Is Laparoscopic Surgery Associated with Specific Hemodynamic Changes?

We read with interest the study by Mann et al. (1), which shows that a specific antagonist of vasopressin receptor suppresses hemodynamic changes associated with CO2 pneumoperitoneum under isoflurane anesthesia in pigs. However, we do not agree with the conclusion that their data support the hypothesis of a specific hemodynamic response to laparoscopic surgery caused by vasopressin release. Indeed, conflicting hemodynamic changes have been reported in association with laparoscopic surgery in humans and in animals (1–7). For example, the cardiac index either decreased significantly (2) or did not change significantly (3) during laparoscopic surgery. Also, afterload indices increased significantly after the induction of pneumoperitoneum (2–4). However, subsequently, afterload variations persisted, until pneumoperitoneum was released (2), or were not sustained throughout the pneumoperitoneum period, even though intraabdominal pressure remained high (4). Nonetheless, vasopressin release has been previously observed in association with hemodynamic changes during laparoscopic surgery (5). However, Odeberg et al. (6), failed to show any significant vasopressin release in association with significant hemodynamic changes in 20 patients undergoing laparoscopic surgery. More importantly, general anesthesia was maintained with only isoflurane in the Mann et al. (1) study, and no opiates were administered for intraoperative analgesia during this procedure (1). Consequently, the authors cannot rule out that they mainly observed and suppressed both a hemodynamic and a humoral response to a nonspecific surgical stress initiated by a noxious peritoneal stimulus. Indeed, surgical stress is associated with a vasopressin release graded to surgical injury (8). Thereafter, in response to surgical stress, vasopressin release (a) causes arterial pressure and afterload increases and (b) subsequently modifies cardiac index (8). In addition, intraoperative opiates administration suppresses both hemodynamic changes and vasopressin release associated with a nonspecific surgical injury (9). In this respect, no hemodynamic changes were observed in association with a CO2 pneumoperitoneum up to 15 mm Hg in pigs when general anesthesia was maintained by using large-dose fentanyl (7). Peritoneum is highly reactive to CO2, as opposed to argon used in the control group (10). This is likely to explain why the pressor response to peritoneal CO2 was higher than the pressor response to peritoneal argon in the present study (1). In contrast with Mann et al.’s (1) conclusions, we suggest that hemodynamic changes and vasopressin release reported with CO2 pneumoperitoneum in their study, and suppressed by using vasopressin antagonists, may have been caused by a noxious effect with no specificity. In this respect, one may question whether an opiate administration could have suppressed hemodynamic changes associated with vasopressin release reported in this study more physiologically than the administration of a vasopressin antagonist. In our opinion, the reality of a specific vasopressin-related hemodynamic response to laparoscopic surgery is still not proven. C. Lentschener MD D. Benhamou MD