Effect of extracellular volume expansion and surgical stress on splanchnic blood flow and cardiac output in anesthetized rats: role of nitric oxide

In a normal volume state, surgical stress decreases rather than increases nitric oxide (NO) production in the vascular system. In our studies, the effect of minor and major surgical stress and three different degrees of volume expansion on systemic and splanchnic circulatory parameters and on the NO dependence of the circulation have been investigated. When the degree of volume expansion was increased, cardiac output and organ blood flow increased without significant change in vascular resistances. Major surgical stress reduced the increase in cardiac output and organ blood flow elicited by the volume expansion. NO synthase (NOS) inhibition significantly increased blood pressure and total peripheral resistance (TPR) and decreased cardiac output in all groups of animals. As the degree of volume expansion was increased, the NO dependence of the circulation in the surgically less- and more-stressed animals was inversely influenced in some cases. With the three degrees of volume expansion (20, 40, and 60 ml/kg), the NOS inhibition increased the TPR from 30.7 R/kg +/- 1.90 to 73.6 R/kg +/- 5.00, from 20.7 R/kg +/- 1.43 to 66.7 R/kg +/- 3.88, and from 19.9 R/kg +/- 1.25 to 49.1 R/kg +/- 3.84 in the surgically less-stressed animals and from 38.6 R/kg +/- 2.14 to 59.8 R/kg +/- 5.62, from 31.9 R/kg +/- 2.70 to 81.7 R/kg +/- 9.89, and from 29.1 R/kg +/- 2.49 to 91.1 R/kg +/- 6.36 in the surgically more-stressed animals. Volume expansion increases the NO dependence of the vascular resistance in the surgically more-stressed animals but decreases it in the surgically less-stressed animals.