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J Am Coll Cardiol, 1998; 32:1389-1396 © 1998 by the American College of Cardiology Foundation |
* Department of Anesthesiology and Intensive Care Medicine, University Hospital of Liège, Liège, Belgium
Department of Gastrointestinal Surgery, University Hospital of Liège, Liège, Belgium
Department of Endocrinology, University Hospital of Liège, Liège, Belgium
Manuscript received April 13, 1998; revised manuscript received June 25, 1998, accepted July 15, 1998.
Address for correspondence: Dr. Jean Joris, Department of Anesthesiology and Intensive Care Medicine, CHU of Liège, Domaine du Sart Tilman, B-4000 Liège, Belgium
mlamy{at}chu.ulg.ac.be
Objectives. 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.
Background. 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.
Methods. 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 µg/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.
Results. 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.
Conclusions. 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.
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