Yilmaz E N, Vahl A C, van Rij G L, Vink G Q, Lange-De Klerk E S, Brom H L, Rauwerda J A
Institute for Cardiovascular Research, Dept. of Vascular Surgery, Academic Hospital Vrije Universiteit, Amsterdam, The Netherlands.
Cardiovasc Surg. 1999 Aug;7(5):539-44. doi: 10.1016/s0967-2109(99)00009-5.
Colonic ischaemia is a serious complication after aortic surgery, and is most frequent after repair of ruptured aortic aneurysms. It was felt that the increased risk of colonic ischaemia during shock might be the result of a local effect of the renin-angiotensin system in the splanchnic circulation, which is exacerbated by poor perfusion. In order to evaluate the activity of the renin-angiotensin system in the colonic circulation, a subtotal occlusion of the distal aorta was induced in nine pigs. A colonic flow reduction of 70% was created for 4 hours. In the experimental group (n = 6), induce hypovolaemic shock, 20 cm3/kg blood was sampled at 45 min before resuscitation was performed with 20 cm3/kg haemaccel. The sham group (n = 3) did not have hypovolaemic shock induced. Blood samples were taken for determinations of angiotensin II, haemoglobin and lactate. Blood gas was obtained from the pulmonary artery and the caudal mesenteric vein for blood gas analysis and lactate determinations. ANOVA and the Wilcoxon sum rank test were used for statistical analysis. There was a significant increase in angiotensin II after induction of ischaemia in both groups. The increase in angiotensin II in the splanchnic circulation was more prominent than the increase in the systemic circulation (P < 0.01). In the experimental group, there was a sustained increase in angiotensin II levels in the splanchnic circulation following shock and reperfusion (P < 0/01). The increase in lactate concentrations, which was significantly higher in the experimental group (P < 0.05), was evidence of intestinal ischaemia. There was a significant decline in cardiac output and blood pressure during the period of shock (P < 0.05). The combination of colonic ischaemia and hypovolaemic shock followed by reperfusion leads to an increase in angiotensin II activity. The increase of the local activity of the renin-angiotensin system in the splanchnic circulation is more prominent after ischaemia and reperfusion. This is probably caused by a selective response of the splanchnic vasculature to shock, ischaemia and reperfusion.
