THE INFLUENCE OF THORACIC EPIDURAL-ANESTH ESIA ON MESENTERIC TRACTIONRESPONSE

Abdominal mesenteric traction (MT) results in decreased mean arterial pressure (MAP), systemic vascular resistance (SVR) and increased cardi ac output (CO) [24, 25, 28]. This response is induced by a considerabl e release of prostacyclin (PGI(2)) [12, 26, 27]. Precipitous falls in systemic arterial pressure related to central and/or autonomic nervous reflex arcs also have been described during operations on the upper a bdominal viscera [14, 22, 29, 30]. Those hypotensive responses to visc eral traction appear to be transmitted along afferent fibres contained within the splanchnic nerves [17]. We investigated the influence of s upplementary thoracic epidural anaesthesia on mesenteric traction resp onse during major abdominal surgery. Methods. With the approval of the Human Investigation Review Board we studied 40 patients scheduled for major abdominal surgery (infrarenal aortic, gastrointestinal and panc reatic surgery) according to a prospective, randomized double-blinded protocol. Patients were randomized to two different anaesthetic regime ns. Patients in group 1 received general anaesthesia (GA n = 20) with 0.1-0.15 mg/kg midazolam and 10 mu g/kg fentanyl prior to skin incisio n. Maintenance included 65% nitric oxide in oxygen and 0.1 mg incremen ts of fentanyl as required. Group 2 patients (EA n = 20) underwent a c ombined technique of dose-reduced general anaesthesia and supplementar y continuous, thoracic epidural anaesthesia (bupivacaine 0.25%, sensor y blockade T4 to L13). In both anaesthesia groups ibuprofen (400 mg i. v.) or a placebo equivalent was administered 15 min before the inducti on of anaesthesia. MT was applied in a uniform fashion. Baseline value s preceded the incision of the peritoneum. Further assessments followe d 5, 15 and 30 min after MT. The plasma concentrations of 6-keto-PGF(1 alpha) (stable metabolite of PGI(2)), TXB(2) (stable metabolite of th romboxan), PGF(2 alpha) KH2-PGF(2 alpha) (stable metabolite of PGF(2 a lpha)) were determined by radioimmunoassay. At all assessments we reco rded systolic and diastolic blood pressure, heart rate and measured ar terial blood gases. Statistical analyses were performed using three-fa ctor ANOVA for repeated measurements after log(x) transformation. A P- value of less than 0.05 was considered significant when the Bonferroni -Holm adjustment was applied. Results. Patients with supplementary epi dural anaesthesia demonstrated lower systolic (P=0.0001) and diastolic (P=0.006) blood pressure than those in the GA group. Nevertheless, in untreated patients in the EA and GA group there was a significant dec rease of about 20-30% in systolic and diastolic blood pressure (P=0.00 01) after mesenteric traction. Irrespective of the anaesthetic procedu re, paO(2) (P=0.0001) decreased after mesenteric traction in the place bo group. The control patients in the GA group exhibited a more pronou nced increase in heart rate after MT. After traction on the mesentery a significant 20- to 30-fold increase in 6-keto-PGF(1 alpha) plasma co ncentrations occurred in the placebo group: GA group 1950/58 (5 min), 1574/59 (15 min) 858/66 (30 min) ng/l, P < 0.0001; EA group: 2002/106 (5 min), 2955/107 (15 min) 1807/70 (30 min) ng/l, P < 0.0001, for plac ebo vs ibuprofen. There was no statistically significant difference be tween the two anaesthetic procedures used. In ibuprofen-pretreated pat ients haemodynamics and paO(2) values were stable, while 6-keto-PGF(1 alpha) plasma concentrations remained within the normal range. Conclus ion. Our data clearly indicate that the mesenteric traction response c onsists in relevant haemodynamic alterations and a significant decreas e of paO(2). Stable haemodynamics and paO(2) following cyclooxygenase inhibition signify an action mediated by prostacyclin. Deafferentiatio n of the splanchnic nerves by supplementary thoracic epidural anaesthe sia did not influence either prostacyclin release or the decrease in b lood pressure and paO(2) after traction on the mesentery root. A centr al nervous or sympatho-adrenergic reflex are transmitted along afferen t fibers of the splanchnic nerves seems to be unlikely as a pathophysi ological determinant of mesenteric traction response.