Joris J L, Chiche J D, Canivet J L, Jacquet N J, Legros J J, Lamy M L
Department of Anesthesiology and Intensive Care Medicine, University Hospital of Liège, Belgium.
J Am Coll Cardiol. 1998 Nov;32(5):1389-96. doi: 10.1016/s0735-1097(98)00406-9.
We investigated endocrine correlates of the hemodynamic changes induced by carbon dioxide pneumoperitoneum (PNO). We then studied whether clonidine might modulate the hemodynamic changes induced by PNO by reducing release of catecholamines and vasopressin.
Both mechanical and neurohumoral factors contribute to the hemodynamic changes induced by carbon dioxide PNO. Several mediators have been proposed, but no study has correlated hemodynamic changes with changes in levels of these potential mediators.
We conducted two studies, each including 20 healthy patients scheduled for elective laparoscopic cholecystectomy. In the first study serial measurements of hemodynamics (thermodilution technique) were done during laparoscopy and after exsufflation. Plasma concentrations of cortisol, catecholamines, vasopressin, renin, endothelin and prostaglandins were measured at the same time points. In the second study patients were randomly allocated to receive 8 microg/kg clonidine infused over 1 h or placebo before PNO. Hemodynamics and plasma levels of cortisol, catecholamines and vasopressin were measured during PNO and after exsufflation.
Peritoneal insufflation resulted in a significant reduction of cardiac output (18+/-4%) and increases in mean arterial pressure (39+/-8%) and systemic (70+/-12%) and pulmonary (98+/-18%) vascular resistances. Laparoscopy resulted in progressive and significant increases in plasma concentrations of cortisol, epinephrine, norepinephrine and renin. Vasopressin plasma concentrations markedly increased immediately after the beginning of PNO (before PNO 6+/-4 pg/ml; during PNO 129+/-42 pg/ml; p < 0.05). The profile of vasopressin release paralleled the time course of changes in systemic vascular resistance. Prostaglandins and endothelin did not change significantly. Clonidine significantly reduced mean arterial pressure, heart rate and the increase in systemic vascular resistance. Clonidine also significantly reduced catecholamine concentrations but did not alter vasopressin and cortisol plasma concentrations.
Vasopressin and catecholamines probably mediate the increase in systemic vascular resistance observed during PNO. Clonidine before PNO reduces catecholamine release and attenuates hemodynamic changes during laparoscopy.
我们研究了二氧化碳气腹(PNO)诱导的血流动力学变化的内分泌相关性。然后我们研究了可乐定是否可能通过减少儿茶酚胺和血管加压素的释放来调节PNO诱导的血流动力学变化。
机械因素和神经体液因素均促成了二氧化碳PNO诱导的血流动力学变化。已经提出了几种介质,但尚无研究将血流动力学变化与这些潜在介质水平的变化相关联。
我们进行了两项研究,每项研究包括20例计划进行择期腹腔镜胆囊切除术的健康患者。在第一项研究中,在腹腔镜检查期间和放气后进行血流动力学的连续测量(热稀释技术)。在相同时间点测量血浆皮质醇、儿茶酚胺、血管加压素、肾素、内皮素和前列腺素的浓度。在第二项研究中,患者在PNO前被随机分配接受1小时内输注8μg/kg可乐定或安慰剂。在PNO期间和放气后测量血流动力学以及血浆皮质醇、儿茶酚胺和血管加压素水平。
气腹导致心输出量显著降低(18±4%),平均动脉压升高(39±8%),全身血管阻力(70±12%)和肺血管阻力(98±18%)增加。腹腔镜检查导致血浆皮质醇、肾上腺素、去甲肾上腺素和肾素浓度逐渐且显著升高。血管加压素血浆浓度在PNO开始后立即显著升高(PNO前6±4 pg/ml;PNO期间129±42 pg/ml;p<0.05)。血管加压素释放曲线与全身血管阻力变化的时间过程平行。前列腺素和内皮素没有显著变化。可乐定显著降低平均动脉压、心率和全身血管阻力的增加。可乐定还显著降低儿茶酚胺浓度,但未改变血管加压素和皮质醇血浆浓度。
血管加压素和儿茶酚胺可能介导了PNO期间观察到的全身血管阻力增加。PNO前使用可乐定可减少儿茶酚胺释放并减轻腹腔镜检查期间的血流动力学变化。