY 10032, USA.
J Thorac Cardiovasc Surg. 2005 May;129(5):1104-10. doi: 10.1016/j.jtcvs.2004.08.025.
To examine whether children with univentricular defects have intrinsic dysfunction in the natriuretic peptide system.
We compared plasma levels of the fluid-regulating hormone vasopressin (antidiuretic hormone), aldosterone, atrial natriuretic peptide, and brain natriuretic peptide in children with congenital univentricular and biventricular defects. We enrolled 27 patients with univentricular defects and 27 patients with biventricular cardiac defects. Children who underwent Fontan and Glenn procedures were considered as patients with univentricular cardiac defects; children who underwent repair of tetralogy of Fallot or subaortic stenosis were considered as controls with biventricular defects.
Preoperative plasma atrial natriuretic peptide, brain natriuretic peptide, antidiuretic hormone, and aldosterone were comparable in both groups. Although plasma cyclic guanosine monophosphate levels were comparable between groups, there was a significant correlation between molar concentrations of plasma cyclic guanosine monophosphate and plasma atrial natriuretic peptide ( r = 0.42) and brain natriuretic peptide ( r = 0.44) in the biventricular group, but not in the univentricular group ( r = 0.19 for atrial natriuretic peptide; r = 0.13 for brain natriuretic peptide). All patients had a significant postoperative increase in plasma antidiuretic hormone. A significant postoperative increase in plasma brain natriuretic peptide was found in the patients with biventricular, but not univentricular, defects. In contrast, a significant increase in plasma aldosterone was observed only in the patients with univentricular defects.
There were distinct differences between univentricular and biventricular groups in their perioperative plasma fluid-regulating hormone responses. Specifically, patients with univentricular defects may have abnormal natriuretic peptide secretion and function. The natriuretic dysfunction may be on the basis of hypoplastic ventricular development.
研究单心室缺损患儿的利钠肽系统是否存在内在功能障碍。
我们比较了先天性单心室和双心室缺损患儿体内调节液体的激素——血管加压素（抗利尿激素）、醛固酮、心房利钠肽和脑利钠肽的血浆水平。我们纳入了27名单心室缺损患儿和27名双心室心脏缺损患儿。接受Fontan和Glenn手术的患儿被视为单心室心脏缺损患者；接受法洛四联症或主动脉瓣下狭窄修复术的患儿被视为双心室缺损对照组。
两组患儿术前血浆心房利钠肽、脑利钠肽、抗利尿激素和醛固酮水平相当。虽然两组间血浆环磷酸鸟苷水平相当，但双心室组血浆环磷酸鸟苷摩尔浓度与血浆心房利钠肽（r = 0.42）和脑利钠肽（r = 0.44）之间存在显著相关性，而单心室组则无（心房利钠肽r = 0.19；脑利钠肽r = 0.13）。所有患者术后血浆抗利尿激素均显著升高。双心室缺损患者术后血浆脑利钠肽显著升高，而单心室缺损患者则无。相反，仅在单心室缺损患者中观察到血浆醛固酮显著升高。
单心室组和双心室组在围手术期血浆液体调节激素反应方面存在明显差异。具体而言，单心室缺损患者可能存在利钠肽分泌和功能异常。利钠功能障碍可能基于心室发育不全。
